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MCM > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Vorinostat

A
  • A histone deacetylase (HDAC) inhibitor
  • In cancer, HDAC’s can be turned ON, and genome is turned OFF
  • This can turn ON the genome, in particular tumor suppressor genes
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2
Q

Werner Syndrome

A
  • Progeria syndrome (pre-mature aging)
  • WRN mutation
  • Helicase assoc. with telomere maintenance
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3
Q

Antimetabolites

A
  • Type of anti-neoplastic agent

- Incorporated into growing DNA instead of dNTP’s

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4
Q

Topoisomerase inhibitors

A
  • Type of anti-neoplastic agent
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5
Q

RNA Polymerases

A 
mRNA - II
miRNA - II
tRNA - III
rRNA (5.8S, 18S, 28S) - I
rRNA (5S) - III
snRNA and scRNA - II and III
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6
Q

Proteosomes

A
  • 20S core (protein breakdown)

- 19S caps (targets poly-ubiquitin tags)

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7
Q

Ubiquitin Ligase

A
  • find degredation signal on target protein

- Adds ubiquitin tag

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8
Q

Actin

A
  • Most abundant cytoskeletal protein
  • G actin = globular
  • F actin = filament
  • Polym. occurs at + end, depolym. at - end
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9
Q

Cell shape/movement

A 
Actin forms cell processes
   - Microvilli
   - Filopodia
   - Pseudopodia
Locomotion
   - Lamellipodia (+ end leads)
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10
Q

Spectrin

A
  • Actin binding protein
  • Assoc. with membrane lipids/proteins
  • Anchors actin to membrane
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11
Q

Microtubules

A
  • ALPHA and BETA (form tube)
  • GAMMA (forms foundation)
  • Polym. at + end, requires GTP
  • Depolym. at - end
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12
Q

Microtubule Organizing Centers (MTOC)

A
  • places in cells where microtubules start to form
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13
Q

Microtubule Basal Bodies

A
  • part of MTOC
  • found at base of cilium/flagellum
  • allow for whip-like, unidirectional motion
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14
Q

Motorproteins

A
  • walk along microtubules
  • kinesins: walk to +, away from nuc, can push OR pull
  • dyneins: walk to-, towards nuc, can ONLY pull
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15
Q

Intermediate filaments types

A

mechanical strength
assoc. with membranes and cytoskel.
types
- keratins (synth. by epithelium)
- neurofilaments (support long, thin axons)
- lamins (undelying all nuc membranes)

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16
Q

Intermediate filament assembly

A
  • homodimers (two together)
  • protofilaments (two of those)
  • filaments (eight of those)
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17
Q

Desmosomes

A
  • cell-cell junctions
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18
Q

Hemidesmosomes

A
  • cell-ECM junctions (at basement membrane)
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19
Q

Basement membrane

A
  • Basal Lamina + Reticular Layer

- a fibrous EC layer

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20
Q

Glucosaminoglycans (GAG)

A
  • sugars with sulfate groups
  • (-) charged, trap + ions and water
  • part of proteoglycan (protein + GAG)
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21
Q

Propyl hydroxylase

A
  • resident ER protein
  • forms hydroxy-Proline from Proline
  • needed for collagen
  • REQUIRES Vitamin C (Scurvy)
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22
Q

Collagen

A
  • 31 kinds
  • Sequence is Gly-Pro-hydroxyPro
  • makes triple helixes (tropocollagen)
  • important in wound healing
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23
Q

Elastin

A

can stretch and recoil
made of
- elastin (randomly coiled and hydrophobic, covalently cross-linked to each other)
- fibrillin (a surrounding network of microfibrils)

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24
Q

Lysyl oxidase

A
  • enzyme that does the cross-linking of elastin molecules to create elastin fibrils from tropoelastin
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25
Q

Fibronectin

A 
principle adhesion protein in conn. tissue
contains multiple adhesion domains
   - collagen
   - GAG (part of ground substance)
   - integrin (cell surface protein)
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26
Q

Laminin

A
  • principle adhesion protein of basal lamina
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27
Q

Integrins

A
  • cell surface receptors
  • bind to ECM (collagen, fibronectin, laminin)
  • anchor to cytoskel.
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28
Q

Focal adhesions

A
  • attach motile cells to ECM

- anchor to actin skel.

