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Cell Biology > Chapter 16 > Flashcards

Chapter 16 Flashcards

1
Q

what are the outcomes to cellular signaling?

A

Survival, cell growth (cell division), inhibition of growth, development (differentiate into something else), apoptosis, DNA synthesis, Protein synthesis, defense against pathogens, change in metabolism

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2
Q

Diabetes

A

Type1
• auto immune - beta cells in the pancreas, no insulin, dependent on insulin
Type 2
• make insulin- insulin resistant, no longer respons as well over 8% of the pop.

Both glucose intolerant- early warning sign

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3
Q

Signal Transduction Information pathways traveling

A

Long distance- endocrine-bloodstream
Local- Paracrine- extracellular fluid diffuse
Touching- contact dependent- physical contact
Self- autocrine- self

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4
Q

What are the essential parts and steps in a signaling pathway?

A
  1. Ligand produced
  2. Ligand travels to target cells
  3. Ligand binds receptor
  4. Signal passed from receptor to additional signal pathways
  5. Response (slow or fast)
  6. Ending the signal
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5
Q

Receptor Proteins

A
  1. Receptors bind to specific ligands-binding specific
  2. G protein coupled receptors and enzyme coupled receptors are examples of cell-surface receptors
  3. Some receptors are also enzymes (common: kinase, adds P)
  4. Ligand are hydrophobic and small (crossing membrane) (intracellular)
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6
Q

What are commonly found in the intracellular signaling pathway?

A
  1. Kinases
  2. Sm G proteins
  3. Adaptor
  4. 2nd messengers -Ca2+ and DAG to cAMP (sm molecules, bind and regulate)
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7
Q

Two types of receptor proteins?

A

Cell surface receptors
Intracellular receptors
Effector specificity- ligand receptor complex mediates a response specific to cell type

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8
Q

Intracellular Signaling

A
  1. Primary transduction
  2. Relay
  3. Transduce and Amplify-important -make signal bigger
  4. Integrate and distribute- CROSSTALK-signaling pathways dont exist alone

Leads to altered metabolism, altered cell shape or movement, and altered gene expression

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9
Q

What are essential to help turn proteins on and off?

A

Kinases and phosphatase through charges in phosphoralation status

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10
Q

What are three types of i2nd messengers in intracellular signaling?

A
  • 3, 5’ Cyclic AMP (cAMP)
  • 1,2 Diacylglycerol (DAG)
  • Ip3I
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11
Q

Why are some signaling pathways slow and some fast?

A

Slow- makes new proteins

Fast- Alter existing protein

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12
Q

What do molecular switches do?

A
  1. Signaling by phsphorylation- SIGNAL IN kinase activates changing ATP to ADP(SIGNAL OUT) and then phosphates inactivates and loses a P and turns the signal off.
  2. Signaling by GTP binding protein - (SIGNAL IN) GTP binding activates and GDP out and GTP in, so signal on (SIGNAL OUT), then GTP hydrolysis inactivates and loses a P and turns the signal off
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13
Q

Termination of Signals

A
  1. Receptor sequestration (bring in receptor and turn off)
  2. Receptor down-regulation (bring in receptor and turn off) (degrading in lysosome)
  3. Reception inactivation (change at surface)
  4. Inactivation of signaling protein (change at surface)
  5. Production of inhibitory protein (negative feed back/ feedback inhibition) (change at surface)
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14
Q

Insulin Resistance

A
  • Glucose intolerant, hypertenstion, obesity, dyslopidemia

* Type 2 diabetes, cardiovascular disease, neurodegeneration, pcos, cancer, fatty liver

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15
Q

Insulin Signaling

A
  • insulin -peptide hormone -endocrine signal

* insulin receptor -tryosine kinase receptor

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16
Q

Enzyme linked receptor proteins

A

Cooperative binding
active when together
activate each other

17
Q

Ras signaling

A
  • Adaptor protein is attached to the activated receptor tyrosine kinase (Grab2)
  • Son of Sevenless attaches to adaptor protein
  • SOS activates an inactive Ras Protein (GDP to GTP)
  • with ras on the signal goes onward
18
Q

Are the receptors binding specific?

