2 Flashcards

1
Q

Galphas

A

activate adenylate cyclase, raise substrate AMP

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2
Q

GalphaIs

A

inhibit adenylate cyclase, lower substrate AMP

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3
Q

Phospholipase A2 can activate

A

arachidonic acid.

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4
Q

Major thing activated by GalphaIs

A

Phospholipase A2.

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5
Q

——- is the source of prostaglandins

A

arachidonic acid

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6
Q

Prostaglandins are

A

used in pain and inflammation signaling

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7
Q

IP3 binds

A

ER to release calcium

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8
Q

PIP2

A

leads to changes in gene expression (transcription factors). Breakdown of Gqs by PLC beta (other product is IP3)

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9
Q

PIP2 serves as substrate for

A

phospholipase C

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10
Q

Phosphatidyl

A

ids something as a phospholipid

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11
Q

DAG activates

A

protein kinase C

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12
Q

*Most isoforms of PKC regulated by

A

DAG (DAG allows the enzyme to bind Ca++ tighter. Therefore, the enzyme can function at lower Ca++ concentrations

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13
Q

the trimeric G protein gets turned on, but

A

turns itself off.

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14
Q

Meanwhile, the agonist-GPCR complex is free to

A

activate other trimeric G proteins with which it comes in contact.

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15
Q

Desensitization of GPCRs by

A

endocytosis - chronic usage

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16
Q

Endocytosed receptors can either be

A

recycled or degraded

17
Q

Ligands

A

: Growth factors, differentiation factors, cytokines

18
Q

Receptor tyrosine kinase:

A

Receptors either contain an intrinsic tyrosine kinase enzyme or an extrinsic tyrosine kinase enzyme

Binding of ligand leads to dimerization of the receptor

Some receptors form homodimers, some receptors form heterodimers, and some receptors do both.

Dimerization leads to transphosphorylation of receptors

Tyrosine phosphorylation of receptors leads to docking of signaling molecules

The positioning of proteins near the membrane leads to different cascades of signaling

19
Q

Receptor tyrosine kinase:

Receptors either contain an

A

intrinsic tyrosine kinase enzyme or an extrinsic tyrosine kinase enzyme

20
Q

Receptor tyrosine kinase:

Binding of ligand leads to

A

dimerization of the receptor

21
Q

Receptor tyrosine kinase:

Some receptors form ——-, some receptors form ———-.

A

homodimers

heterodimers, and some receptors do both

22
Q

Receptor tyrosine kinase:

Dimerization leads to

A

transphosphorylation of receptors

23
Q

Receptor tyrosine kinase:

Tyrosine phosphorylation of receptors leads to

A

docking of signaling molecules

24
Q

Receptor tyrosine kinase:

The positioning of proteins near the membrane leads to

A

different cascades of signaling

25
Q

JAK-STAT signaling mediates….

A

mediates immune proccesses, development.

Used for a quick change in gene expression

26
Q

JAK-STAT;

A
  1. Binding of ligand (cytokine) leads to phosphorylation of receptor by JAK kinase
  2. This leads to binding of STAT protein (one of six) to the phosphorylated receptor
  3. These leads to phosphorylation of STAT protein by Jak kinase
  4. This leads to dimerization of STAT protein
  5. This leads to translocation of STAT dimer to nucleus and transcriptional activation of panels of genes
27
Q

STAT monomers contain both an SH2 domain and a tyrosine that can be

A

phosphorylated

28
Q

Nuclear Hormone Receptors

A

Steroid hormone receptors - inside cell somewhere.

29
Q

Class 1 nuclear receptors

*Exist as a complex with ———– in the absence of ligand.

A

heat shock proteins in the absence of ligand

30
Q

Class 1 nuclear receptors

*Ligand binding induces the complex to

A

fall apart, form a homodimer, and bind to its specific DNA response element

31
Q

Class 1 nuclear receptors

*Once bound to its specific response element it binds —————– to stimulate transcription

A

coactivators

32
Q

Class 2 nuclear receptors

*Binds to target DNA at its specific response element in the

A

absence of ligand

33
Q

Class 2 nuclear receptors

*Binds ——— in the absence of ligand and repressses transcription

A

corepressors
*Form homo and heterodimers

take acetyl group off lysine, making histone more positively charged and strenthening interactions between DNA and protein.

34
Q

Class 2 nuclear receptors

*Ligand binding produces a switch from binding ——-to binding—————

A

corepressors

coactivators

35
Q

Class 1 nuclear receptors cause histones to be

A

less positively charged, weakening the interaction with chromatin.