Histo Final 2

Front 1

Cortex of cytoplasm – location + “main” cell:

Back 1

underlying the plasma membrane anchored to membrane proteins• the best known for erythrocytes (a meshwork of the filamentous spectrin)

Front 2

Membrane is impermeable for:

Back 2

water soluble molecules.

Front 3

There are 3 classes of transport proteins:

Back 3

carrier proteins

Front 4

Which molecules can more rapidly it will diffuse across a lipid membrane:

Back 4

The smaller the molecule and themore soluble in lipids (the more hydrophobic /nonpolar)

Front 5

in ATP-dependent ion transport:

Back 5

P

Front 6

P-class pump =

Back 6

phosphorylation of one subunit is necessary (Na+- K+ pump)

Front 7

F-class pump =

Back 7

transport protons in reverse way –utilize energy of H+ gradient to synthesis of ATP (ATP synthase of inner mitochondrial membrane)

Front 8

V-class pump =

Back 8

H+ pump of lysosomesin ATP-dependent manner

Front 9

ABC-class pumps - Involved in transport of:

Back 9

ions

Front 10

ABC-class pumps Example::

Back 10

CFTR : Function as chloride ions channel in epithelial cells

Front 11

Which GLUT in pancreas?

Back 11

GLUT 2 - Insulin-insensitive

Front 12

Active transport of glucose occurs in:

Back 12

Choroid plexus -Proximal convoluted tubules of kidneys -Epithelial cells of small intestine

Front 13

Receptors for hydrophilic ligands are localized in:

Back 13

the cell membrane (membrane receptors).

Front 14

Receptors for hydrophobic ligands are localized:

Back 14

inside the cell (intracellular receptors)

Front 15

Paracrine signals:

Back 15

signals are released by cells into the extracellular fluid in their neighborhood and act locally

Front 16

Autocrine signals:

Back 16

signals act on the secreting cell

Front 17

Intracellular receptors – Ligands:

Back 17

steroid hormones

Front 18

Effectors of G proteins -Membrane proteins:

Back 18

- Adenylyl cyclase (cAMP) - Phospholipase C

Front 19

Binding of ligand to its receptor coupled with G protein ->:

Back 19

conformational changes of receptor -> α subunit activation -> decreased affinity to GDP -> GTP binds -> α subunit leaves complex ->α subunit hydrolyzes GTP to GDP

Front 20

Ligands that activate adenylyl cyclase (g-protein):

Back 20

adrenaline

Front 21

which receptors are fast/slow:

Back 21

Fast: Metabotropic Slow: Catalytic receptors

Front 22

Inner membrane of mitochondria has what:

Back 22

cardiolipin(cardiolipin contains four

Front 23

Peroxisomes contain

Back 23

oxidative enzymes

Front 24

Functions of peroxisomes:

Back 24

β-oxidation of long-chain fatty acids

Front 25

enzymatic marker of peroxisomes:

Back 25

D-AMINO ACID OXIDASE

Front 26

Enzymes belonging to the cytochrome P450 family participate in:

Back 26

detoxification processes

Front 27

Pinocytosis =

Back 27

„cell drinking” is the nonspecific (random) uptake of the extracellular fluid and material in solution into pinocytic vesicles.

Front 28

Receptor-mediated endocytosis ==

Back 28

is the specific uptake of a substance (e.g.

Front 29

Transcytosis=

Back 29

(endocytosis + exocytosis; the transported molecules are not changed inside the cell)

Front 30

Receptor-mediated endocytosis – type of coat:

Back 30

clathrin-coated s rapidly lost

Front 31

Receptor-mediated endocytosis Ligands:

Back 31

-Transferrin -low-density lipoproteins = LDLs -protein hormones

Front 32

Clathrin:

Back 32

-consists of:

Front 33

Adaptins do what:

Back 33

(adaptor proteins) -participate in the formation of clathrin-coated vesicles -recognize both clathrin triskelions and cargo receptors

Front 34

It encircles and pinch neck of forming vesicle =?

Back 34

Dynamin has GTPase activity

Front 35

Autophagy =

Back 35

autophagocytosis

Front 36

Polyubiquitination =

Back 36

at least 4 molecules of ubiquitin are attached

Front 37

Monoubiquitinated proteins are directed to:

Back 37

lysosomes for degradation.

Front 38

Polyubiquitinated proteins are directed to:

Back 38

proteasomes for degradation.

Front 39

Nuclear pore diameter:

Back 39

approx. 80 nm - 9 nm channel opening

Front 40

Direction of DNA replication:

Back 40

5’ -> 3

Front 41

Topoisomerases:

Back 41

unwind DNA double helix

Front 42

Helicase:

Back 42

separates two annealed DNA strands

Front 43

DNA ligase:

Back 43

binds Okazaki fragments together

Front 44

A basic promoter =

Back 44

a DNA sequence that binds an RNA polymerase

Front 45

basic transcription factors do what:

Back 45

Bind to the basic promoter and allow for binding of RNA polymerase.

