Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS 2 > Mechanisms of Cell Signalling > Flashcards

Mechanisms of Cell Signalling Flashcards

1
Q

Response types and examples

A

Reversble-become motile/change shape

Irreversible-divide, differentiate/remain undifferentiated, die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cells sense environment bye

A

Specialized receptor proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ligands+specificity

A

Molecule that triggers signal by binding to receptor

-specificity governed by tertiary structure and non-covalent bonds between AA groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Agonists vs antagonists

A

agaonists-induce receptor activation
-occupies ligand binding site and stimulates receptor activity

antagonists-block receptor activation
-occpies ligand binding sites and exclusde agonists /change conformation of receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where do drugs act

A

either receptors or enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ion channels

A

Pore forming protein that allow flow of ions across membranes down electrochemical gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ligand gated channel

A

Bind ligand to open channel to allow flow of ion across membrane-or close to slop flow

Basis for nerve transmission and muscle contraction

Channels are oligomeric (can form groups that do not let anything through)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CFTR

A

Cystic fibrosis transmembrane conductance regulator

  • recessive disease-loss of function mutation
  • abnormal salt transport-mucous buildup
  • ligand=ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

GOF mutations to ion channels

A

Domnant inheritance-create defects in other ion channels b/c oligomeric bonding
-only 1 bad receptor fucks up others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mutations in voltage=dependnent Na” channels

A

GOF

Results in defective inactivation and late Na+ currents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Tetrodotoxin

A

Pufferfish toxin

-Na+ channel blocker-blocks action potentials in nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nucelar Steroid hormone receptors

A

Derived from cholestorl-control gene expression

Hydrophobic hormones-cross cell membrane

Bind to receptors in cyto or nuc

Chaperone may help prior to ligand binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Estrogen

A

Enter cell, binds to chaperone, binds to receptor, receptor causes estrogen dissociation from chaperone and exposes nuclear import signal=homodimerizaiotn and nuclear entry occur

Bind to ERE (dna promoter) to activate gene trx

Estrogen receptors are overexposed in breast cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Endocrine therapy for breast cancer

A

Use selective estrogen receptor antagonists-tamoxifen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Protein Kinase receptors Pathway

A

Ligand binds to extra cellular domain
Subunits dimerize-cytosolic protein kinase domains are now in proximity
Kinases phosphorylate each other (usually multible P’s)
Additional cytosolic proteins recruited to receptors (bind to phosphorylated tails)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Phosphorylation

A

Reversible
On/Off switch
Can turn hydrophobic portion of a protein into hydrophilic
Conformational change-facilaitate interaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Grb

A

G-protein receptor binding

Binds to phosphylated g receptors

Constains SH2-doman that recognizes phosphorylated kinase (tyr-P)

18
Q

Tyr-P

A

AA that gets phosphorylated in protein receptor kinase cascade

19
Q

SoS

A

GEF=son of sevens

-bnds to grb and activates small G-prtoeins such as Ras

20
Q

Ras

A

Monomeric small g=protein, activated by SoS

21
Q

GEFs

A

Guanine nucleotdie exchange factors

Activate G proteins (like RAS) by catalyzing exchange of GDP for GTP

22
Q

GAPs

A

GTPase activating proteins

Promote inactivation o G prpteins by cleaving phosphate group from GTP to make GDP

23
Q

G-proteins

A

Bind guanine nucleotides and act as molecular switch during signalling

24
Q

DRAW-NUCLEOTIDE EXCHANGE REACTION AND G PROTEIN=SLIDE 30

A

SoS recruited to actiate protein kinase receptor-induce exchange of GDP for GTP on Ras

  • Ras is inactive with GDP bound
  • SoS is ras GEF
  • Ras is now activated-weak gap function, hydrolyzes GTP to GDP slowly (weak gap function) there is also gap proteins that push process along wit proper timing to allow inactivation of as from GTP to GDP
  • intrinisic and other proteins push along GTP to GDP
25
Q

