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Comprehensive Exam > Molec Bio White > Flashcards

Molec Bio White Flashcards

1
Q

signal transduction

A

cell to cell communication

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2
Q

leptin

A

released from fat

signals hypothalamus that you are full

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3
Q

endocrine signaling

A

long distance, blood stream, diffusible

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4
Q

paracrine signaling

A

acts locally on nearby cells

short lived

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5
Q

synaptic signaling

A

acts locally on nearby cells

short lived

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6
Q

autocrine signaling

A

cells responding to themselves

ex. cancer growth factors

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7
Q

direct cell signaling

A

ex. immune cells

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8
Q

transmembrane receptors

A

most ligands/hormones are hydrophilic or large SO

use G protein coupled receptors (7 transmembrane receptor)

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9
Q

G protein coupled receptor

A

extracellular domain - binds ligand
transmembrane domain - anchors receptor
cytoplasmic domain - G protein
heterotrimeric (a, b, y) (guanine)

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10
Q

cholera

A

cholera toxin modified G protein keeping Ga active indefinitely
pump Cl and water out of intestine

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11
Q

PKA

A

has 2 catalytic and 2 reg subunits

  • 2 cAMP binds to reg subunits –> release of active C subunits
  • adds two (-) charges (phosphorylation)
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12
Q

receptor tyrosine kinase

A
  • used for response to growth factors
  • enzymatic domain = cytoplasmic tail of integral membrane protein
  • adds phosphate to tyrosine on proteins
  • extracellular domain
  • cytoplasmic domain (transmits signal)
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13
Q

receptor tyrosine kinase steps

A

ligand binds –> conformational change in receptor –> dimerization of 2 monomers –> autophosphorylation –> receptor is scaffold –> binds SH2 domain on Grb2 protein–> SH3 domain of Grb2 binds prolines in SOS –> binds Ras –> binds Raf –> MAPK cascade

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14
Q

Ras

A

first discovered human oncogene

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15
Q

Src

A

first discovered oncogene

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16
Q

Jak-Stat receptor steps

A

ligand binds receptor –> dimerize –> bind JAKs –> they phosphorylate eachother and receptor –> phosphorylates STATs –> STATs separate from receptor, dimerize –> enter nucleus –> transcription

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17
Q

serine-theronine receptor and Smad

A

receptor binds R-Smad (by phosphorylation) –> binds Co-Smad –> nucleus –> transcription

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18
Q

if serine-theronine receptor and Smad is wrong

A

point mutation: Gly to Val

activates Ras

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19
Q

what makes cells different

A

differences in gene expression

they have the same genes but different set of protein

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20
Q

control of gene expression order

A
  1. transcriptional control
  2. RNA processing control
  3. RNA transport and localization control
  4. translation control
  5. mRNA degradation control
  6. protein activity control
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21
Q

Helix turn helix

A

simplest
2 a helices with short chain of AA making the “turn”
longer helix binds to major groove
-binds DNA as dimers

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22
Q

zinc finger domain

A

Zn atom

binds major groove

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23
Q

leucine zipper

A

2 a helices
grabs DNA like clothes spin
Leucine at every 7 AA

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24
Q

helix loop helix

A

short a and longer a helix chain
homo or heterodimers
3 domains: DNA binding, dimerization, activation

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25
Q

committee

A

gene activation

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26
Q

regulation by RNA stability

A
  1. decapping from 5’ end
  2. mRNA degaded fomr 3’ end through poly-A tail
    ^^ both act like a timer
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27
Q

post translational modifications

A

need proteins to be FUNCTIONAL
must fold into 3D conformation
chaperones have fold correctly

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28
Q

protein degradation via proteasome

A

destroys protein via ubiquitin
one E1 activations
30 E2 activations
100s E3 accesory proteins

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29
Q

other controls of gene expression (2)

A

methylation/genomic imprinting: what genes get expressed (or not) from mom/dad

X chromosome inactivation: even things out, 2X vs 1X chromosome (XX, XY)

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30
Q

cell cycle checkpoints (3)

A
  1. Start: commits to entry and chromosome duplication
  2. G2/M: chromosome alignment (is all DNA replicated)
  3. metaphase to anaphase transition: are all chromosomes attached to spindle
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31
Q

Cdk

A

HEART OF CELL CYCLE CONTROL SYSTEM

  • activities of Cdks change, NOT LEVELS
  • without cyclins, not active
32
Q

cyclin

A

levels vary

regulate and activate Cdk

33
Q

APC/C

A

anaphase promoting complex
initiates metaphase to anaphase transition
-targets S-cyclin and M-cyclin
-activated by M-Cdk to complete mitosis

34
Q

when is cdk active

A

inactive: without cyclin or CAK (T loop blocks active site)
partially active: cyclin bound (removes T loop from site)
fully active: CAK phosphorylates cdk at T loop

35
Q

Wee1 kinase

A

inhibits Cdk activity by phosphorylating roof site

36
Q

Cdc25 phosphotase

A

increase cdk activity by dephosphorylating roof site that was previously phosphorylated

37
Q

CKI

A

cdk inhibitory protein (inhibits cyclin-cdk complex)