Front 46

Transcription factors =

Back 46

Proteins that bind to specific DNA sequences (beyond the basic promoter) and activate or enhance initiation of transcrption.

Front 47

maintain the three-dimensional structure of the cell – which structure:

Back 47

Intermediate filaments

Front 48

The formation of the 2nd pair of centrioles occurs during:

Back 48

the late S and G2 phase

Front 49

centromeres begin to move apart – when:

Back 49

anaphase

Front 50

The longest phase:

Back 50

G1 25h

Front 51

G2/M checkpoint look for + needed cyclin/cdk:

Back 51

• proper cell size • DNA replication is completed • MPF (cyclinB + Cdk1)

Front 52

M checkpoint look for:

Back 52

• proper alignment of chromosomes on mitotic spindle

Front 53

Restriction point look for:

Back 53

• proper cell size • proper external environment • presence of growth factors

Front 54

The importance of the restriction point R (G1 phase checkpoint):

Back 54

• Cell must decide whether to: - leave the cell cycle temporarily (state of quiescense) - Finally leave the cell cycle (aging)

Front 55

Cyclins/Cdk which are constant:

Back 55

Cdk

Front 56

The role of the Rb protein in the cell cycle:

Back 56

Complexes Cdk4

Front 57

increase of concentration of MPF =

Back 57

cell enters the prophase

Front 58

decrease of concentration of MPF =

Back 58

cell enters the anaphase – cell division ends – cell cycle stops

Front 59

high level of MPF leads to:

Back 59

- condensation of chromosomes; - damage of the nuclear envelope; - mitotic spindle formation

Front 60

Activity of cyclin-Cdk complex is regulated by:

Back 60

degradation of cyclins by ubiquitination

Front 61

nuclear envelope breaks up how:

Back 61

MPF (cyclin B

Front 62

APC (Anaphase Promoting Complex) do what +how:

Back 62

Promoting Anaphase! by tagging specific proteins for degradation (ubiquitination) like mitotic cyclins for degradation

Front 63

The inhibition of G1 phase terminates when:

Back 63

G1 cyclins accumulate after stimulation of the cells to divide by growth factors

Front 64

The role of p53 in cell cycle control:

Back 64

DNA results in phosphorylation of p53 protein -> p53 protein stimulates the synthesis of p21(inhibitor of cyclin-dependent kinases (CDKs))

Front 65

inhibitors of cyclin-dependent kinases (CDKIs):

Back 65

The INK4 family: p15

Front 66

The INK4 family consist of+ act on:

Back 66

p15

Front 67

The CIP/WAF family consist of+ act on:

Back 67

p21

Front 68

The most important tumor suppressor genes associated with cell cycle contro:

Back 68

RB + P53

Front 69

RB protein prevents:

Back 69

passing through the G1 phase and entry into S phase by cells with damaged DNA

Front 70

Intestinal epithelial cells are completely replaced within:

Back 70

a few days;

Front 71

The bone is completely replaced within:

Back 71

10 years;

Front 72

The epidermis is renewed within:

Back 72

two months.

Front 73

mitogens do what:

Back 73

stimulate cell division primarily by relieving intracellular negative controls that block progress through the cell cycle.

Front 74

Mitogens works how:

Back 74

relieve the inhibitory effect of Rb protein by activation of intracellular signalling pathways leading to the activation of G1-Cdk and G1/S-Cdk complexes

Front 75

anti-apoptotic proteins:

Back 75

Bcl-2

Front 76

pro-apoptotic proteins:

Back 76

Bax

Front 77

caspases associated with initiation of apoptosis:

Back 77

(caspases 2

Front 78

caspases associated with effector phase of apoptosis:

Back 78

(caspases 3

Front 79

cytochrome c which binds to:

Back 79

Apaf-1 protein + capsapse 9 ->apoptosome inducing caspase cascade).

Front 80

Apoptosome =

Back 80

complex composed in mammaliancells of Apaf-1 protein

Front 81

stress-induced apoptotic pathway (intrinsic) – is induced by:

Back 81

increased concentration of calcium ions in the cell

Front 82

death receptor – initiated apoptotic pathway (extrinsic) –is initiated by

Back 82

engagement of plasma membrane death receptors (TNF-R

Front 83

apoptosis - Intrinsic pathway -involves the action of:

Back 83

sensors and effectors of the Bcl-2 family

Front 84

Apoptosis - Extrinsic pathway -engagement of:

Back 84

death receptors leads directly to caspase activation

Front 85

DNA cell disintegrates into fragments of random lengths – due to:

Back 85

necrosis

Front 86

Glycosaminoglycans=GAGs are build up by:

Back 86

long unbranched polysaccharides + repeating disaccharide units: Uronic acid(Glucuronic acid) + Hexosamine

Front 87

hyaluronic acid GAG is how long:

Back 87

25k sugars

Front 88

whats special with hyaluronic acid?

