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42 Cards in this Set

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Mitochondria
-converts glucose to ATP(powerhouse)
-has lots of proteins made in cytop. & they're imported to mito after xlation
- have 2 membranes
-have DNA from mom
Peroxisomes
-contain enzymes
-detox of toxic
subs.oxidation of fatty acids,make phospholipids & bile
-make H2O2 & catalase uses it for oxidation of stuff
-lots in liver
Zellweger's Syndrome
-inherited
-proteins can't be imported & peroxisomes are empty
-death shortly after birth
Lysosomes
-degrade cellular components through memb. fusion
-have low PH b/c of proton pumps inside
-coated w/ carbos on inside
-in kidney
-
Lysosomal storage diseases
-linked to mutation of acid hydrolase gene
-metabolites can't be degraded & accumulate
Tay-Sachs disease
-Jews most affected
-motor,mental deterioration @6mo. age
-death @ 2-3 yrs old
-no hexosaminidase A that breaks down glycolipids
-neurons are swollen w/ glycolipids & are destroyed
Endoplasmic Reticulum
-protein (RER) & lipid synth(SER)
-Sequesters Ca plas a big role in cell signaling
SER
-SER makes lipids & phospholipids on cytostolic leaflet
-flipase maintains = growth of bilayer leaflets
-lipids reach other
-lipids reach other cells by:
*vesicles that bud off then fuse where they need to (vesc. traffic)
*diff through ER to SER (diff to continuous organelle)
*xfer proteins
-in testis(steroid sec cells),liver(enzymes to degrade hormones/detox subst)
ER signal sequence
-directs ribo to ER membrane
-import of proteins to ER are cotranslational w/ translocons
-import into nucleus & organelles is post translational
Modification of proteins in ER
helps in folding:
-signal peptidase cleaves N terminal sig
-N linked glycosylation
-disulfide bonds
-addition of a GPI anchor
acts as signal sorter to direct memb proteins to certain areas on PM
-chaperones fold protein & it leaves ER
Cystic Fibrosis
-mutation in CFTR gene that codes for a protein that transports Cl ions out of epi into lumen= cl imbalance in cell & it swells,can't secrete H2O
Vesiculation
-needs coat proteins that are soluble & induce curvature of memb. face
3 types:
-clathrin (golgi PM)
-cop1 (golgi cisternae)
-cop2 (ER)
Secretory pathway
from ER->golgi stacks->secreted proteins go to vesicles then PM
Golgi
-makes & packages complex molecules i.e. glycolipids,glycoproteins,lipoproteins
What happens to proteins as they move through golgi?
-some get N linkage taken off & get O linked sugars
-glycocalix is added to extracellular domains of memb proteins for protection
Regulation of secretion
before anything is released from trans golgi by forming vesicles to PM=hormone sigs/neurotransmitters/ACh are needed
-Ca causes release of vesicles a lot
-dynein & kinesin move vesicles along MTs till they get to actin/myosin then they take over
Signal for targeting of a protein to lysosomes
-N-linked sugar added in ER
-In the golgi, a phosphorylated mannose is added to the n-linked sugar (at the 6 position of the mannose).
-The specificity comes from the sugar transferase that adds the M6P. It only adds it to the specific amino acid sequence specific to lysosomal proteins.
-The M6P then binds to the M6P receptor in the golgi and enters a vesicle.
Other sorting signals
-ER retention KDEL seq in localized proteins
-golgi retention signals
-diversion of secretory proteins to regulated secretory vesicles
3 pathways to degredation in lysosomes
-Endocytosis
-Phagocytosis
-Autophagy – degrades its own organelles.