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29
Q

Scurvy

A

defective collagen formation

  • impaired wound healing
  • capillary hemorrhage
  • vit C deficiency (ascorbic acid)
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30
Q

Kinetochore microtubules

A
  • attach to sister chromatids

- depolymerize

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31
Q

Astral microtubules

A
  • attach to membrane

- polymerize

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32
Q

Cell cycle: Restriction point

A
  • late G1
  • controls cell cycle and entry into DNA duplication
  • Is environment favorable?
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33
Q

Cell cycle: G2/M checkpoint

A
  • during G2
  • is all DNA copied?
  • Is environment favorable?
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34
Q

Cell cycle: Metaphase-to-anaphase checkpoint

A
  • During M

- Are all chromosomes attached to spindle?

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35
Q

Cell cycle: DNA damage checkpoints

A

Found in

  • G1
  • S
  • G2
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36
Q

Cyclin dependent kinases

A

Phosphorylate proteins that regulate cell cycle
G1/S cyclin
- trigger progression through restriction point
- peaks in G1
S cyclin
- trigger chr duplication
- Peaks through S and G2
M cyclin
- trigger process through G2/M checkpoint
- Peaks in M

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37
Q

Regulation of Cyclin-Cdk complex

  • Cdk-activating kinase
  • Wee1
  • Cdc25
  • Cdk Inhibitor proteins (CKI)
A

Cdk-activating kinase (activates complex by P active site)
Wee1 (inhibits complex by P inhibition site)
Cdc25 (actiates complex by de-P inhibition site)
Cdk Inhibitor proteins (CKI)
- creates Cyclin-Cdk-CKI complex
- inhibits Cyclin-Cdk activity
- ex: p27, p21, p16

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38
Q

Securin

A
  • hold sister chromatids together
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39
Q

APC/C

A
  • anaphase promoting complex/cyclosome
  • actived by Cdc20
  • ubiquitin ligases target securin (hold sister chr together) for degradatin ——-> anaphase
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40
Q

Origin replication complexes

A
  • complexes found at origins of replication
  • remain assoc. with origins throughout cell cycle
  • include DNA helicases
  • these are Phosphorylated to initiate replication
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41
Q

Cohesins

A
  • ring-like structures around sister chr to keep them together
  • cleaved by separase
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42
Q

M phase control

A

M-Cdk Phosph. targets

  - Condensin (promotes chr condensation)
  - Mitotic spindle
  - Nuclear pore complexes
  - Nuclear lamina
  - APC/C
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43
Q

[Glucose] in cell

A
  • 5mM

- 90 mg/dL

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44
Q

Phosphofructokinase

A
  • 3rd step of Glyc.
  • F6P ——> F-1,6-BP
  • Activated: AMP, F-2,6-BP
  • Inhibited: ATP, citrate
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45
Q

Hexokinase (I and IV)

A 
Commitment step of Glyc.
Glu -----> G6P
Inhibited by G6P (product)
Hexokinase I
- high affinity, low Km
- NOT super specific for Glu
- Inhibited by its product
Hexokinase IV
   - "Glucokinase"
   - In liver and pancrease
   - NOT inhibited by G6P
   - Larger Km, though
   - highly specific for Glu
- Acts as a sensor for B-cells in pancrease (high Glu -->  more HK IV activity --> insulin secreted)
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46
Q

Pyruvate Kinase

A
  • 10th step of Glyc.
  • PEP —–> Pyruvate
  • Activated: AMP, F-1,6-BP
  • Inhibited: ATP, Acetyl-CoA
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47
Q

Arsenic

A

Found in
- Rat poison
- Herbicides
- Industrial cleaners
Inhibits Pyruvate Dehydrogenase (Pyruvate —> A-CoA)
“Garlic smell” = PDH deficiency = lactic acidosis

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48
Q

Carboxylases

A 
Require ABC
   - ATP
   - Biotin
   - CO2
Pyruvate carboxylase (gluconeogen.)
Acetyl-CoA carboxylase (FA synth.)
Propionyl-CoA carboxylase (Prop. acid pathway)
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49
Q

TLCFN

A 
TLCFN
   - TPP (thiamin, Vit B1)
   - alpha-Lipoiic Acid
   - CoA
   - FAD (riboflavin, Vit B2)
   - NAD+ (nicain, Vit B3)
3 enzymes require
   - Pyruvate DH (pyruv ---> A-CoA)
   - a-ketoglutarate DH (a-KG ---> succinyl CoA)
   - branched chain ketoacid DH (Val/Iso/Leu ---> Propionyl CoA) "maple syrup urine disease"
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50
Q

Hutchinson-Gilford Progeria Syndrome

A 
normal dev. 3-6 months
LMNA mutation
   - Lamin A, of nuc. lamina
fragile nuclei, genomic instability
mean death 13.5 years
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51
Q

Beriberi

A 
Thiamine deficiency (Vit B1)
Need TPP for TLCFN enzymes
   - Pyruvate DH
   - a-Ketoglutarate DH
Loss of neural function
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52
Q

Fluoroacetate

A
  • Inhibits aconitase of TCA cycle
  • metabolizes to fluorocitrate
  • in some acacia trees in Australia/Africa
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53
Q

Tyrosine-Kinase Associated Receptors

A 
act through CYTOplasmic tyr. kinases
soluble tyr. kinases in cytosol associate with activvated receptor
ligands
   - cytokines
   - interleukins
   - integrins
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54
Q

Receptor Tyrosine Kinase

A 
aka "Tyrosine-linked receptors"
contain intracellular tyrosine kinase domain
two monomers cross-Phosph. each other
ligands
   - growth factors
55
Q

Philadelphia chr

A
  • chromosomal translocation
  • Bcr-Abl fusion protein
  • Abl is always ON (it’s a Tyr Kinase)
  • chronic myeloid leukemia
  • treated by Imatinib (Gleevac)
56
Q

PDGFR

A 
platelet derived growth factor receptor
stimulated mitogenic activity (MAPK/PI3K)
oncogenic mutation
   - chronic myeloid leukemia
   - GI stromal tumors
57
Q

GSD Type 1

A 
von Gierke's
Glu-6-Phosphatase
symptoms
   - severe hypoglycemia
   - hepatomegaly
   - hyperlipidemia
58
Q

GSD Type 2

A 
Pompe's
acid a-glucosidase (a1-4 linkages)
symptoms
   - cardiomegaly
   - death by 2 y/o
59
Q

GSD Type 3

A 
Cori
glycogen debranching enzyme/glycogen phosphorylase
symptoms
   - mild hypoglycemia
   - hepatomegaly
60
Q

GSD Type 4

A 
Andersen
Glycogen branching enzyme
Symptoms
   - cirrhosis
   - failure to thrive
   - hypotonia
   - death by 2 y/o
61
Q

GSD Type 5

A 
McArdle's
Muscle glycogen phosphorylase
Symptoms
   - muscle weakness
   - cramps on exercise
   - rhabdomyolysis
62
Q

GSD Type 6

A

Hers
Liver glycogen phosphorylase
Symptoms
- hepatomegaly

63
Q

Ion Flow (Na, Ca, H, K, Cl, HCO3)

A 
In
   - Na
   - Ca
   - H
Out
   - K
   - Cl
   - HCO3
64
Q

Wernicke-Korsakoff Disease

A

brain syndrome cause by lack of Vit B1 (thiamine)
transketolase has low affinity for TPP due to point mutation (part of HMP Shunt)
symptoms
- ataxia
- psychosis
- confusion
Also, alcohol inhibits thiamine absorption

65
Q

Citrate synthase

A 
A-CoA + Oxaloacetate ---> Citrate (Krebs)
Inhibited
   - citrate
   - succinyl-Coa
   - NADH
   - ATP (this can be reversed by AMP)
66
Q

Pyruvate DH

A 
Pyruvate ---> Acetyl-CoA
TLCFN
Activated:
   - NAD+
   - CoA
   - Ca (in muscle only)
Inhibited
   - A-CoA
   - ATP
   - NADH
67
Q

Complex 1 (ETC)

A
  • NADH-ubiquinone oxidoredutase
68
Q

ETC/OP Inhibitors (I - 2, IV - 3, OP - 2)

- “Br-cac, DO”

A 
Complex I
   - Barbiturates
   - Rotenone (fish poison)
Complex IV
   - Cyanide (Fe3+)
   - CO (Fe2+)
   - Azide
ATPase
   - Oligomycin (antibiotic, plugs opening of F0)
   - DCCD
69
Q