Back 88

does not form proteoglycans(PG) + absence of sulfate groups.

Front 89

Proteoglycans=PG consist of:

Back 89

Glycosaminoglycans + protein chain (core)

Front 90

types of GAGs in PG:

Back 90

– dermatan sulfate – chondroitin sulphate– keratan sulphate – heparan sulphate

Front 91

Aggrecan typically consists Of:

Back 91

about 100 chondroitin sulfate chains and about 30 keratan sulfate chains linked to a serine-rich core protein of almost 3000 amino acids.

Front 92

Aggrecan aggregate consists of :

Back 92

about 100 aggrecan monomers noncovalently bound to a single hyaluronanchain

Front 93

Glycoproteins important in :

Back 93

– interactions between cells and matrix – adhesion of cells to their substrate (Protein-Carbohydrates:)

Front 94

Common ECM glycoproteins is called:

Back 94

fibronectin=FN

Front 95

fibronectin=FN function:

Back 95

it mediates cell adhesion to ECM by binding to FN receptors on the cell surface. RGD sequence!

Front 96

Other glycoproteins of the ECM(more then fibronectin):

Back 96

Entactin or NIDOGEN - t binds laminin and links it with type IV collagen in the lamina densa. ++ Laminin

Front 97

Laminin location:

Back 97

located in basal laminae

Front 98

Laminin shape:

Back 98

large cross-shaped molecule have binding sites for cell-surface receptors (integrins) heparan sulfate

Front 99

Laminin function:

Back 99

mediates interaction between epithelial cells and the extracellular matrix by anchoring the cell surface to the basal lamina.

Front 100

most abundant protein in the body:

Back 100

Collagen (up to 30% dry weight)

Front 101

Collagen function:

Back 101

provides strength and flexibility• stiff and inextensible

Front 102

Structure of a tropocollagen molecule:

Back 102

three alpha-chains arranged in a triple helix -> basic protein unit that polymerizes to form collagen fibrils

Front 103

Typical structure of one collagen chain:

Back 103

1000 amino acids long - triplet Gly-X-Y sequences

Front 104

Collagen – between the three αchains there is a molecule:

Back 104

Glycine

Front 105

Aminoacids – which ones:

Back 105

Glycine

Front 106

Collagen fibers – “stages” during build up:

Back 106

tropocollagen molecules -> microfibrillar subunits –> fibrils -> fibres -> collagen bundles

Front 107

Preprocollagen consist of:

Back 107

one α-chain

Front 108

intracellular events of formation of a collagen fibril:

Back 108

Synthesis of Pro-a-Chain -> Hydroxylation of selected prolines and lysosines -> glycosylation of selected hydroxylysines -> self assembly of 3 Pro-a-Chains -> leave ER into cytosol -> secretion

Front 109

Extracellular events in the formation of a collagen fibril:

Back 109

Cleavage of propeptides by procollagen peptidases-> tropocollagen Spontaneously aggregate near the cell surface

Front 110

Collagen type 1 – main site:

Back 110

Bones

Front 111

Collagen type 1 – Special features:

Back 111

Most abundant

Front 112

Collagen type 2 – main site:

Back 112

Hyaline + Elastic cartilage

Front 113

Collagen type 3 – main site:

Back 113

Reticular fibers

Front 114

Collagen type 3 – Special features:

Back 114

Very thin

Front 115

Collagen type 4 – main site:

Back 115

Basal lamina <-> endothelial cells

Front 116

Collagen type 4 – Special features:

Back 116

Amorphous + forms networks

Front 117

Collagen type 5 – main site:

Back 117

Basal lamina

Front 118

Lack of vit. C will lead to:

Back 118

( Scurvy) synthesis of poorly hydroxylated tropocollagen -> bad bonds

Front 119

Procollagen peptidase defect leads to:

Back 119

Ehlser danlos syndrome.

