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Cell Bio > Membranes III > Flashcards

Membranes III Flashcards

exam 1

1
Q

the first ___-____ aa translated will determine if the protein continues to be translated in the cytoplasm or contains the _____ ____ that will cause the ribosome/nascent protein complex to relocate to the ER to finish translation of the protein

A

the first 20-25 aa will determine if the protein continues or contains the Signal Sequence

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2
Q

possibles fates of proteins that are translated completely on cytoplasmic ribosomes (4)

A

(1) cytoplasm
(2) nucleus
(3) mitochondria
(4) peroxisomes

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3
Q

possible fates of proteins that finish translation in the ER (5)

A

(1) plasma membrane
(2) ER
(3) golgi
(4) lysosomes
(5) secretion

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4
Q

mucopolysaccharidoses is an

A

LSD

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5
Q

why is I-Cell disease important?

A

it revealed the mannose-6-phosphate address label for lysosomal enzymes, opened up the whole field of LSDs, and taught us how lysosomes and several other organelles are made

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6
Q

In I Cell disease, the defect is in the ________________ enzyme that _________ the 6-position on specific ______ residues

A

the defect is in the phosphotransferase enzyme that phosphorylates the 6-position on specific mannose residues

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7
Q

targeting signal for all lysosomal enzymes

A

6-position on mannose residue

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8
Q

lysosomal enzymes are secreted from the cell, leaving lysosomes as an empty bag devoid of degradation enzymes

A

I-Cell

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9
Q

consequence of the I-Cell defect

A

lysosomes fill up with all the substrates they usually degrade and appear under the microscope as large, dark inclusion bodies

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10
Q

Protein targeting sequence 1

A

S-K-L is the tripeptide sequence that targets proteins to the peroxisome

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11
Q

Protein targeting sequence 2

A

short (typically 5-6) basic aa sequences are the NLS

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12
Q

Protein targeting sequence 3

A

mannose-6-phosphate targets proteins to the lysosome (its the only non-peptide address label)

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13
Q

Protein targeting sequence 4

A

a longish (about 75 aa) sequence near the N-terminal end of the protein directs proteins to mitochondria

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14
Q

Protein targeting sequence 5

A

K-D-E-L is the tetrapeptide sequence targeting proteins to the ER (it is actually an ER retention signal)

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15
Q

peroxisome targeting disease

A

Neonatal adrenoleukodystrophy (NADL) and Zellweger syndrome

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16
Q

nuclear targeting disease

A

Huntington’s

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17
Q

invagination

A

RME- receptor mediated endocytosis

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18
Q

clathirin is on the ____ side for RME

A

cytoplasm

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19
Q

clathirin coated vesicles are called

A

endosomes

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20
Q

homozygous condition on the dark side of RME leading to high LDL

A

familial hypercholesterolemia

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21
Q

Infleunza and rabies virus gets into the cell by

A

RME

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22
Q

Many viruses use RME to get inside the cell, then fuse with the _________

A

endosomes

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23
Q

true or false: clathirin help concentration of the ligands by sending a signal

A

true

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24
Q

true or false: all protein synthesis occur in the cytoplasm

A

true

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25
Q

SKL

A

presoxisomes

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26
Q

KDEL

A

ER “keep in the ER”

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27
Q

long, N-terminal aa sequence

A

mitochondria

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28
Q

short, basic aa sequence

A

nucleus

29
Q

important signal for dilated mycocardiopathy

A

plasma membrane

30
Q

recognize miss-folded proteins

A

chaperones

31
Q

inducible by conditions that cause unfolding of newly synthesized proteins

A

Heat shock proteins

32
Q

transmembrane protein in the ER membrane needs a

A

stop-transfer sequence

33
Q

stacks of cisterne

A

golgi

34
Q

cis golgi

A

close to the nucleus

35
Q

trans golgi

A

close to the plasma membrane

36
Q

phosphorylation of proteins destined to be _______ _______occurs at the ______ golgi

