Cell Signaling Flashcards

1
Q

What does absence of signaling cause

A

Apoptosis

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2
Q

5 types of signaling

A

Endocrine- hormonal, long range. Blood stream
Paracrine- nearby, diffusion
Neuronal- very close, synapses
Contact dependent- cells linked by signal
Autocrine- cell signals self

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3
Q

Signal components

A

Ligand, receptor, intracellular signal proteins, target proteins

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4
Q

Is ligand concentration high or low

A

Low, and affinity is very high

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5
Q

Two types of receptor

A

Cell surface and intracellular. Intra requires small hydrophobic signal like a steroid

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6
Q

Domains of intracellular signal protein

A

Dna binding, ligand binding, transcription activation, inhibitory or promoter

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7
Q

Types of cell surface receptors

A

Ion channel linked(bind to allow ions in), G protein linked (7 pass), and enzyme linked (single pass)

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8
Q

Secondary signal protein uses

A

Turn signal on or off, amplify signal, or split signal

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9
Q

Can response proteins do different things with same signal, or same with different?

A

Yes

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10
Q

Which is slower: dna pathway or altered protein pathway

A

DNA pathway

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11
Q

G protein receptor pathway

A

Receptor binds signal, causing protein to bind G protein. Makes gtp, and splitting trimer into two. Alpha unit activates target and makes gdp, rebinding to trimer

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12
Q

cAMP pathway

A

G protein. Activates a protein that makes cAMP, activates protein kinase A, which goes to nucleus to phosphorylate.

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13
Q

Ca signaling pathway

A

G protein activated. Activates phospholipase C, which releases inositol, opening Ca channel in ER, activating Protein kinase c

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14
Q

Enzyme pathways

A

Generally receptor tyrosine kinase. Involve dimer signals. Which dimerize tyrosine kinase, P itself to make signal complex

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15
Q

What do phosphorylation sites on RTKs do?

A

Serve as protein docking sites

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16
Q

What are signal transduction switches and what types?

A

Turn signal on or off. Kinase type and gtpase type.

17
Q

SRC domains and functions

A
N and C lobe- ATP between
SH1- kinase
SH2- phosphotyrosine binding 
SH3- protein binding 
SH4- binds membrane
18
Q

SRC pathway

A

Nonreceptor TKR. Tail Dephosphorylated to open, then loop is phosphorylated, opening catalytic cleft. Three states

19
Q

RAS basics

A

RTK linked to GTPase. Tethered to membrane.

20
Q

RAS pathway

A

Activated by GEF, forcing in GTP. Then signals, and GAP induces GTP hydrolysis inactivation, turning off. Activates MAP kinase cascade.

21
Q

JAK-STAT pathway

A

RTK. Cytokine binds, binding JaK to itself. Then it phosphorylates itself twice, where STAT binds and dimerizes

22
Q

NF-kB path

A

Activates inhibitor kinase, which degrades inhibitor of NF-kB

23
Q

TGF- b pathway

A

Type 2 receptor binds signal(BMP), which binds and phosphorylates type 1. Activates smads

24
Q

Wnt pathway

A

Frizzled binds receptor, activating disheveled, which prevents GSK from degrading beta catenin

25
Q

Hedgehog pathway

A

Sonic binds, preventing patched from inhibiting smoothened, which prevents GLI from being cut. Normally repressor, now inducer.

26
Q

Cell contact path (Notch)

A

Delta binds notch, connecting cells. Pulls up notch, allowing cleavage. Lowers notch, further cleavage. Bit inside goes to nucleus. Differentiation.

27
Q

Types of combinatorial action

A

Integration, divergence, cross talk, specialization.