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BIOCHEMISTRY > EXAM1_L6_Cytoskeleton_vesicular_Transport > Flashcards

EXAM1_L6_Cytoskeleton_vesicular_Transport Flashcards

1
Q

What structure and proteins of Intermediate filaments?

A

Dimers- self assemble- end to end/side to side
Keratin (EC’s)
Vimentin (fibroblasts)
Neurofilaments (neurons)

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2
Q

Intermediate filament protein in Epithelial cells called.

A

keratin

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3
Q

Vimentin

A

intermediate filament protein found in fibroblasts

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4
Q

What is intermediate filament protein found in fibroblast cells?

A

Vimentin

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5
Q

What causes ALS?

A

mutations in neurofilaments (intermediate filaments in the neurons)

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6
Q

Abnormal growth/accumulation of neurofilaments?

A

progressive loss of motor neurons> muscle atrophy, paralysis, death

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7
Q

A patient does something to cause blistering and cell separation with the slightest touch. What may cause this?
What is the actual dysfunction?

A

EBS (epidermolysis bullosa simplex)

Desmosomes-keratin- cell structural stability-tearing/shearing forces- intermediate filaments

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8
Q

What end does microfilaments add on to in G actin? What end does microtubules assemble from?

A

Actin-the plus end

Microtubules- Both ends at different rates–can reorganize

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9
Q

What 3 structures of actin (examples)

A 
Parallel bundles (Mv), 
Contractile bundles (focal adhesions),
Networks (cell cortex- shape/movement)
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10
Q

Myosin I and myosin II. functions

A

1- membrane vessicles/cargo shipping

2- muscle movement

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11
Q

Microfilaments (actin)
Intermediate filaments (Keratin)
Microtubules (tubulin)
Function:

A

microfilaments- adherens junctions (between cells) & focal adhesions (cell to ECM)

Intermediate filaments- desmosomes (cell-cell) & hemidesmosomes (cell-ECM)

Microtubules- MTOC cell division

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12
Q

Cytoplasmic microtubules. What might happen with dysfunction?

A

mitotic spindles & spacial trafficking of vesicles and other organelles.

Cells won’t divide correctly-
Chromosomes may not separate correctly
Organelles may not be able to go where they need to go

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13
Q

Axonemal microtubules

A

Central axoneme shaft of cilia and flagella

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14
Q

Microtubule growth

A

heterodimers of a/b tubulin bound to GTP bind to either end of growing MT.
-Occurs faster at PLUS end where GTP-tubulin concentrations high.
If rate is slow- GTP hydrolysis catches up and tip favors depolymerization (catastrophe)

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15
Q

MTOC

A

Neg end anchored to MTOC-Pos extends out-site of NUCLEATION

Centrosome=two centrioles in pericentriolar material

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16
Q

Colchicine

A

Inhibits MT growth-inhibits neutrophils to reduce gout inflammation.

17
Q

Vincristine/vinblastine

A

causes tubulin aggrigation-block tumor cell growth

18
Q

Paclitaxel (taxol)

A

microtubules stuck in mitosis- block tumor cell growth

19
Q

Kinesin & Dynein. What might happen in dysfunction?

“dine in” “in towards the center neg end)

A

Microtubule dependent motor proteins
Kinesin-vesicles toward Pos end (periphery)
Dynein-transport vesicles central to Neg end
Uses ATP.
dysfunction-intercellular transport may be disrupted?

20
Q

KARTAGENER SYNDROME

“kindergardner syndrome- dying b/c of school”

A

No Dynein in microtubules: flagella (sperm) and cilia (respiratory) resulting in male sterility and chronic respiratory infections

21
Q

If the TGN has dysfunction what might happen? What won’t be affected?

A
  • protein sorting intracellular or extracellular destinations will have problems. constitutive/regulatory secretion may be affected.
  • Post-transcriptional processing (glycosylation, proteolysis etc) happen throughout the golgi and probably won’t be affected
22
Q

Proteins residing in the cell are marked with ___ sequence.

A

KDEL (lys-asp-glu-leu) on the C terminus of the protein.

23
Q

Constitutive exocytosis

A

default-(ie: albumin, membrane proteins nakatpase, sphongolipids)

24
Q

regulated exocytosis

A

ALWAYS mediated by Ca signaling.

ie- hormones (insulin, glucagon), NTM (epinephrine, acetylcholine), digestive enzymes

25
Q

Pathway of Lysosomal enzymes/proteins that stay in the the lysosome.

tq: What could happen if no M6p? what happens if no receptor.

A

add M6P in golgi->calthrin coat & receptor-dep transport to endosome- P removed in acid cytosol of endosome-m6p receptor recycled back to Golgi for reuse.

Icell disease

26
Q

I-cell disease- POST TRANSLATIONAL-Genetic

A

deficiency of enzyme that adds M6P to lysosomal proteins in TGN. (endosomes can’t become lysosomes_) leads to buildup of macromolecules that should have been degraded by lysosomes.
Pathology:
- Developmental delays
-Short-trunk/dwarfism
-lethal by 7yrs (congestive heart failure or respiratory tract infections)

27
Q

Increased lysosomal proteins in the blood and identification of inclusion bodies at LM

A

I-Cell Disease

  • phosphotransferase dysfunction in golgi
  • lysosomal enzymes don’t get M6P Tag/Label & exocytose via Golgi default pathway.
  • accumulation of molecules inside lysosomes waiting for degradation
28
Q

Lysosomal diseases

A

Most- fail to degrade molecules- dysfunction of lysosomal hydrolases (~50 genetic diseases)

ICELL & others affect biogenesis of lysosomes (icell interrupts vesicular transport).

29
Q

2 lysosomal storage disorders/enzymopathies of degradation & their disorders respectively

A

Sphingolipidosis (neimann-pick, tay-sachs, gaucher)

Mucopolysaccharidosis (huler,hunter)

30
Q

Neimann-Pick disease. What kind of disease?

enzyme deficiency and accumulation?

A

Sphingomyelinase Enzyme deficiency-
accumulating sphingomyelin
dysfunctional metabolism of sphingolipids (found in cell membranes)

31
Q

Deficiency in degrading sphingolipids, glycosaminoglycans, and glycogen

A

dysfunction degrading sphingolipids (Tay-sachs, Neimann-Pick, gaucher).
Diseases of degrading GAG’s (Huler, Hunter)
Glycogen (Pompe’s syndrome)

32
Q

Sphingolipids

A
  • Signal transduction and cell recognition
  • Derivatives of ceramide (sphingosine FA esterification)
  • localized in CNS white matter
  • Hereditary defects in lysosomal enzymes that break down sphingolipids cause sphingolipidoses (lysosomal storage diseases) Tay-sachs, gauchers, nieman-pick
33
Q

Tay-Sachs disease

A
  • Hexosaminidase A enzyme deficiency
  • GM2-ganglioside Accumulates

-Retinal red dot-autosomal recessive- no cure/treatment-nerve cell death in brain.

34
Q

Gaucher disease

A

B-Glucosidase deficient- glucosylceramide accumulates- large liver/spleen- sphingolipidosis

35
Q

Hurler Syndrome

A

Mucopolysaccharidosis
Iduronidase deficient;
Heparan sulfate/dermatan sulfate accumulates

36
Q

Hunter Syndrome

A

Mucopolysaccharidosis

BIOCHEMISTRY (33 decks)

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