Front 120

Ehlser danlos can be due to:

Back 120

defect in Procollagen peptidase or lysyl hydroxylase

Front 121

Reticular fibers function:

Back 121

provide a very delicate network supporting individual cells in certain organs (bone marrow

Front 122

Actin filaments consist of:

Back 122

two-stranded helical polymers of the protein actin

Front 123

Fimbrin =

Back 123

actin cross-linking protein important in the formation of filopodia;

Front 124

Two main forms of structures involved in cell migration:

Back 124

1)Filopodium- rojection that extend beyond the leading edgeof lamellipodium 2) actin thin sheet on themobile edge of the cell

Front 125

Cellular adhesion molecules (CAM) are what kind of protein:

Back 125

transmembrane proteins

Front 126

Types of CAM:

Back 126

• Cadherins • Selectins • Integrins

Front 127

Cellular adhesion molecules (CAM) function:

Back 127

Key elements in the recognition/adherence/binding of other cells orintercellular molecules;

Front 128

Cadherins needs what:

Back 128

Ca ++

Front 129

Cadherins do what:

Back 129

bind with similar proteins of the same tissue and with cytoskeleton filaments

Front 130

Selectins do what:

Back 130

make weak intercellular connections by binding to specific oligosaccharide groups of glycoproteins and glycolipids (also need Ca++).

Front 131

Integrins do what:

Back 131

make strong connections between cell and ECM macromolecules

Front 132

E-cadherins do what:

Back 132

E-cadherins of 2 cells ‘glue’ each other –they are responsible for tight adherence of epithelial cells.

Front 133

There are also N- and P-cadherins – found where?

Back 133

in CNS

Front 134

Selectins initiate movement of :

Back 134

white blood cells = leukocytes(WBC) toward tissues across thevessel wall = extravasation

Front 135

Synthesized only when required – what:

Back 135

E-SELECTINS

Front 136

E-SELECTINS are involved in:

Back 136

recruiting leukocytes such as neutrophils (white blood cells) and macrophages to the inflammation sites.

Front 137

XX mediates much slower rolling than XX?

Back 137

E-selectin slower then P-selectin.

Front 138

Selectin locations:

Back 138

•blood platelets – may bind von Willebrand factor (vWF) and fibrinogen – clot formation •endothelial cells (on demand)

Front 139

E-selectins location:

Back 139

on endothelial cells

Front 140

Extracellular domains of the integrin bind directly:

Back 140

to ECM components (fibronectin

Front 141

cytoplasmic domains of the integrin binds to:

Back 141

indirectly via several intracellular anchor orconnecting proteins (α-actinin

Front 142

inside-out signalling =

Back 142

Integrins respond to intercellular events by changing their adhesive properties with respect to ECM molecules

Front 143

The most important pathological processes that depend on CAM:

Back 143

Blood clotting. Inflammatory reaction

Front 144

Zonula occludens (TIGHT JUNCTION) – location::

Back 144

in the apical part of adjacent cells

Front 145

Zonula occludens (TIGHT JUNCTION) – which molecules:

Back 145

special cadherins (claudin and occludin) - bind the actin filaments of the 2 cells

Front 146

Zonula adherens (belt desmosome) – location:

Back 146

usually localized below tight junction in the apical part of the cell.

Front 147

Zonula adherens (belt desmosome) – which molecules:

Back 147

E cadherins – actin filaments.

Front 148

The actin filamants of belt desmosome Build:

Back 148

a terminal web. It anchors bundles of actin filaments of microvilli.

Front 149

spot-like structures that hold cells together =

Back 149

cula adherens (desmosome)

Front 150

desmosome function in side cell:

Back 150

Anchoring sites for intermediate filaments.

Front 151

main component of a dense plaque(desmosome):

Back 151

Desmoplakin bind Cytoplasmic tails of desmoglein and desmocollin.

Front 152

CADHERINS of desmosome:

Back 152

desmoglein and desmocollin.

Front 153

Hemidesmosome =

Back 153

unctions between epithelial cells and basal lamina of the underlying connective tissue

Front 154

Hemidesmosome molecules:

Back 154

DYSTONIN

Front 155

GAP JUNCTIONS molecules:

Back 155

6 connexin subunits

Front 156

GAP JUNCTIONS molecules with a mass of less than x? Da can pass into the other cell

Back 156

1500 DA

Front 157

INFERTILITY – can be due to:

Back 157

Gap junction coupling in the ovarian follicle. - granulosa cells are coupled to each other by gap junctions

Front 158

Connexin 50 mutations leads to:

Back 158

blindness

Front 159

BASEMENT MEMBRANE made by:

Back 159

Lamina reticularis + BASAL LAMINA

Front 160

BASAL LAMINA made by:

Back 160

Lamina lucida + Lamina densa

Front 161

Most common collagen in lamina densa of basal Lamina:

Back 161

Type IV collagen

Front 162

Proteins involved in DOCKING/FUSION OF TRANSPORTING VESICLES:

Back 162

SNAREs (v/t)

Front 163

v-SNARE – located on:

Back 163

transporting vesicle