Biochem - M🐈 (Ez,aa,dna,gene Control Mutation)

Front 1

Glutamine code

Back 1

Gln- Q

Front 2

Lysine and Leucine 3-1 code

Back 2

Lys K and Leu L

Front 3

Asparagine,Aspartate,Alanine,Arginine (3,1)

Back 3

Asn N, Asp D , Ala A, Arg R

Front 4

Which AA has no chiral carbon

Back 4

Glycine

Front 5

Which two AA are alpha helix breakers and why

Back 5

Gly and Pro

Front 6

Where is Cysteine in reduced form and in oxidised form

Back 6

Intracellular and extracellular respectively

Front 7

What is pI and How to find pI

Back 7

Neutral. Average of pKA of all functional groups.

Front 8

What happens to AA if pH is above pI . What form ? And how does carboxylic acid and amino group looks like

Back 8

Deprotanated. NH2 AND COO- . CHARGE NEGATIVE

Front 9

Ez that creates peptide bond

Back 9

Ribonucleases

Front 10

Name 4 Ez startegies or method of actions

Back 10

1. Acid/base catalysis 2. Covalent catalysis 3. Electrostatic catalysis4.proximity and orientation catalysis

1. Acid/base catalysis 2. Covalent catalysis 3. Electrostatic catalysis4.proximity and orientation catalysis

1. Acid/base catalysis 2. Covalent catalysis 3. Electrostatic catalysis4.proximity and orientation catalysis

1. Acid/base catalysis 2. Covalent catalysis 3. Electrostatic catalysis4.proximity and orientation catalysis

Front 11

Whats the cofactor that helps DNAP to stabilize DNA(-ve charge) during replication and what strategy of catalysis is this

Back 11

Mg2+, electrostatic catalysis

Front 12

What does proximity and orientation effect does in enzyme catalysis? In your conceptual understanding.

Back 12

Increases frequency of collision of molecules that enables successful reactions

Front 13

Highest energy point on the path from A(reactant) to B(product) in reaction coordinate diagram

Back 13

Transition state G‡

Front 14

What's ΔG‡ : free energy of activation?

Back 14

Difference between initial state(energy) and Transition state energy.

Front 15

Net free energy? Difference between Initial state and end state? Does it get changed by the enzyme?

Back 15

Standard free energyΔG°

No

Front 16

A negative ΔG!

Back 16

a negative ΔG suggests that the reaction can occur on its own without needing an external push. It's like saying the reaction "wants" to happen because it leads to a more stable and lower-energy state. This is often associated with processes moving towards equilibrium, where the system becomes more balanced and stable over time. ( Final- initial .. negative) Learn thermodynamics

Front 17

Which AA forms disulfide bond

Back 17

CYS/C

Front 18

What's does the Ez lowers in reaction to speed up?

Back 18

ΔG‡ : free energy of activation

Front 19

Ez of peptide bond formation

Back 19

Peptidyl transferase

Front 20

Lyases

Back 20

Dissociate molecule in to 2 without water or oxidation or reduction.

Their role is mainly in rearranging chemical structures to facilitate bond cleavage or formation.

Front 21

Difference between Cofactor and Coenzymes. They both assist Enzymes

Back 21

Cofactor: -Nature: Inorganic or non-protein molecules. -Examples: Metal ions (zinc, magnesium). - Function: Stabilize proteins or participate in catalysis.Coenzyme: Nature:Organic molecules, often from vitamins. -Examples: NADH, FADH2. - Function: Carry/transfer functional groups or electrons in enzymatic reactions.

Front 22

What happens when Cells Na+/K+ stops working?

Back 22

Gets hypotonic and swell(water gets inside)

Front 23

What is Km in Michaelis-Menten eqn

Back 23

Km is the [S] when our rate of reaction or speed of Rxn is half the Vmax or Vmax/2

Front 24

What's Michaelis-Menten eqn

Back 24

Vo= Vmax[S]/Km+[S]

Front 25

When does Enzyme has highest affinity to its Substrate? @ low Km or High Km.

Back 25

Low Km.

In the Michaelis-Menten equation, a lower Km (Michaelis constant) indicates a higher affinity of the enzyme for its substrate.

Front 26

What's the eqn that says Enzymes turnover number?

Back 26

Kcat = Vmax/[E]t

Front 27

What's steady state assumption in Enzymes? This brings out the Michaelis-Menten eqn for a hint

Back 27

Formation of ES = Loss of ES, ES is always loaded

Front 28

What's the use of Michaelis-Menten equation and what are the variables

Back 28

The Michaelis-Menten equation is used to describe the rate of enzymatic reactions. It relates the initial reaction rate Vo to the substrate concentration [S] where substrate is the molecule upon which the enzyme acts. The equation is:Vo= Vmax[S]/Km+[S]

Km= Mentalis constant( [S] at 1/2 Vmax)This equation helps understand how quickly an enzyme can convert substrate to product under different substrate concentrations.

Front 29

What's Cooperativity:

Back 29

substrate binding changes substrate affinity

Front 30

Homotropic inhibitor

Back 30

a molecule that serves as both a substrate and a regulator for an enzyme. In the context of ATP and phosphofructokinase in glycolysis, ATP is indeed a homotropic regulator, as it acts both as a substrate for the enzyme and as an allosteric inhibitor, influencing the enzyme's activity based on its concentration.

Front 31

Herterotrophic activator

Back 31

Substrate and Allosteric regulator are different molecules

Front 32

Coenzymes are organic _____ molecule,

Whereas Cofactors takes part in _____

Back 32

Carrier, Catalysis

Front 33

Catalytic efficiency eqn

Back 33

Kcat/Km

Front 34

Difference b/w competitive binding and allosteric

Back 34

Competitive ligands bind in the active site of a protein while allosteric ligands exhibit their effect from a remote location on the protein

Front 35

List all non-ez protein types

Back 35

Receptors,channels,transport,motor,antibodies

Front 36

What are suicide inhibitors

Back 36

Ez inhibitors that covalently and permanently binds the target.