-used for control of G1/S-Cdk and S-Cdk in early cycle

38
Q

condensin

A

causes chromosome condensation and resolution

39
Q

activation of APCC to complete mitosis steps

A

APCC adds ubiquitin –> destroys securin –> separase now active –> cleaves cohesin –> sister chromatids come apart –> anaphase begins

cohesin: holds sister chromatids together
securin :protects cohesion (inhibitor of separase)
separase: enzyme that cleaves cohesin

40
Q

apoptosis

A

programmed cell death

-important in development of mature forms

41
Q

procaspases

A

inactive precursor for caspases

42
Q

initiator caspase

A

activates downstream caspases

43
Q

executioner caspases

A

destroys actual targets ( executes apoptosis)

esp. caspase 3

44
Q

intrinsic pathway of apoptosis

A

cytochrome c is released from mitochondria –> binds Apaf1 –> forms apoptosome

45
Q

BH123 protein

A

pro-apoptotic

activated –> forms aggregation in mit outer mem –> induce release of cyt C –> apoptosome formed

46
Q

Bcl2

A

regulate intrinsic apoptosis

  • anti-apoptotic protein (inhibits apoptosis)
  • controls release of cyt C into cytosol
47
Q

BH3 only protein

A

pro-apoptotic

inhibits BCl2 protein from inhibiting release of cyt C

48
Q

IAP

A

inhibitor of apoptosis (good thing)

binds/inhibit caspases and prevents them from autoactivating

49
Q

anti-IAPs

A

neutralize IAP and liberate caspases
if apoptotic signal causes release of anti-IAPs from mit to block IAP activity –> executioner caspases activated when IAPs blocked

50
Q

cancer

A

disease of aging

51
Q

oncogenes

A

overactivity mutation
gain of function
single mutation –> proliferation

52
Q

tumor suppressor genes

A

underactivity mutation
loss of function
needs two mutations to cause problems (recessive)

53
Q

activation of oncogenes (4)

A

deletion or point mutation in coding sequence
regulatory mutation
gene amplification
chromosome rearrangement

ALL ARE DOMINANT

54
Q

2 categories of tumor suppressor genes

A
  1. proteins that normally restrict cell growth and proliferation
  2. proteins that maintain integrity of genome
55
Q

hereditary/familial retinoblastoma

A

both eyes affected. 40% (more common)
one copy of Rb is fucked up, you still have one good gene
somatic event occurs – eliminates good copy and forms tumor
loss of heterozygosity

56
Q

sporadic retinoblastoma

A 
one eye affected, no family history 
60% (more rare)
no mutation of Rb 
both copies of Rb mutated
first Tb mutation then second
57
Q

polyp

A

precursor of colorectal Ca
10 years
can develop into adenoma

58
Q

mutations in colorectal ca

A

majority: loss of Apc (tumor suppressor gene)
then loss of p53
then activation of K-Ras

59
Q

actin filaments

A

mardi gras beads

determine shape of cells surface and necessary for whole cell locomotion, secretion, endocytosis

60
Q

microtubules

A

slinky
tube like structure
determine position of organelles
directs intracellular transport

61
Q

intermediate filaments

A

grinders in building
mechanical strength
resist mechanical stress
formation of hair and fingernails

62
Q

polymerization of actin

A

actin monomer contains binding site for ATP or ADP

arranged head to tail –> generates structural polarity

63
Q

polymerization of tubulin

A 
formation of microtubules 
heterodimer of a tubulin and b tubulin with noncovalent bonds 
binding site for GTP 
(+) end = growing end 
(-) end = shrinking end
64
Q

if cytoskeleton of RBC is defective then

A

leads to hemolytic anemia

hereditary spherocytosis

65
Q

spectrin

A

primary component of RBC cytoskeleton
tight capillary spaces

-if defective, Hereditary spherocytosis

66
Q

listeria

A 
bacteria that invades intestine
attaches to receptors on RBC 
behavior based on actin cytoskeleton
faster than submarine 
involves ARP complex (accessory protein) cause branching actin
67
Q

DMD = duchenne muscular dystrophy

A 
severe, loss ability to walk by 12 y.o
dead by 20s
X linked recessive 
lack of dystrophin  
clinical: necrosis of muscle, replace with CT or fat
kids: Gower Maneuver
68
Q

dystrophin

A
  • function: provide stability to muscle cell membrane during cycles of contraction and relaxation
  • 4 functional domains
  • cysteine rich and C terminus domains
69
Q

becker muscular dystrophy = BMD

A 
mild
lose ability to walk by 16 y.o
heart failure
X linked recessive 
has dystrophin by abnormal quantity/size
70
Q

mitochondrial diseases

A 
ragged red fibers
maternally inherited 
self replicated 
higher mutation than nuclear 
threshold effect 
need a mutation AND threshold effect
affects brain/CNS, heart, skeletal m
71
Q

heteroplasmy

A

mixture of normal and mutant mitochondria

72
Q

MEERF

A

myoclonic epilepsy
ataxia
ragged red fibers
majority: mutation due to A => G

73
Q

MELAS

A

mutation in tRNAleu
seizures
most common
ragged red fibers

74
Q

kearns-sayre syndrome

A 
retinitis pigmentosa 
cardiac conduction abnormality 
cerebellar ataxia 
majority: due to mtDNA rearrangements 
ragged red fibers
75
Q

CPEO

A

ragged red fibers

ptosis

76
Q

LHON

A

only affects optic n
no muscle involvement
vision loss
mutation in complex 1 proteins

Comprehensive Exam (3 decks)

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