Autophagosome
-all worn out organelles are degraded by the lysosome in autophagosomes
2 types of vesicular traffic from PM
-Pinocytosis
-Phagocytosis
Phagocytosis
-in specialized cells macrophage/neutrophils
- a cell needs an eat me sig. to be persued:
*chemoattractants
*AB activated
Pinocytosis
-extracellular fluid is pinched off by the plasma membrane and internalized
-Receptor mediated endocytosis involves the specific internalization of extracellular fluid upon stimulation of receptor i.e. LDL receptors
Clathrin cycle
-a mix of diff memb rec. cluster in a clathrin coat & are internalized by the cell when the vesicle pinches off
-adaptin helps bind lignd in clathrin coat
Receptor mediated endocytosis
-coated vesicle is endocytosed
-is uncoated
-fuses w/ endosome
-early endosome forms:has low PH= dissaoc. of ligand from recep.
-receps are recycled & carried by vesocles to PM
Primary vs. Secondary vs.Early endosomes
-Primary:
vesc. has just budded off of golgi going to lysosome hasn't fused w/ another vesc.w/ cargo to be digested yet
-Secondary:
has its cargo
-Early:
*vesc. & tubuels near PM
*endocytic uncoated vesc.fuses w/ another uncoated enocytic vesc,no fusion w/ vesc.w/ lyso enzymes
*when it fuses it's a secondary lysosome
Hypercholesterolemia
-too much cholesterol in bld
-defects in uptake of LDL
Down-regulation of receptors
-ater binding of the ligand, receps. cluster in coated pits
-after internalization receps & ligands are sorted to lysosome for destruction after continual signaling
3 functions of caveolae
-conc. subs from xtracell space & move into cytosol
-transport material across cells by transcytosis
-signal transduction
2 forms of cell death
-necrosis
-apoptosis
Necrosis
-cell swells and bursts
-loss of plasma membrane
-spilling of cellular contents
-lack of alterantion in nucleus
-from toxic stimulus/massive injury to cell
-can cause potentially damaging inflammatory response=tissue damage
Apoptosis
-mild convolution
-chromoatin compaction and segregation
-condensation of cytoplasm
-nuclear fragmentation (blebbing)
-cell fragmentation
*In apoptosis, the dead or dying cell is phagocyteosed by phagocytic cells (macrophages and neutrophils)
-no leakage of cellular contents
-no inflammation
-imperceptible to organism.
Purpose of apoptosis in dev.
-deleting unwanted structures
-sculpting specific tisues
-controls cell #'s
-eliminates abn cells in dev.
Purpose of apoptosis in adults
homeostasis
-maintins cell death:
too much=neurodegen disorders,osteoporosis,AISs
too little:=CA,viral inf.,autoimm disorders
-eliminating damaged,mutated cells
-reg of irreversible dev of orgns songbird-> brain cell death
Which is the default pathway in multicellular organisms in apoptosis?
-cells require a constant input of signals that tell cells to stay alive
-If not received, the cells will automatically undergo apoptosis
-by the withdrawl of positive signals or receipt of neg signals
4 stages of prog cell death
-signaled:making up its mind
-apopotosis:pulling the trigger
-phagocytosis:hiding the corpse
-degradation:destroying the evidence
Factors that drive apoptosis
regulators
adaptors
effectors
Effectors
–caspases (death proteases) = executionary arm of the apoptotic machinery
-caspases cleave critical proteins in the cell
-makes it incompatible with life
Regulators
– Bcl-2 family members
-Receptors for different ligands
-Depending if they are activated, they can bind adaptors, which then activate the effectors
Activation of apoptosis from OUTSIDE the cell (extrinsic pathway)
-killer lymphocytes induce apoptosis in target cell by binding it,
-transmits a signal intracellularly for the cell to commit apoptosis
Activation of apopotosis from INSIDE the cell (intrinsic pathway)
-release of cytorchrome C from mitochondria can result from damage to the mitochondria, or as a result of a specific signal triggered by a signaling cascade from plasma membrane
-what causes the release of cyt c? Damage, signaling pathway
What is the “eat me” signal on apoptotic cells that attract phagocytic cells?
-exposure of PS on external leaflet of membrane
-phosphatidylserine (PS) is a negatively charged phospholipids that normally present on the internal leaflet of the plasma membrane
-there is NO PS facing the extracellular space, b/c there is not a flippase for it
-100% stays inside the membrane leaflet