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42 Cards in this Set
- Front
- Back
Mitochondria
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-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 |
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Peroxisomes
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-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 |
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Zellweger's Syndrome
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-inherited
-proteins can't be imported & peroxisomes are empty -death shortly after birth |
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Lysosomes
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-degrade cellular components through memb. fusion
-have low PH b/c of proton pumps inside -coated w/ carbos on inside -in kidney - |
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Lysosomal storage diseases
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-linked to mutation of acid hydrolase gene
-metabolites can't be degraded & accumulate |
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Tay-Sachs disease
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-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 |
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Endoplasmic Reticulum
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-protein (RER) & lipid synth(SER)
-Sequesters Ca plas a big role in cell signaling |
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SER
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-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) |
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ER signal sequence
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-directs ribo to ER membrane
-import of proteins to ER are cotranslational w/ translocons -import into nucleus & organelles is post translational |
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Modification of proteins in ER
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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 |
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Cystic Fibrosis
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-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
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Vesiculation
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-needs coat proteins that are soluble & induce curvature of memb. face
3 types: -clathrin (golgi PM) -cop1 (golgi cisternae) -cop2 (ER) |
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Secretory pathway
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from ER->golgi stacks->secreted proteins go to vesicles then PM
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Golgi
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-makes & packages complex molecules i.e. glycolipids,glycoproteins,lipoproteins
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What happens to proteins as they move through golgi?
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-some get N linkage taken off & get O linked sugars
-glycocalix is added to extracellular domains of memb proteins for protection |
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Regulation of secretion
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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 |
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Signal for targeting of a protein to lysosomes
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-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. |
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Other sorting signals
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-ER retention KDEL seq in localized proteins
-golgi retention signals -diversion of secretory proteins to regulated secretory vesicles |
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3 pathways to degredation in lysosomes
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-Endocytosis
-Phagocytosis -Autophagy – degrades its own organelles. |
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Autophagosome
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-all worn out organelles are degraded by the lysosome in autophagosomes
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2 types of vesicular traffic from PM
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-Pinocytosis
-Phagocytosis |
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Phagocytosis
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-in specialized cells macrophage/neutrophils
- a cell needs an eat me sig. to be persued: *chemoattractants *AB activated |
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Pinocytosis
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-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 |
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Clathrin cycle
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-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 |
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Receptor mediated endocytosis
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-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 |
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Primary vs. Secondary vs.Early endosomes
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-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 |
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Hypercholesterolemia
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-too much cholesterol in bld
-defects in uptake of LDL |
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Down-regulation of receptors
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-ater binding of the ligand, receps. cluster in coated pits
-after internalization receps & ligands are sorted to lysosome for destruction after continual signaling |
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3 functions of caveolae
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-conc. subs from xtracell space & move into cytosol
-transport material across cells by transcytosis -signal transduction |
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2 forms of cell death
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-necrosis
-apoptosis |
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Necrosis
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-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 |
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Apoptosis
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-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. |
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Purpose of apoptosis in dev.
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-deleting unwanted structures
-sculpting specific tisues -controls cell #'s -eliminates abn cells in dev. |
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Purpose of apoptosis in adults
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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 |
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Which is the default pathway in multicellular organisms in apoptosis?
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-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 |
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4 stages of prog cell death
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-signaled:making up its mind
-apopotosis:pulling the trigger -phagocytosis:hiding the corpse -degradation:destroying the evidence |
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Factors that drive apoptosis
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regulators
adaptors effectors |
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Effectors
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–caspases (death proteases) = executionary arm of the apoptotic machinery
-caspases cleave critical proteins in the cell -makes it incompatible with life |
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Regulators
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– Bcl-2 family members
-Receptors for different ligands -Depending if they are activated, they can bind adaptors, which then activate the effectors |
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Activation of apoptosis from OUTSIDE the cell (extrinsic pathway)
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-killer lymphocytes induce apoptosis in target cell by binding it,
-transmits a signal intracellularly for the cell to commit apoptosis |
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Activation of apopotosis from INSIDE the cell (intrinsic pathway)
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-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 |
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What is the “eat me” signal on apoptotic cells that attract phagocytic cells?
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-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 |