Chylomicrons

A
  • packages of fat from diet

- Ride on Apoprotein B48

70
Q

VLDL

A
  • very low density lipopotein
  • it is made of excess Glucose from diet
  • Glu –> Pyruvate –> A-CoA –> fatty A –> fat (then exit liver)
  • drop off FA at adipose, return glycerol-P to liver
71
Q

lipoprotein lipase

A
  • cuts the FA’s off of the fat in VLDL

- drops off FA at adipose tissue for storage, glycerol will return to liver

72
Q

GLUT4

A
  • Glu transporter
  • found in muscle and adipose
  • stays in vesicles, waiting for insulin to arrive at cell, then it’s on surface
73
Q

Main source of fuel, 4 hours after eating

A

Liver glycogen

74
Q

Main source of fuel, `8 hours after eating

A

Fatty acids (adipose tissue

75
Q

Main source of fuel, 5 days after eating

A

Ketone bodies

- Adipose tissue fat –> (b-ox) –> fatty a –> fatty a albumins –> Liver –> A-CoA –> ketone bodies

76
Q

4 main starvation adaptations

A
  1. fat hydrolysis in adipose
  2. gluconeogenesis in liver and kidney
  3. ketogenesis in liver
  4. protein degridation in muscle
77
Q

CTD Tail

A

C-terminal end of RNA Pol II

Must be phosph. to initiate transcription

78
Q

DNA Methylation

A

Done at CpG islands (C’s that proceed G’s)
Transcriptional REPRESSION
Heritable (epigenetic)

79
Q

siRNA

A
  • small interfering RNA
  • can induce transcriptions silencing
  • usually exogenous (artifically introduced)
80
Q

miRNA

A
  • micro RNA
  • an regulate mRNA degredation by base pairing with existing mRNA, targets it for destruction
  • usually endogenous
81
Q

GLUT2

A

Found in Liver and Pancreatice B-cells
Uptake and release of Glu (liver)
Glu-sensing (B cells)
- GLUT2 –> ATP:ADP ratio –> membrane depolarization –> open Ca channel –> Ca enters –> Insulin vesicles secreted

82
Q

3 different hemolytic anemias

A

1st most common
Sickle cell
- Hb has mutation –> distorts RBC –> RCB life expectancy drops –> RBC lysis

2nd most common
Pyruvate kinase deficiency
- Back up of Glyc. –> no ATP –> RBC has no other source of ATP –> can’t power Na-K pumps –> cell hypotonic –> swells –> lysis

G6PD deficiency
- No entry into HMP Shunt –> can’t make NADPH (reduced glutathione) –> oxidative damage to RBC –> lysis

83
Q

MetHb

A
  • Methemoglobin
  • Heme group has Fe3+ not Fe2+
  • Cannot carry O2
  • Reverted to Hb by MetHb reductase, which requires NADPH
  • “methemoglobinuminia”
84
Q

Heinz bodies

A

Small budding dots on RBC’s

Found in G6PD hemolytic anemia, but not PK

85
Q

2,3-BPG

A
  • Part of Glycolysis
  • Binds to Heme groups in Hb and lowers O2 affinity
  • Necessary for dumping O2 in tissue
  • It binds the B subunit of Hb and “kicks off” the O2 there
  • HbF (fetal) has alpha and gamma subunits, so unaffected by 2,3-BPG
86
Q

Pyruvate Dehydrogenase

A
  • Pyruvate to A-CoA
  • Inhibited by Arsenic (rat poison, herbicides, moonshine)
  • TLCFN

Thiamine deficiency

  • common in alcoholics (alcohol inhibits absorption of thiamine)
  • and IV solution of glucose can kill alcoholics because lactic acidosis
87
Q

Cell response to hypertonicity (in surroundings)

A

Activate Na-H exchanger (Na in, H out) —> This activates Cl-HCO3 exchanger —> Cl enters
Net uptake of Na and Cl —> water follows

88
Q

Cell response to hypotonic (in surroundings)

A

Activate solute efflux (either Cl and/or K channels) —> Water exits

89
Q

Idiogenic osmolytes

A

Some cells can increase tonicity by producing these
Response to long-term hyperosmolality
OR because Na and Cl can interrupt cell processes

90
Q

Na-H exchanger

A

“acid extruder”

  • Uses Na gradient to move H out
  • activated by intracellular metabolic acidosis
  • inhibited by very high pH
  • induces Cl-HCO3 exchanger by creating high pH
91
Q

Cl-HCO3 exchanger

A

“acid loader”

  • uses Cl gradient to move HCO3 out
  • activated by intracellular metabolic alkalosis
  • inhibited by very low pH
  • induces Na-H exchanger by creating low pH
92
Q

Intracellular respiratory acidosis

A

high E CO2 pushes CO2 into cell
low pH in cell
CO2 + H20 —> H + HCO3 (carbonic anhydrase)
Activate Na-H exchanger

93
Q

Protein sorting signals

A

encoded in aa sequence
usually at N-terminus
or can be “signal patches”, not near each other in aa sequence, but in 3d are near each other
no signal = destined for cytosol

94
Q

Importins

A

Recognize nuclear localization signals on proteins
Brings them to/through nuclear pore complex
Have two binding sites
- nuclear localization signal
- nuclear pore complex

95
Q

Exportin

A

Recognizes nuclear export signal
RanGTPase binds the protein-exportin complex and exits the nuclear pore with them
- RanGTPase used to dissociate the complex in the cytosol

96
Q

Vesicle coats from different sources

A

Clathrin-coated (from plasma membrane)
COP I-coated (from Golgi)
COP II-coated (from ER)

97
Q

ER retrieval signal

A

KDEL
Usually at C-terminus
Proteins can only leave ER after this sequence has been cleaved

98
Q

SNARE

A

v-SNARE (vesicle)
t-SNARE (target)
Need SNARE-SNARE interaction for vesicle fusion

99
Q

Co-translational import

A

rER “catches” the protein as it’s coming out of the ribosome
SRP recognizes the early budding protein, brings it to SRP receptor on ER
Two types of proteins are usually co-translated
- transmembrane proteins
- water soluble protein (for secretion)

100
Q

Lysosome maturation

A

Endocytotic vesicle —> Early endosome —> Late endosome (mildly acidi pH 6, zymogens) —> Endolysosome (fusion with pre-existing lysosome, activates zymogens, pH 4.5-5) —> lysosome

101
Q

Mannose-6-P

A

Signals lysosomal proteins for lysosomes

M6P receptors are on the inside of Trans-Golgi

102
Q

UDP-glucose phosphorylase

A

G1P —> UDP-Glu (to be added to glycogen)

Required UTP

103
Q

Glycogen synthase

A

UDP-Glu —> Glycogen (a1-4 linkages)
Activated by Insulin
Works alongside Glycogen branching enzyme (a1-6 linkages, every 8-14 residues)

104
Q

Gluconeogenesis

A

Mainly in liver/kidneys (only places with G6Pase)
E to power gluconeogenesis comes from triacylglycerides (TG)
Hormone Sensitive Lipase (HSL) breaks fat —> FA + Glycerol

105
Q

Cori cycle

A

LIVER
Lactate —> Pyruvate —> Glu (gluconeogenesis)

BLOOD
Transport

MUSCLE
Glu —> Pyruvate —> Lactate

  • this cycle produces lactic acidosis
106
Q

Glucose-Alanine Cycle

A

LIVER
Alanine —> Pyruvate —> Glu (alanine transaminase)
Urea excreted

BLOOD
Transport

MUSCLE
Glu —> Pyruvate —> Alanine (alanine transaminase)

107
Q

Transketolase

A

Part of HMP Shunt
Requires TPP (but not the rest of TLCFN)
Wernicke-Korsakoff Disease (mut in TK gene, enzyme won’t bind TPP)
- treat with increased thiamine in diet (Vit. B1)

108
Q

G6PD deficiency

A

Most common enzymatic deficiency in world
X-linked recessive
10-14% of African-American males have it

  1. Immunodeficiency
    - In neutrophil, no NADPH made
  2. Heinz bodies
    - Hb denaturation in RBC’s because oxidative damage because no reduced gultathione because no NADPH
  3. Hemolytic anemia
109
Q

Trophic factors

A

Cells require these signals to “keep living”

110
Q

Cell signaling dessensitization

A

Receptor sequestration
Receptor down-regulated
Receptor inactivated
Inhibitor protein production

111
Q

Mitogen

A

Signaling molecules that stimulate cell division

Activate G1/S-Cdk activity

112
Q

Intracellular receptors

A
  1. Steroids
    - hydrophobic enough to diffuse in to cell
    - intracellular receptors dimerize and then go to nuc as TF’s
  2. Nitric Oxide
    - gas, small enough to diffuse
    - acts locally, short half life
    - Activates guanylyl cyclase (GTP —> cGMP)
113
Q