A

phosphorylation of proteins destined to be lysosomal enzymes occurs at the cis golgi

37
Q

processing and sorting occurs at the ______ golgi

A

trans

38
Q

lysosomes are full with ______ enzymes that work best at the ____ ph achieved by the _____ pump

A

lysosomes are full with degradative enzymes that work best at the low ph achieved by the H+ pump

39
Q

low ph in an endosome allows for

A

a vesicle to be pinched off containing the receptor to be recycled

40
Q

deficiency in iduronate 2-sulfatase

A

MPS dx–> hunter’s disease

41
Q

caused by a defective phosphototransferase, such that lysosomal enzymes do not get properly tagged

A

I-Cell

42
Q

where do the proteins destined for the lysosome acquire a phosphate group on the 6-positon mannose

A

Cis golgi body

43
Q

if the first 20-25 amino acids on a proteins N-terminal are not hydrophobic, the completed protein’s default destination is the

A

cytoplasm

44
Q

a protein will be transported to the ____ if it has a hydrophobic signal peptide

A

ER

45
Q

4 fates of protein that finishes translation in cytoplasms

A
  1. Nulceus
  2. Mitochondria
  3. Peroxisomes
  4. Cytoplasm
46
Q
  1. fates of protein that finished translation in membrane-bound ribosome
A
  1. E.R.
  2. Plasma membrane
  3. Secretory Vesicles
  4. Lysosomes
  5. Golgi
47
Q

Nucelar localization signal (sequence)

A

Lys-Lys-Lys-Arg-Lys

48
Q

Diseases of peroxisomal targeting (2)

A
  1. Zweller Syndrome

2. NALD

49
Q

Golgi membrane between cis and trans

A

Medial region

50
Q

3 fates of proteins that go through golgi

A
  1. Lysosome
  2. Plasma membrane
  3. Secretory vesicle
51
Q

pH of lysosomes

A

5

52
Q

Low lysosomal pH is achieved by

A

H+ pump

53
Q

Lysosome deficiencies are due to a single _______

A

Lysosome deficiencies are due to a single enzyme deficiency

54
Q

Targeting signal of nucleus

A

Short basic aa sequence

55
Q

Pathology of problem with targeting signal of nucleus

A

Huntington

56
Q

Targeting signal of peroxisome

A

SKL tripeptide

57
Q

Targeting signal of mitochondria

A

70-80 aa sequence near N-terminus

58
Q

Problem with targeting signal of mitochondria

A

mitochondriopathies

59
Q

Targeting signal of lysosome

A

Mannose-6-phosphate

60
Q

Problem with targeting signal of lysosome

A

I-cell disease

61
Q

Targeting signal of ER

A

KDEL tetrapeptide

62
Q

Problem with targeting signal of ER

A

Dilated cardiomyopathies

63
Q

Sphingolipid metabolism defect; first LSD successfully treated with enzyme replacement therapy

A

Fabry

64
Q

Sphingolipid metabolism defect; also successfully treated with enzyme replacement therapy

A

Gaucher

65
Q

Sphingolipid and glycosaminoglycan (GAG) metabolism defect prevalent in Ashkenazi Jews

A

Tay-Sachs

66
Q

Defect in one of the several enzymes needed to break down GAGs (aka mucopolysaccharides); several are now treated with enzyme replacement or enzyme enhancement therapies

A

Mucopolysaccharidoses (MPS)

67
Q

Defect in the phosphoryltransferase that puts a phosphate group on the 6-position of specific mannose residues; no lysosomal enzymes get to lysosomes, thus all substrates constipate the lysosome; rare disease that revealed mechanisms for LSD pathogenesis and lysosomal/organellar biogenesis

A

I-Cell Disease

68
Q

Key Point: While each individual LSD has an incidence of 1 in 100,000 or less, there are so many of them that the overall likelihood of an individual having an LSD is about 1 in _____

A

3000

Cell Bio (10 decks)

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