A

Yes, there are multiple tryosines, the receptor activates at least 3

19
Q

Mutations in the receptor pathway

A
  • 30% human cancers have a Ras mutation- no longer hydrolyzes (stuck in “on”)
  • amp DNA, turn on receptors with too many copies
  • melanoma -Raf, turned on (MAP= mitogen activated protein)
20
Q

MAP Kinase cascade

A
  1. Active Ras protein activates MAP kinase-kinase-kinase
  2. RAT phosphorlates (ATP to ADP gains P) activates MAP- kinase- kinase
  3. MEK phosphorlates (ATP to ADP gain a second P) activates MAP-kinase
  4. Leads to fast (changes in protein activity) or Slow ( changes in gene expression) (Goal to turn on G1 to S phase-turn on cell cycle)

Three places for other signals to affect this pathway

21
Q

How does amplification affect kinase?

A

each kinase phosphorlating many, ramps up the signal- high and fast

22
Q

Insulin Receptor signaling pathway

A
  • activates Ras kinase pathway- cell growth/differentiation

* survival signal, turn on matabilism of glucose and lipid synthesis

23
Q

PI3K signaling

A

Goal: relocalize

  1. Activated RTK activates PI3-kinase and inositol phospholipid
  2. goes to phosphorylated insoitol phospholipid
  3. goes to protein kinase 1
  4. activated Akt and protein kinase 2
  5. the signal is relayed onward
24
Q

What happens when PI3K signaling is on? off?

A

Turn on: survival and metabolism
Turn off: use lipid phophortase, protein phophortase, RasGAP- rasGTP to ras GDP, and edocytose the receptor by degrading ligand and degrade ligand and receptor

25
Q

How does glut 4 containing vesicles transport to plasma membrane?

A

passive transport of glucose

26
Q

G protein coupled receptors

A

Fight or flight
GEF attaches to adrenalin epmophrian and the GDP with alpha, beta, and gamma are off until the conformation change and GTP binds with alpha while beta and gamma are seperate. This leads to G alpha S (stimualtes)

27
Q

Brian Kobilka’s Structures

A

Special structure:

  1. inactive and active states
  2. membrance protein difficult to crystalize
28
Q

Heterotrimeric G proteins

A

Turn off: hydrolize GTP

  1. phosphoralte receptor
  2. internalize receptor
29
Q

Adenylyl cyclase

A

Caffeine inhibits

adenylyl cyclase makes it and cyclic AMP turns off

30
Q

Activation and inactivation of G alpha

A
  1. Activation of a target protein by the alpha subunit
  2. hydrolysis of GTP by the alpha subunit inactivates this subunit and causes it to dissociate from the target protein
  3. inactive alpha subunit reassembles with beta gamma complex to refrom an inactive G protein
31
Q

PKA activity fast

A
  • releasing more glucose to increase
  • phophorylate and inhibit glycogen synthase- active PKA
  • glycogen n - glycogen n-1 +glucosel P
32
Q

PKA activity Slow

A
  • turn on transcription to make new proteins

* phosphoralate transcription factor CREB

33
Q

PhospholipaseC

A
  • PKA -binds to DAG - BInd to Ca2+ for a response

* 3 second messengers (DAC, IP3, and Ca2+)

34
Q

What happens with energy is utilized?

A

increase metablic rate

35
Q

Vibrio Cholerae

A

adds chemical group and G alpha s is always on, no longer hydrolyze GTP

36
Q

Membrane lipids can function as signaling second messengers

A

depends on cell what it does
•armpit-sweat
•mouth- salivate

secretion and metabolism

37
Q

There are many G protein subunits

A

Contact dependent
•Stimulatory G protein complex- activates Adenylyl cyclase and increases cAMP and increase PKA
•Inhibitory G protein complex- inhibits adenylyl cyclase, inhibit cAMP, and inhibits PKA

38
Q

Convergent signaling

A

CROSSTALK different pathways can affect other pathways

Dont act along modified and affected by other pathways

39
Q

Combinatorial control of gene transcription

A

a lot of singlaing happens at genes combo of signals positive or negative

Cell Biology (2 decks)

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