Front 37

An organ secrete the zymogen, that turns into it a useful proteases by covalent modification catalyzed by an enzyme, in intestine. What's the organ ,name of the zymogen and name of the protease it turns into and Enzyme that catalyze this turning.

Back 37

Pancreas, Trypsinogen,Trypsin ,enterokinase

Front 38

Ribosomes subunits of euk and prok

Back 38

60s;40s 50s;30s

Front 39

Directionality of reading .

(Whats read not what is produced)

1.DNA replication (DNAP):

2.Reverse transcripts(Rev,transcriptase)

3. Transcription

4.Translation

Back 39

1.DNA replication (DNAP): 3'=>5'( copy 5' to 3')

2.Reverse transcripts(Rev,transcriptase).3'=>5'

3. Transcription. 3'=>5' (like replication).

4.Translation 5' to 3"

So every dna Synthesis is read I'm 3 to 5 and protein is 5 to 3

Front 40

Every nt acid strand Synthesis reads template strand in what direction

Back 40

3' to 5'

Front 41

What prevents reannealing during DNA replication.

Back 41

Single-stranded DNA-binding proteins (SSBs) play a crucial role in preventing reannealing during DNA replication

Front 42

What relieves tension in DNA strands by introducing temporary breaks, facilitating unwinding during processes like replication.

Back 42

Topoisomerase

Front 43

What does primase do in replication

Back 43

Primase synthesizes short RNA primers that provide starting points for DNA polymerase during DNA replication.

Front 44

What does DNAse do?

Back 44

DNase breaks down and hydrolyzes DNA by cleaving the phosphodiester bonds between nucleotides, playing a role in DNA degradation and removal.

Front 45

What are telomeres and Telomerase, and function

Back 45

Repeats at the end ,to prevent erosion effect during replication and Chromosomes sticking together.

Telomerase lengthens the Telomeres

Front 46

Where is repetitive dnas found on Chromosomes

Back 46

Towards the middle/centromere

Front 47

What has High mutation rate, Repeatative or Single Copy DNA?

Back 47

R

Front 48

What has important genes, Single Copy or Repeatative DNA

Back 48

S

Front 49

What unwinds DNA temporarily for replication?

Back 49

Topoisomerase. Mainly in replication. In Transcription RNAP does most

Front 50

Around what speed is DNAP action

Back 50

700+ base/sec

Front 51

Around what precision is DnAP

Back 51

Approx 1 mistake per 10^9 nt, after proofreading ( 1 per 10^7 before pr)

Front 52

Whats the start codon and AA it's characteristics

Back 52

AUG: Met,M, methionine: nonpolar aliphatic Sulphur containing AA

Front 53

Catalytic efficiency eqn

Back 53

Kcat/Km

Front 54

What direction does the DNA grows

Back 54

5' to 3'. Nucleotides get added to 3' end of existing strand

Front 55

What does Kcat or Turnover number gives

Back 55

Vmax/Et

this ratio gives you insights into the efficiency of the enzyme by considering the speed at which it operates (maximum velocity) relative to the total enzyme concentration.

Front 56

How many Codons possible?

Back 56

3 spots,4 Bases => 4×4×4=64

Front 57

How many stop codons? And what are they

Back 57

UAA,UAG,UGA

Front 58

What are the 3 sites of RBsM

Back 58

Aminoacyl-tRNA site,Peptidyl-tRNA,Exit site, = APE

Front 59

What's the rbsm binding spot on prok

Back 59

Shine-Dagarno sequence

Front 60

First AA of prokaryote

Back 60

Formylmethionine(fMet)

Front 61

What's 5' cap in euk mRNA? What is it modified from? How is it linked to the mRNA

Back 61

7-methylguanosine, The 5' cap is a modified guanosine triphosphate (GTP) molecule linked to the mRNA through an unusual 5'-5' triphosphate bridge.

Front 62

What's at the 3'end of mRNa..? Roughly how long is it.

Back 62

Poly A tail 250++

Front 63

Rbsm binding spot of euk mRNA

Back 63

5'cap

Front 64

First AA of euk protein and what's the codon

Back 64

Methionine; AUG

Front 65

A brief overview of DNAP-III? Does it do exonuclease activity? What's the direction of that activity? How does this do

Back 65

It synthesise DnA as well as proofread and repair by exonuclease activity. It sense the mistake and reverse and correct it. Therefore 3' to 5' activity .

Front 66

A brief overview of DNAP-I? Does it do exonuclease activity? What's the direction of that activity? How does this do

Back 66

It's mainly for repair unlike DNAP-III (both). It has exonucleatic activity in both direction, 5 to 3 and 3 to 5 .

It's involved in removal of RNA primers from okazaki fragments and add nucleotides there.

Front 67

What's mismatch repair mechanism? How it operates

Back 67

It's repair after replication

First make a cut ✂️ at the mismatch

Then exonuclease removes

Then DNAp adds correct nt

Then DNA ligase sticks.

How does it know which one is a mismatch? I don't know

Front 68

What does UV rays cause on DNa

Back 68

Pyramidine dimers- melanoma

Front 69

Name a famous endogenous dna damager

Back 69

Reactive oxygen species;

Superoxide anions, peroxides( comes from ETC byproducts) so it's very common. Highly reactive: oxidative s

Antioxidants helps here. Vitl C E

Front 70

Difference between exonuclease activity and endonuclease activity

Back 70

Endonucleases cut within the nucleic acid chain at specific sites, while exonucleases remove nucleotides from one or both ends. Endonucleases play roles in repair and restriction, and exonucleases contribute to processes like proofreading during DNA replication. Both activities are essential for maintaining genetic integrity.

Front 71

Nucleotide excision repair

Back 71

DnA damage repair mechanism.