Ras-MAPK pathway

DRAW

A

ras stimulates phosphrylation cascade

  • MAPK, KK, KKK etc.
  • target is TF in nucellus-activate it and allow regulation of gene expression
  • result=cell division
26
Q

Ras functions

A

Cell growth/dividion, cytoskeleton, membrane traffic-many more

Depends on what is downstream

27
Q

Oncogenic mutations in Ras

A

Turn all downtstream pathways on

  • two position-gl-12/13 or gln-61
  • abolish weak intrinsic function of as to dephosphorylate self
  • cant hydrolyze GTP to GDP
28
Q

Neurofibromatosis Type 1

A

Mutation in NF1 gene

  • Encodes a Ras GAP
  • catalyizes converson of GTP to GDP
  • overactive Ras if can’t
29
Q

Noonan Syndrome

A

Mutation in PTPN11 gene which encodes SHP2

-GOF which leads to hyperactive ras

30
Q

7 alpha helix receptors

A 
Must abundant
-7 transmembrane alpha helixes with large extra cellular domains
(also have intracellular part)
-Most drugs target at these
-Coupled to large G-proteins
31
Q

Roles of 7 a helix receptors

A

vision, smell, mood, autonomic nerve system

32
Q

7 alpha helix receptor pathway

A

Ligand binding causes exhchange of GDP by GTP and activates G-protein
-alpha domain has GTP whhile beta and gamma spread away

33
Q

Functions of gsalpha, go-alpha, and gpalpha

A

Stem from G-alpha

Gs-stimulating pathway downstream
Gi-inhibiting pahtway
Gs/Gi-function through adenylate cyclase-target PKA
Gq-alpha-actviates and targets PKC

34
Q

B andrenergic receptor (DRAW)-42/43

A

7-alpha helix receptor
-binds to epinephrine and norepinephrne

-ligand bound receptor is substrate of BARK

  • Phosphorylated receptor is bound by beta arresting
    • terminates signal even in presence of ligand
    • BETA ARRESTIN BINDS ONTO THE B ANDREGENIC RECEPTOR-no alpha, beta, gamma subunits recombine to resend signal

Blocks interaction with Gs

DESENSITIZATION PATHWAY

35
Q

Gs alpha/Gi-alpha DRAW-44

A

Target is protein kinase a (PKA)

  • blocks reaction of inactive adenylate cyclase to active adenylate cyclase
  • cuclic amp then goes on to activate protein kinase a
  • regulates untra cellular calium
  • gsalpha and gi alpha antagonistically work to regulate PKA activity
36
Q

AC/PKA induced Ca 2+ signalling

A

Cyto Ca 2+ is maintained at very low concentration by calium pumps in PM and SER

  • receptor mediated calium influx triggers many events in cell
  • ligand/recepptor doesn’t really matter-depends on what g protein is linked
37
Q

Gq proteins acticate PKA via Ca2+ and PLC

A

Regulate PKC

  • PLC on cell membrane
  • hydrolyze Pip2-make DAG and IP3
  • DAG goes to activate PKC directly-allows Ca 2+ to go in
  • IP3 in presence of Ca goes into cell, allows more calum from lumen of SER to go to sit
  • DAG plus calcium from IP3 regulate protein kinase C
38
Q

Why need calcium and ligand for protein kinase c (DRAW 48)

A

PKC is inactive b/c active site is filled with N=terminal psuedosubstrate peptide held in place by C1 and C2 domains

  • C1 domain binds DAG in membranes
  • Presence of Ca2+ in C2 domain binds phosphatidyl serine-found in inner leaflet of PM
  • This removes psuedosubstrate from active site and PKC becomes active
  • Can then be cleaved and kinase now is permanently active
39
Q

Calmodulin

A

Binds to Ca2+ (4 at once) and regulates activity of many proteins
-activates calmodulin-activated protein kinase (CAMK)

40
Q

CAMK

A

Calmodulin with 4 Ca2+ bind to it, active site is not accessible
-linked to learning, memory, cancer, and musculoskeletal diseases

BMS 2 (41 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions