EXAM 2 - Cell Signaling Flashcards

1
Q

PKA

A

-Activated by cAMP
-Phosphorylates VDCCs allowing an increase in Ca2+ entry
-Phosphorylates RYRs allowing an increase in Ca2+ entry from the SR

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2
Q

DNA-PK

A

-Activated by DNA damage produced by ROS
-Phosphorylates and activates P53

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3
Q

GC

A

-Activated by NO binding
-turns GTP to cGMP

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4
Q

Matrix Metalloproteases (MMPs)

A

-Affect cancer cell mobility, degrades the ECM
-GoF

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5
Q

CAS (Caspases)

A

-mediate apoptosis
-initator caspases activate exectutioner (effector) caspases
-Executioner caspases chop up proteins

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6
Q

AngII

A

-activated by renin in the kidneys
-promotes increased contraction of vasc. smooth muscle
(activates alpha-q when bound to ATII receptor. alpha q actives PLC, PLC cuts PIP2. IP3 activates IP3 gated channels, influx of Ca2+ from the SR, Ca2+ binds to PKC. PKC binds to DAG and phosporylates VDCCs, more Ca2+ promotes increased contraction = increased arteriole resistance + decreased venous compliance = increased MAP)

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7
Q

MLCP

A

-phosphorylated and activated by PKG
-dephosphorylates myosin, inhibiting contraction of smooth muscle

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8
Q

Oncogene

A

-GoF mutations that promote a cancerous phenotype
-Ex: growth factor receptors, Akt, Bcl-2

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9
Q

PKG

A

-Activates and phosphorylates MLCP
-Activates and phosphorylates Potassium channels allowing an efflux of K+ which leads to hyperpolarization of the cell (interferes with VDCCs on smooth muscle)

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10
Q

Cas-9

A

-zymogen form = pro-caspase-9
reruited by the APAF/cyt-c complex
-when bound to the complex, pro-casp-9 undergoes cross-proteolysis leading to the active caspase-9

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11
Q

cGMP

A

-Activated by GC (GTP-cGMP)
-Activates PKG

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12
Q

Mdm-2

A

-Part of the intrinsic apoptotic pathway
-Activated by Akt
-Targets p53 for degradation

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13
Q

Bcl-2

A

Proteins that regulate pores that allow the release of cyt-c for apoptosis
3-categories:
-pro-survival
-pro-apoptosis
-BH3 (blocks pro-survival proteins)

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14
Q

PI3K

A

Turns PIP2 into PIP3
-Part of the intrinsic apoptotic pathway

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15
Q

MKP

A

-Inhibits JNK (in the signaling pathway of apoptosis)
-Is activated by ROS

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16
Q

AKT

A

-Activated by PIP3
-Phosphorylates and inhibits BH3
-Activates Mdm-2

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17
Q

What are some Tumor Suppressor Genes?

A

P53, PTEN, BH3

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18
Q

DAG

A

-Part of the cleaved PIP2
-Ca-PKC binds and activates
-This complex then activates VDCCs in smooth muscle

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19
Q

Myc

A

-promotes cell proliferation (cancer!)
-activated by MAPK

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20
Q

cAMP

A

-Activated by AC (ATP -> cAMP)
-Activates HCN channels
-Activates PKA

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21
Q

ASK-1

A

-Activated by ROS
-Activates JNK

22
Q

RAS

A

-Activates MAPK
-monomeric G-protein

23
Q

ROS

A

-can be generated by high levels of NO
-made in the ETC
-associated with ischemia
-can cause DNA damage
-can promote apoptotic cell death

24
Q

PTEN

A

dephosphorylates PIP3 -> PIP2

25
Q

Examples of Pro-Survival/Anti-Apoptotic mutations

A

LoF of P53
GoF of Akt

26
Q

NOS

A
  • Activated by Ca-CAM complex
  • Generates N.O.
27
Q

GRK

A

-Activated by an accumulation of beta/gamma g-protein subunits
-Phosphorylates GPCRs (P leads to recruit of B-arrestin which inactivates GPCRs)

28
Q

AC

A

-Activated by Gs protein
-Inhibited by Gi
- When activated, generates cAMP from ATP

29
Q

2 modes of vascular control?

A

Direct = arteriole resistance
Indirect = venous compliance

30
Q

PDE

A

cAMP -> AMP
cGMP -> GMP

31
Q

PKC

A

-Activated when bound to Ca2+ and DAG
-Phosphorylates and increases activity of VDCCs and RYRs

32
Q

P53

A

-Phosphorylated and activated by DNA-PK and JNK
-Triggers cell cycle arrest when levels are low
-Triggers apoptosis (via release of BH3 from nucleus) when levels are high

33
Q

PLC

A

Cleaves PIP2 to IP3 and DAG

34
Q

APAF

A

Scaffolding that binds to cyt-c and then recruits pro-caspase-9

35
Q

Rho-GTPase GoF

A

increases cancer mobility

36
Q

E-cadherin LoF

A

increases cancer cell mobility

37
Q

N.O.

A

-Produced by NOS
-Can be turned into ROS in the ETC
-Activates GC in smooth muscle cells

38
Q

cyt-c

A

-moves e- in the ETC
-release of cyt-c from the Mt induces apoptosis

39
Q

Beta arrestin

A

-Recruited when GRK phosphorylates the GPCR
-inactivates the GPCR

40
Q

Alpha-1 Adrenergic Receptor

A

-Located in smooth muscle and myocytes
-NE binds to this receptor

41
Q

PIP2

A

-Cleaved by PLC into IP3 and DAG

42
Q

IP3

A

-Activated when PLC cleaves PIP2 into IP3 and DAG
-Binds to IP3 gated channels on SR allowing an influx of Ca2+

42
Q

Example of a pro-proliferative mutation

A

GoF of growth factor receptors

43
Q

Ach

A

-Released from PNS
-Binds to muscarinic receptors (M3)

44
Q

MLCK

A

-Activated when bound to Ca-CAM complex
-Phosphorylates myosin in smooth muscle, promotes contraction

44
Q

JNK

A

-Activated/phosphorylated by ASK-1
-Activates/phosphorylates P53

45
Q

CAM

A

-Activated when bound to Ca2+
-Activates NOS to generate NO
or
-Binds to MLCK to Phosphorylate Myosin for contraction of smooth muscle

45
Q

Clathrins

A

-recuited to the GPCR/Beta-Arrestin complex
-clathrin coating triggers endocytosis of GPCRs (sequestration)

46
Q

NE

A

-Released from the SNS
-binds to adrenergic receptors

47
Q

VDCC

A

-depolarization allows these channels to become more active and let more Ca2+ into the cell
-PKA phosphorylates VDCCs increasing activity
-Ca-PKC-DAG complex phosphorylates VDCCs increasing activity

48
Q

HCN Channel

A

-allows Na+ into the cell
-Activated by cAMP