Specialized proteins (endonucleases) recognize the damage, excise the affected section, and allow DNA polymerase and ligase to replace and seal the gap,

Front 72

What are 3 consequences if Dna damage doesn't get repaired and damaged get accumulated

Back 72

1. Dormant DNA

2. Apoptosis

3. Cancer

Front 73

What are three models of DNA replication and what came proved of these 3 and what experiment concluded that

Back 73

Conservative,Dispersive,Semi-conservative.- Meselson-Stahl experiment

Front 74

What are two modification of protein: and which one is common, give an example of each

Back 74

Co translation : acetylation of first A

Post translation(common) : glycosylation

Front 75

P. Post modification ,that's on the membrane.

Give a brief description of eacch.

Where does the modification occurs

Back 75

Glycosylation : on receptor P. , addition of CarbH eg: blood group

Lipidation: addition of lipids. To anchor proteins to membrane.

Eg: GPI anchor

ER/GA

Front 76

What is ubiquitinuation

Back 76

It is a post-translational modification.

Adding Ubiquitine to P.

It mark down P. For degradation.

Front 77

What's proteolysis mod of P.

Back 77

It cuts inactive P. (Zymogens) To activate them .

Eg: insulin

Front 78

What has lac operon,, euk or Prok

Back 78

Prok. Eg : Ecoli

Front 79

What has lac operon,, euk or Prok

Back 79

Prok. Eg : Ecoli

Front 80

What are 3lac operon genes and their product: and functions?

Back 80

Lac y: lactose permease ( brings lactose)

Lac Z: B galactosidase

Lac A: beta-galactoside transacetylase. Something for lactose metabolism, don't worry

Front 81

Which carbon of deoxribose of DNA has no Oxygen

Back 81

2'

Front 82

Where does new nucleotide connects to existing strand.

What'd the bond

Back 82

5' of Pi, connect to 3' OH of existing strand . Phosphodiester bond

Front 83

What enzyme is involved in forming of phosphodieterbond in DNA Synthesis. And what's this process called

Back 83

DnA polymerase. Dehydration synthesis

Front 84

A and T has how many acceptor and How many Donor, of hydrogen Bond?

What about C and G

Back 84

- A&T: 1 Hbond acceptor ,1 donor each , (so two bonds)- C&G: 1Hbond Donor,2 acceptor; One acceptor and 2 Donor ,respectively.(so 3 bonds)

Front 85

Scientist who studied complementary base pairing

Back 85

Erwin Chargaff

Front 86

How many codes by codon. How many are Protein coding

Back 86

64

61codes AA (3 stops)

Front 87

Talk about acetylation in Gene regulation .

Back 87

In Gene regulation Acetyl is like a key🔑 that goes on the histone drawer where DNa is wrapped, and once the key is inserted, it unravel DnA and cause Gene expression. And it's removal keep the DnA locked.Histone AcetylTransferase(HAT) is the enzyme that add Acetyl.

Deactylation (by histone deactylases- HDACs) locks the DNa

Front 88

Methylation In Gene regulation ?

Where is methyl group added?

What does it do?

Back 88

Adding Ch3- group to CgP islands.

Recruit methyl-CpG binding domain proteins, which can lead to chromatin compaction and inhibition of transcription factor binding..

Gene silencing and repression.

Inheritable epigenetic regulation

Front 89

Main function of miRNA

Back 89

Binds to 3' UTR.

Once bound, miRNAs can inhibit translation of the mRNA into protein or promote degradation of the mRNA, leading to reduced levels of the corresponding P.

Front 90

What's operon

Back 90

An operon is a unit of genetic material in bacteria and archaea consisting of multiple genes under the control of a single regulatory region. Eg : lac operon

Front 91

Draw the order of regions in lac operon

Back 91

Promoter--operator--lacz--lacy--laca--

Front 92

1. How is Glucose availability doesn't express Lac operon?

2. How about when Glucose Low?

3. How is glucose availability cause to stop lactose binding on repressor protein hence the expression of Lac operon?

Back 92

1. Glucose is plenty. Good for energy. Low concentration of cAMP. And lact operon kept repressed.

2.when Glucose is low. cAMP goes up, forms cAMP-CRP complex which increasing RNAP binding to the promoter of lac operon. And allolactose (isomer of lactose and its metabolite) binds to repressor P. And expression of operon.

3. When Glucose gets available, [Inducer Exclusion] : intermediary P. Binds to Lactose Permease and inhibits activity that is bringing anymore Lactose to cell,that repress the repressor

Front 93

How many histones in one nucleosome(octamer)- what are each kind.And how many DNA wrapped around one nucleosome

How many histones in one nucleosome(octamer)- what are each kind.And how many DNA wrapped around one nucleosome

Back 93

4 x 2= 8 histones

4 types are H2A,H2B,H3,H4.

About 147 bp of DNA.

Front 94

What terminal of histone, acetylation done. What enzyme does this?

What removes the acetyl?

Back 94

Amino trail.

HAT and HDAC, respectively.

Front 95

Whats unpacked chromatin called(by acetylation)?

What's packed chromatin called(deactylation)?

Back 95

Heterochromatin. (H for hug)

Euchromatin

Front 96

What is epigenetics? And three ways of epigenetic mechanism.

Back 96

Epigenetics refers to heritable traits that are not a consequence of DNA sequence. Three classes of epigenetic regulation exist: DNA methylation, histone modification, and noncoding RNA action.

Front 97

What does Methylation does

Back 97

Gene silencing

Front 98

How does methylation impedes transcription

Back 98

● it cause a P. To bind on it (MBD) which recruits other Proteins such as HDAS => which modifies histones=> leading to increasing compaction of Chromatin or Heterochromatin.* can become binding of P. That recruits chromatin remodeling complex, that remodels DNa in a way restricts access and thus gene silencing.* it can also blocks TF from binding DNA for Transcription

● can become binding region of P. ,that recruits chromatin remodeling complex, which inturn remodels DNa in a way that restricts access to it and thus gene silencing.