Eicosanoid

A

Lipids that bind cell surface recptors
Short half life, act locally
Induce clotting and inflammation

114
Q

Ion-channel-coupled

“Ionotropic”

A

Rapid signaling in electrically-excitable cells
Action: opens/closes ion channels to change excitability state of cell
Ligands: Neurotransmitters

115
Q

G Protein coupled receptors

GPCR

A

7TM (7 pass transmembrane proteins)
Ligands: eicosanoids, neurotransmitters, peptide hormones
Special senses: smell, sight, taste

Coupled to three protein inside
alpha (binds GTP)
beta-gamma (they stay together)

alpha subunit will be activated and will activate/inhibit adenylyl cyclase
Gs (activates) vs. Gi (inhibits)

116
Q

Receptor serine/threonine kinases

A

Ligands: TGF-beta
Action: form heterodimers –> one chain activates other –> activates Smad pathway

117
Q

Notch

- Do Not Work For HP

A

Receptor for direct cell-cell signaling
Ligand: Delta
Action: Delta induces proteolytic cleavage of cystolic tail of Notch —> to nuc as TF

118
Q

Frizzled

- Do Not Work For HP

A

Receptor
Ligand: Wnt
It stops the bully from phosphorylating and ubiquinating beta-catenin

119
Q

Patched

- Do Not Work For HP

A

Receptor
Ligand: Hedgehog
Actions: Activated smoothened —> inhibits phosphorylation of Ci —> Ci becomes TF

120
Q

Death receptors

A

Ligands: cytokines, growth factors, pathogen assoc. molecular patters (MAMP)
Action: binding of one ligand induces clustering of cytosolic Death Domains
Ex: Caspase

121
Q

Inegrins

A

At cell-matrix junctions (focal adhesions, hemidesmosomes)

Induce proliferation, gene expression, survival

122
Q

cAMP

A

A secondary messenger

Activates protein kinase A

123
Q

PIP2

A

Cleaved by phopsholipase C into IP3 + DAG (two secondary messengers)
IP3 - activated ligand-gated Ca channels
DAG - activates protein kinase C

124
Q

PI3 Kinase

A

Phosphorylates PIP2 to PIP3
This activate Akt, a kinase that influences cell survival and protein synth.
A secondary messenger

125
Q

JAK/STAT

A 
JAK
- cytokine receptor
- non-receptor protein Tyr kinase
- phosphorylates nearby STAT's ---> STAT's dimerize ---> TF's
STAT
- The secondary messenger
126
Q

NF-kB

A

regulates proliferation and survival
activates through death receptors
Ligands: Cytokines, growth factors, pathogen assoc. molecular patters (MAMP) (this is same as death receptors)
Action: Receptor activates 1kB kinase —> phosphorylates and ubiquinates 1kB (which had been covering a NF-kB dimer) —> free NF-kB dimer —> TF
It’s a secondary messenger

127
Q

Rho (secondary messenger)

A

Regulates cytoskeletal changes
Activated through integrins, growth factor receptors
Promotes actin growth, and phosphorlationg of myosin

128
Q

Sickle Cell Disease

HbS

A

Affects shape/life span of RBC’s
Mutation in B chain, non-polar Val for Glu
Creates hydrophobic knobs that aggregate and pcpt

129
Q

Sickle Cell Symptoms

A

Anemia

Growth failure
- long term effect of anemia

Infection
- reduced splenic function

Vaso-occlusive events

  • local vessel obstruction, further promotion of hypoxia/acidosis
  • causes extreme pain

Organ failure
- long term effect of hemolysis and clogging

130
Q

Sickle Cell Treatment

A

Hydroxyurea

  • stimulates HbF production
  • mechanism noe 100% known but…
  • Activates NOS
  • ribonucleotide reductase
131
Q

Ionotropic

receptor class

A
  • ligand-gates ion channels

- typically fast neurotransmitters

132
Q

Metabolic

receptor class

A
  • G protein coupled

- coupled with effector protein, ion channel, or TF

133
Q

Enzyme-linked

receptor class

A
  • act on TF’s

- cell growth, differentiation, division, apop., inflammtion

134
Q 
Nuclear receptors
(receptor class)
A
  • act directly as TF’s

- located in cytosol/nucleus, ligand must diffuse in

MCM (3 decks)

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