● it can also blocks TF from binding DNA for Transcription

Front 99

Components of Basic Transcription apparatus for mRNA

Back 99

Gen TF,RNAP,mediator multiple complex.

Front 100

What does activators do ?

Back 100

Enhances RNAp and promoter interaction.

Front 101

How does activators works?

Back 101

Either by interacting with subunits of RNAP or indirectly by changing the structure of DNA.

Eg : CAP in Lac operon. I hope you remember what does it do. If not go this way,

Find what happens with Lac operon during Glucose starvation

Front 102

What are Enhancers, in Gene regulation

Back 102

Enhancers are DNA sequences that enhance gene transcription by binding transcription factors. They can regulate genes over long distances by forming DNA loops that bring them (initiation complexes) into proximity with gene promoters, facilitating gene expression.

Front 103

What are silencers

Back 103

It's like enhancer seq upstream or downstream of promoter, where repressor P. Binds to prevent RNAP binding and thus gene expression

Front 104

Difference b/w prokaryotic and eukaryotic gene regulation

Back 104

Prokaryotic gene regulation primarily occurs at the transcriptional level, often involving operons in a single circular DNA molecule. Eukaryotic gene regulation is more complex, involving multiple levels (transcriptional, post-transcriptional, translational, and post-translational) in the context of a nucleus housing linear chromosomes.

Front 105

3 fn of 5'cap

Back 105

>prevents degradation by exonucleases

>regulation of nuclear export of mrNA

>binding of Rbsm

Front 106

Ez for poly A tail

.function?

Back 106

polyadenylate polymerase.- Act as a buffer for exonucleases thus prevents degradation.- Help with promoting translation and nuclear export

polyadenylate polymerase.- Act as a buffer for exonucleases thus prevents degradation.- Help with promoting translation and nuclear export

Front 107

Rna editing

Back 107

RNA editing is a process by which the nucleotide sequence of an RNA molecule is altered after transcription, leading to changes in the final RNA product. This can involve substitutions, insertions, or deletions of nucleotides. RNA editing occurs through enzymatic reactions that modify specific RNA sequences, resulting in diversity in RNA transcripts and potentially generating protein isoforms with different functions.

Front 108

An example of RNA editing: A to I.

Catalyzed by ? How?

Back 108

Ez Adenosine Deaminase (ADAR): hydrolytic deamination.

Front 109

Name 3 non coding RNA

Back 109

rRNA,tRNA,miRNA

Front 110

What is snoRNA? What does it do

Back 110

Small nucleolar RNA- Guides covalent modification of rRNA,tRNA,snRNA=>Primarily through methylation or pseudouridylation

Front 111

snRNA

Back 111

: process pre-mRNA,

Components of spliceosome ( plus 150 P.)

Front 112

Simple action description of Spliceosome

Back 112

binds to specific seq⇒does 2 sequential transesterification rxn and then ligate the 2 exons.

Front 113

Three,situations where Proto-Oncogene becomes oncogenes

Back 113

1. Deletion/point mutation ⇒ hyperactive P. Or overexpressed P.2. Gene amplification or increase mRNA stability⇒ prolonged existence leads to overexpression of Protein.3. Chromosomal rearrangement⇒ translocation of a gene to nearby regulatory sequences ⇒overexpression or fusion to actively transcribed gene which overexpress the fusion P. Or hyperactive fusion P.- So inC: either overexpress or produce hyper active one

Front 114

List famous protooncogenes and their brief description

Back 114

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The SRC gene codes for a protein called c-Src, which is a tyrosine kinase involved in cell signaling. It plays roles in cell growth, adhesion, and movement. When mutated or overactive, it can contribute to cancer development.RAS genes encode proteins involved in cell signaling( like switches), crucial for growth and differentiation. Mutations in RAS genes are common in cancer and are important targets for cancer therapy. Codes P.(GTPase). HRAS,NRAS,KRAS are all RAS family.The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation. Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

The MYC gene encodes a protein called c-Myc, which regulates cell growth and is often deregulated in cancer, making it a key target for cancer therapy research. Codes fir TF that induces cell proliferation.

Eg: Burkitts lymphoma: due to common translocation b/w xsome 8(myc gene found) and Xsome 14.

RTK oncogenes are specific genes encoding receptor tyrosine kinases that, when mutated or overexpressed, promote cancer development by driving abnormal cell signaling pathways.( it phophorylates Y on P. ,according to the signal. In cancer: signal constitutively.

Front 115

3 examples of RTK and prominent in causing cancer when dysregulated

Back 115

- vascular endothelial growth Factor(VEGF)- Epidermal Growth Factor( EGFR)- Platelet derived Growth Factor(PDGF).

Front 116

Whats Philadelphia Xsome

Back 116

The Philadelphia chromosome is a chromosomal abnormality caused by a specific translocation between chromosomes 9 and 22. It results in the formation of a fusion gene called BCR-ABL, which is associated with chronic myeloid leukemia (CML) and some cases of acute lymphoblastic leukemia (ALL).

Front 117

What are tumor suppressor G.

Back 117

- Genes whose product has either halting effect on regulation of cell cycle or can promote apoptosis or sometimes both.

Front 118

Whats Two Hit Hypotheses

Back 118

Two Hit Hypotheses : both alleles must be mutated, before the effect is manifested

Front 119

What's p53, what gene codes it .

Back 119

p53 is a protein that safeguards cells from becoming cancerous. It does so by regulating DNA repair, pausing cell division for repair, and triggering cell death if damage is irreparable.

TP53.

Front 120

What's two hit hypothesis in Tumor suppressor genes and name a P. That is tumor suppressor some kinds of which doesn't follow this hypot

Back 120

According to this hypothesis, both copies of a tumor suppressor gene must be inactivated or mutated (hit) in a cell to lose its tumor-suppressing function and contribute to cancer development..

P53

Front 121

What's the mutation in Sickle cell disease, and the consequences?

Back 121

Mutation in gene HBB, that codes Beta Globulin . GLU=>VAL. Results in HbA to Hbs, which becomes Sickle shaped in low O2 condition

Mutation in gene HBB, that codes Beta Globulin . GLU=>VAL. Results in HbA to Hbs, which becomes Sickle shaped in low O2 condition

Front 122

Stem cell and the process name ,of RBC generation

Back 122

Hematopoetic stem cell .

Hematopoesis.

Front 123

Typically,Level of mutation occurs and level at which it's effect is seen

Back 123

DNA; Protein

Front 124

Spontaneous mutation cause , list 4

Back 124

Replication error, environmental factors(UV radiation), endogenous (reactive Oxygen species), poisons

Front 125

Nonsense mutation

Back 125

Makes codon to a stop codon. Stops protein Synthesis in middle

Front 126

3 types of missense mutation

Back 126

Conservative, Silent,Non-Conservative

Front 127

3 causes/occurrence route of point mutation

Back 127

Transition, Transversion

Mispairing/mismatch

Front 128

Translocation and Inversion: mutation at Xsome level

Back 128

Translocation: swap b/w non-hmlogs Xsome

Inversion: Gene change b/w same Chromosomes.

*These mutation can also affect gene regulation.

Front 129

What are the endogenous mutagen that is related to O2.

What does they do

Back 129

Reactive oxygen species, such 02-,H202.

Base modification, double strand break,dNa depurination or depyrimidination,DNA-P. Cross link etc

Front 130

2 Example of (exogenous)

Back 130

Intercalators- Et Br

Base analogs- 5BU

Front 131

Gene in cystic fibrosis

Back 131

CFTR -

Front 132

Example of mutation that is both bad and good

Back 132

Sickle cell disease .

Aneamic but useful in malaria

Front 133

Complete,codominance, incomplete. Use an example to define

Back 133

Red over white, Red and white, Pink respectively

Front 134

to memorize for future calculations . Gives genotype and phenotype(complete) in answer.

1. AA x Aa

2. aa x Aa

3. AA x aa

4. Aa x Aa

Back 134

1. 50% AA 50% Aa : 100% A

2. 50% aa 50% Aa : 50%a 50%A

3. 100% Aa : 100% A

4. 25%AA 50%Aa 25%aa : 75%A 25% a

Front 135

Hardy-Weinberg assumptions

Back 135

No selection, large population, no mutation. For stable allele freq

Front 136

Hardy-Weinberg eqn and what is each term.

Back 136

P+q =1

p2+2pq+q2= 1.

p2 => homozygous Dominance

q2 => homozygous recessive

2pq=> heterozygous

Front 137

Gel Electrophoresis

Back 137

**Gel Electrophoresis**:- **Purpose**: Separate and analyze DNA, RNA, or proteins based on size and charge. - **Setup**: Gel (agarose or polyacrylamide) in tray with buffer solution and wells for sample loading.- **Process**: Apply electric current; molecules move towards positive electrode. Smaller molecules move faster, larger ones slower.- **Separation**: Molecules separate based on size as they move through the gel.- **Visualization**: Stain gel, visualize bands under UV light. Or ethidium bromide intercalators, fluorescent under UV light - **Analysis**: Compare band positions to molecular weight markers to determine sizes.

Front 138

PCR

Back 138

**PCR (Polymerase Chain Reaction)**:- **Purpose**: Amplify specific DNA sequences for analysis.- **Steps**: 1. **Denaturation**: Heat separates DNA strands. 2. **Annealing**: Primers bind to target sequences. 3. **Extension**: DNA polymerase synthesizes new strands.(taq polymerase) - **Cycles**: Repeated multiple times (usually 20-40 cycles). - **Result**: Exponential amplification of target DNA.- **Applications**: DNA sequencing, genotyping, gene expression analysis, forensics.

Front 139

What is used to form cDNA from RNA

Back 139

Reverse transcriptase

Front 140

What makes dsDNa from cDNA

Back 140

dna polymerase

Front 141

What's used to cut dsDNA,

What cuts RNA

Back 141

Restriction enzymes.

Ribonucleases

Front 142

In Gene cloning. What is done to select bacteria containing plasmid of gene of interest from other bacteria colonies

Back 142

Antibiotic resistance gene is added to plasmid. Grown in Antibiotic mixed nutrients culture

Front 143

Microarray experiment

Back 143

Helps to study and compare upregulation/downregulation.

During a microarray experiment, fluorescently labeled nucleic acid samples (such as cDNA or RNA) from the organism of interest are allowed to hybridize to the DNA probes immobilized on the microarray surface. The labeled nucleic acids bind specifically to their complementary sequences on the array, forming double-stranded hybrids.

Front 144

Southern blotting

Back 144

**Southern Blotting:** A method to detect specific DNA sequences by transferring DNA fragments from a gel to a membrane, then hybridizing them with a labeled probe.

Front 145

What's the nucleotide added in DNA sequencing. What's the process called

Back 145

**Sanger Sequencing:**A technique for determining the sequence of nucleotide bases in a DNA molecule. It involves DNA replication in the presence of chain-terminating dideoxynucleotides (ddNTPs), which stop elongation at specific positions. Fragments of varying lengths are generated, separated by gel electrophoresis, and the sequence is deduced based on the size of the terminated fragments.

Front 146

What is Mentelis Eqn of Ez? When it is used / application ?

Back 146

Vo =(Vmax × [S])/Km+[S]

It says the observed

Rate Vo of an Ez- catalyzed reaction to the substrate conc. [S] by the constants Vmax and Km.

Any 3 values known, 4th can be calculated.

Front 147

What's specific activity of an Ez

Back 147

Front 148

Line weaver plot for inhibitions of Ez activities

Back 148

Front 149

What's the simple eqn for Vmax

Back 149

Vmax = Kcat x [S]

Front 150

What does Hills coefficient says in Enzymes

Back 150

Degree or nature of cooperativity. Denoted by 'n'If n>1 positiveIf n<1 negativeIf n=1 no cooperativity

Degree or nature of cooperativity. Denoted by 'n'If n>1 positiveIf n<1 negativeIf n=1 no cooperativity

Degree or nature of cooperativity. Denoted by 'n'If n>1 positiveIf n<1 negativeIf n=1 no cooperativity

Degree or nature of cooperativity. Denoted by 'n'If n>1 positiveIf n<1 negativeIf n=1 no cooperativity

Degree or nature of cooperativity. Denoted by 'n'If n>1 positiveIf n<1 negativeIf n=1 no cooperativity

Front 151

What kind of Ez is phosphatase

Back 151

Hydrolase- removes phosphate group by addition of water.

Front 152

6 categories of Ez

Back 152

6

Front 153

High yield characteristics of AA

Back 153

Front 154

When finding the charge of amino acids, what are some points to consider. Given a pH

Back 154

Count only the pkA at C terminus and N terminus . And also if there is any side chain. Pka of the group involved in amide bond is ignored.

Front 155

When finding the charge of amino acids, what are some points to consider. Given a pH

Back 155

Count only the pkA at C terminus and N terminus . And also if there is any side chain. Pka of the group involved in amide bond is ignored.

Front 156

Radom: What causes miosis and mydriasis at the Neuron level

Back 156

acetylcholine is responsible for pupil constriction (miosis). The dilation of the pupil (mydriasis) is primarily mediated by the sympathetic nervous system, specifically through the release of norepinephrine (noradrenaline) from sympathetic nerve endings onto the radial muscle of the iris. Therefore, activation of the sympathetic nervous system leads to pupil dilation, while activation of the parasympathetic nervous system, which releases acetylcholine, causes pupil constriction.

Front 157

What does mEselson Stahl experiment, discovered. Main player

Back 157

Dna replication is semiconservative.Heavy isotopes of Nitrogen and comparison of its mass with normal. "the most beautiful experiment in biology".

Dna replication is semiconservative.Heavy isotopes of Nitrogen and comparison of its mass with normal. "the most beautiful experiment in biology".

Dna replication is semiconservative.Heavy isotopes of Nitrogen and comparison of its mass with normal. "the most beautiful experiment in biology".

Front 158

All proposed model of DNA replication which one is true?

Back 158

Semiconservative

Front 159

Is Alzheimers caused by prions

Back 159

No, Alzheimer's disease is not caused by prions. It is primarily associated with the accumulation of abnormal protein aggregates, such as beta-amyloid plaques and tau tangles, in the brain. Prions are infectious proteins associated with diseases like Creutzfeldt-Jakob disease and mad cow disease, but they are not implicated in Alzheimer's.

Front 160

Why is DNAP, low error rate than RNAP

Back 160

DNAP has proofreading domain

Front 161

What genes code for DNA repair proteins

Back 161

Tumor suppressor genes

Front 162

Are histones acidic?

Back 162

No , basic

Front 163

All L - AA has S configuration, except for ?Why's it R and rest AA have S ?

All L - AA has S configuration, except for ?Why's it R and rest AA have S ?

Back 163

Cysteine.

We find config by numbering priorities ,

In L- AA, NH2 is on right

And in All except Cys, 1st priority is Amine group,2nd is Carboxy giving it S (anticlockwise).

In cysteine, the SH gets 2nd priority and it's R (clockwise)

Front 164

Identify L and D amino acid in Fischer projection

Back 164

In Fischer projections, if the Amino group is on the left side, it's a D-amino acid, and if it's on the right, it's an L-amino acid. This rule specialised for amino acids is the opposite of the general rule for Fischer projections.

Front 165

What AA has side chain Pka of greater than physiological (7.4) so that it's positive (protonated)

Back 165

KR

Front 166

Typical pKa value of ionizable group in proteins

Back 166

Pka values

Front 167

What's the charge of aspartic acid in physiological pH

Back 167

-ve

Front 168

What 2 AA are not good fit, with in the Alpha helix. Why

Back 168

Proline(kinker) and Glycine( small R group, instability)

Front 169

Side group of which AA are target for phosphorylation in biological settings

Back 169

YST

Front 170

Whats the rbsm binding site In prokaryotes

Back 170

The Shine-Dalgarno sequence is a ribosome binding site found in prokaryotic mRNA, aiding in translation initiation by facilitating the interaction between the mRNA and the ribosome.

Front 171

What group of cellular amino acid remains protonated in Physiological pH

Back 171

Amine group. It will stay as NH3+.

Front 172

What happens to amino acid in high pH,

And lowest pH

Back 172

Everything deprotanated .

Everything protonated

Front 173

What's the charge of Lysine at physiological pH

Back 173

+ve.

One deprotanated carboxylix acid.

2 -protonated amine group and R group.

Front 174

Groups will be protonated if pH of solution is ____ than pka and deprotanated if ______ than pla

Back 174

Lower ..

Higher

Front 175

What two levels of protein structures are affected by disulfide bridges

Back 175

3° and 4°

Front 176

Western blotting

Back 176

Western blotting, also known as protein immunoblotting, is a widely used laboratory technique to detect and analyze proteins. It involves separating proteins by size via gel electrophoresis, transferring them to a membrane, and then detecting specific proteins using antibodies that bind to them. This technique is valuable for studying protein expression, post-translational modifications, and protein-protein interactions in biological samples.

Front 177

How many peptide bonds in hexapeptide

Back 177

5.

(n-1)

Front 178

Pka of aspartic and glutamic acid

Back 178

4.1

Front 179

What's the R group of C

Back 179

Thiol or sulfhydryl group.

Front 180

AA with + and -ve charge in physiological pH

Back 180

-ve => ED

+ve => HRK

Front 181

Primary structure means

Back 181

The sequence

Front 182

Reason behind zig zag pattern, In beta pleated sheet

Back 182

Planar geometry of the C--C and C--N bonds.

Front 183

What kind of bond is disulfide bridge

Back 183

Covalent

Front 184

Only covalent bond that aids in Protein folding

Back 184

Disulfide bridge

Front 185

A protein that aid in folding of other proteins

Back 185

Chaperone

Front 186

Factors that denature protein: how

Back 186

pH : charge interaction b/w residues. Temperature: can disrupt hydrogen Bonding.Reducing Agent: disrupt Disulfide bridges.

pH : charge interaction b/w residues. Temperature: can disrupt hydrogen Bonding.Reducing Agent: disrupt Disulfide bridges.Organic solvent: can flip the Hydrophobic regions out,that generally hides when folded in aqueous environment.

pH : charge interaction b/w residues. Temperature: can disrupt hydrogen Bonding.Reducing Agent: disrupt Disulfide bridges.Organic solvent: can flip the Hydrophobic regions out,that generally hides when folded in aqueous environment.

Organic solvent: can flip the Hydrophobic regions out,that generally hides when folded in aqueous environment.

Front 187

3 Ez In Glycolytic pathway that can be allosterically regulated.

Name their +/-

Back 187

HexoK- (+ glucose, - G6P)

PhosphoFructoK-1 (+F26bp, - ATP)

Pyruvate K (+F16bp,-ATP)

Note: +F26bp,(this is made by pfk-1, activated by Insulin and inhibited by glucagon.

Front 188

6 classes of Ez

Back 188

Hydrolase,

Lyases,

Isomerase[epimerase],

Transferase,

Oxidoreductase,

Ligase.

Front 189

What activates and deactivates A-coa carboxylase.

Back 189

DePhosphorylation and Phosphorylation (inhibits)

Front 190

What activates and deactivates A-coa carboxylase.

Back 190

DePhosphorylation and Phosphorylation (inhibits)

Front 191

What does Adenylate Kinase do?

Back 191

Adenylate kinase is an enzyme involved in the transfer of phosphate groups between nucleotides. Specifically, it catalyzes the reversible transfer of a phosphate group from ATP to AMP, forming two molecules of ADP. This reaction helps maintain the balance of adenine nucleotides (ATP, ADP, and AMP) within cells, which is crucial for energy metabolism and various cellular processes.

Front 192

Amylase ?

Back 192

Amylase is an enzyme that breaks down starch and glycogen into simpler sugars.

Front 193

Lock and key,confinational selection, induced fit difference.

Back 193

While both "lock and key" and "confirmational selection" describe enzyme-substrate interactions, the former emphasizes the specificity of the interaction based on pre-existing shapes, while the latter highlights the dynamic nature of enzyme conformations and substrate selection.

the main difference lies in whether the enzyme's conformational state is static (confirmational selection) or dynamic (induced fit) upon substrate binding.

Front 194

Talk about intrinsically disordered region(IDR)

Back 194

Intrinsically disordered regions (IDRs) are segments within proteins characterized by the absence of a stable tertiary structure under physiological conditions. Unlike structured regions of proteins, IDRs typically lack hydrophobic residues and instead contain a high proportion of polar and charged amino acids. This structural flexibility enables IDRs to adopt multiple conformations and interact with various binding partners, contributing to their functional versatility in cellular processes such as signaling, regulation, and molecular recognition.

Front 195

What's Zymogen

Back 195

A zymogen is an inactive precursor form of an enzyme, requiring activation to become functional.

Front 196

Whats Ubiquitination?

Back 196

Ubiquitination is a cellular process where ubiquitin, a small protein, is attached to other proteins, regulating their functions, including degradation, signaling, and localization. It involves enzymes like E1, E2, and E3 ligases.

Front 197

Cofactors and Coenzymes

Back 197

cofactors are usually inorganic molecules or metal ions that directly participate in enzyme catalysis, while coenzymes are organic molecules that facilitate enzyme activity by carrying or transferring chemical groups or electrons.

Front 198

The Ez with higher Km value compared to another ,has ______ for its substrate.

Back 198

Lower

Front 199

What's specificity constant

Back 199

Kcat/Km

A higher specificity constant indicates a more efficient enzyme, as it reflects a higher turnover number or a lower Michaelis-Menten constant (indicating higher affinity for the substrate) or both. Enzymes with higher specificity constants can achieve higher reaction rates at lower substrate concentrations.

Front 200

Where does transcription happens

Back 200

Nucleus

Front 201

What's the space between two bilayers of Nucleus called

Back 201

Perinuclear space

Front 202

Bacteria ribosome and Eukaryotic ribosomes subunits and total weight

Back 202

50S + 30S => 60S

60S + 40S => 80S

Front 203

Bacteria ribosome and Eukaryotic ribosomes subunits and total weight

Back 203

50S + 30S => 60S

60S + 40S => 80S

Front 204

Cooperativity and

Back 204

Cooperativity refers to the influence of one ligand's binding on subsequent ligand binding in multi-subunit proteins, while allosteric regulation involves the modulation of a protein's activity through the binding of a regulatory molecule at an allosteric site, inducing conformational changes.

Front 205

What's hills coefficient for +ve cooperativity.

What's hills coefficient for +ve cooperativity. -ve cooperativity And non cooperativity

-ve cooperativity

And non cooperativity

Back 205

n>1

n<1

n=1

Front 206

What type of Ez is phosphatase

Back 206

Hydrolase.

It adds water to remover Phopshate

Front 207

Does methionine contains Sulfhydryl group

Back 207

No, methionine does not contain a sulfhydryl group. It contains a thioether functional group, which consists of a sulfur atom bonded to two carbon atoms. The sulfhydryl group, also known as a thiol group, consists of a sulfur atom bonded to a hydrogen atom (-SH), which is not present in methionine.(but cysteine does)

Front 208

Apart from peptide bond what bond does glutamine forms

Back 208

Hydrogen bonds

.

Front 209

What's transversion mutation

Back 209

A transversion mutation is a type of point mutation in which a purine base (adenine or guanine) is replaced by a pyrimidine base (thymine or cytosine), or vice versa, within the DNA sequence. This mutation results in the substitution of one type of nucleotide with another type of nucleotide that differs in both size and chemical structure. Transversion mutations are less common than transition mutations, which involve the substitution of a purine base with another purine or a pyrimidine base with another pyrimidine.

Front 210

Where and does bacterial cells lie in Hershey-Chase centrifuge

Back 210

Bottom as a pellet

Front 211

Where and does bacterial cells lie in Hershey-Chase centrifuge

Back 211

Bottom as a pellet

Front 212

How many Aa coding codons

Back 212

61

Front 213

Where does Repressor P. Binds to in Lac operon

Back 213

Operation site

Front 214

Missense mutation

Back 214

Type of point mutation where a single NT change leads to change in Aa

Front 215

What's isoelectric point

Back 215

pH value at which total Protein charge is neutral.

Front 216

Isoelectric focusing technique principle.

Back 216

Setup Immobilized Ph Gradient . With anode and cathode at ends

Protein starts to move from a starting pH towards anode or cathode, depending on its charge.

And stops at the pH=pI

Protein starts to move from a starting pH towards anode or cathode, depending on its charge.And stops (why) when the pH=pI.

B/c Protein becomes electrically neutral.

Front 217

Apart from the pKa of functional groups on amino acids of P.

What else affects pI of protein

Back 217

Addition of any ionizable post translational modification. Such as phosphate.

Also tertiary structure formation(folding) can alter the theoretically pI ,they alter the charges through interactions

Front 218

What does p-value ,tells us

Back 218

The p-value in statistics is calculated based on the null hypothesis, which is a statement that there is no effect or no difference between groups. The p-value represents the probability of obtaining results as extreme as or more extreme than the observed results, assuming that the null hypothesis is true.The calculation of the p-value depends on the statistical test being used. Here are a few common methods:1. **For t-tests:** In a t-test, the p-value is typically calculated using the t-distribution based on the test statistic (t-value) and the degrees of freedom.2. **For chi-squared tests:** In a chi-squared test, the p-value is calculated using the chi-squared distribution based on the test statistic (chi-squared value) and the degrees of freedom.3. **For ANOVA tests:** In analysis of variance (ANOVA), the p-value is calculated based on the F-distribution using the F-statistic and the degrees of freedom.4. **For regression analysis:** In regression analysis, the p-value is typically associated with each coefficient and is calculated based on the t-distribution.Once the appropriate distribution and test statistic are determined, the p-value is calculated using software or statistical tables. If the p-value is below a predefined significance level (often 0.05), the null hypothesis is rejected, indicating that the observed results are unlikely to have occurred by chance alone.

Front 219

In Ez Kinetics,

Whats First order Kinetics and zero order kinetics

Back 219

First orderWhen Rate of reaction depends on [S](rising graph-MME) (ie; rate= k[S]^1)

Zero order

First orderWhen Rate of reaction depends on [S](rising graph-MME) (ie; rate= k[S]^1)Zero order When rate of reaction doesn't depend on substrate coordination (plateuo at the top of graph-MME)Rate= k.

When rate of reaction doesn't depend on substrate coordination (plateuo at the top of graph-MME)

Rate= k.

Front 220

How is values for lineweaver plot derived

Back 220

Front 221

Rote memorization alert.

Changes in

Competitive Inhibition(CI)

Non-Competitive Inhibition(NCI)

Uncompetitive inhibition (UI)

Back 221

CI => Km📈

NCI =>Vmax 📉

📉

UCI =>Vmax 📉 Km📉

Front 222

Perturbation and Le chateliers principle

Back 222

Perturbation in a chemical reaction refers to any change that disrupts the equilibrium state. This disruption affects the balance between reactants and products, shifting the reaction towards equilibrium. The reaction quotient (Q) and equilibrium constant (K) help gauge the reaction's progress towards equilibrium. Le Chatelier's principle guides how the system responds to perturbations, shifting to counteract the disturbance and eventually reach equilibrium where Q equals K.

Front 223

Why is F6P to F1,6P in glycolysis, is favorable and not the otherwise

Back 223

Because, ATP presence makes it favorable to form F16P.while F6P may have lower free energy than F1,6P, the hydrolysis of F1,6P to form F6P requires an input of energy, resulting in a positive (ΔG) for the reaction.

Because, ATP presence makes it favorable to form F16P.while F6P may have lower free energy than F1,6P, the hydrolysis of F1,6P to form F6P requires an input of energy, resulting in a positive (ΔG) for the reaction.

while F6P may have lower free energy than F1,6P, the hydrolysis of F1,6P to form F6P requires an input of energy, resulting in a positive (ΔG) for the reaction.

Front 224

In competitive inhibition what happens to Km . What changes on lineweaver plot

Back 224

Km increases

Slope increases ( km/vmax)

So 1/Km decreases. So -1/Km moves to right.

(Note: It moves to left in uncompetitive, b/c Km decreases, . And no change in Km for noncompetitive )

Front 225

Mnemonic for 3 blotting. Easier than snow drop

Back 225

Southil my DNA

Northil RSS(RNA)

Westil protein(gym-rich)

Front 226

Extra blots

Back 226

Eastern blot- detects post translational modification (sanskrit)

South-western: protein-DNa interactions.

North-western: Protein-RNA interactions

Front 227

Why is Bovine Serum Antibodies added in western blot

Back 227

To prevent antibodies supposed to bind proteins from binding to membrane. BSA binds all the spaces in membrane except area with the protein.

Front 228

Three most common AA that are post translational phosphorylation site

Back 228

STaY ( remember ,"STaY there, let me put this phosphate on your 'OH'le)

Front 229

PCR calculatio

Back 229

Amount of DNA = Initial amount of DNA × (amplification factor(its 2 for PCR)^n