Cell Communication Flashcards

1
Q

Bacteria Communication

A

bacteria colonies have a small peptide, when in low bacteria conc, its conc is low too.
receptors on surface of organism to recieve signaling molecule
Signaling peptide: 17 peptides
As bacteria grow, signaling molecule conc incs, more likely to interact with receptor on cell surface
allow DNA molecs to be taken up by cells
receptor recieves signal, turn on genes, express proteins, bring DNA in from environment

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2
Q

Elements for Cell Cell Comunication

A

Signaling cell
signalling molec
receptor molec
receptor cell

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3
Q

When signaling molec recieved

A

recptor turned on

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4
Q

Steps of signaling

A

receptor activation (molec binds signal, conf change)
Signal transduction
Response
Termination

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5
Q

Signal transduction

A

conversion of signal from one form to another as its transduced from where its recieved to final response
environment
other cells

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6
Q

Receptors are

A

highly specific to specific signal molecules

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7
Q

Endocrine transmission

A

furthest distance
molecules travel through blood stream
signalling cell releases signaling molecule
estrogen/testosterone (hydrophobic, made from lipids, can diffuse right through membrane)

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8
Q

Paracrine transmission

A

diffusion over shorter distance
cells close to each other
embryonic development
Growth Factors

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9
Q

autocrine transmission

A

cell signaling itself (immune)

embryonic development, maturing cell types for immune system

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10
Q

juxtacrine transmission

A

2 cells in physical contact signal each other
transmembrane protein embedded in one cell interacts with that of an adjacent cell
tells you where you are in relation to other cells
Nervous system

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11
Q

Kholer and Limptom

A

grew fibroblast cells, gave them either plasma (unclotted blood) or serum (clotted blood).
look at density grown in either
more in the one with serum
Platelets: cause clotting
something released from platelets a possible growth factor.
then grew with just platelet proteins, so proved this.
signaling molecule is PDGF (platelet derived growth factor

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12
Q

Notch (nervous, juxtacrine)

A

become Glial Cells

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13
Q

Delta (nervous, juxtacrine)

A

become neurons

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14
Q

ligand

A

signaling molecule

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15
Q

Ligand binding site

A

receptor where ligand binds
specific affinity for the ligand
can bind tight and be kept for a long time or not

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16
Q

cell surface receptor

A

polar molecules
cant pass through PM
signal recieved at surface of cell on PM
conf change in receptor, once bound transduces signal

17
Q

Intracellular Receptor

A

small, non polar signaling molecs
can pass through PM (also hydrophobic)
recieved by signaling molec in cytoplasm
conf change in molec, transduction

18
Q

When receptor has bound signaling molec

A

turned on

if not bound, turned off

19
Q

G-protein coupled receptors

A

G protein on cytoplasmic side
inteacts with receptor embedded in membrane recieving signal from outside.
Conf change in receptor allows it to interact with G protein
G protein changes from GDP to GTP
when GTP: ACTIVE, interacts with another molec, interact with other molecs and up regulate
most drugs

20
Q

Receptor Kinases

A

adds a phosphate group to a molecule (phosphorylation)
turn molec on
ligand bound to receptor
receptors go under dimerization (receptors interact with each other once bound)
signal transduced

21
Q

Ligand Gated Ion Channels

A
bind ligand to receptor
pathway opens
inos flood into cell
can change electrochemical
signal transduction
22
Q

G Protein Activation

A

3 subunits, alpha beta and gamma
alpha bound to GDP or GTP
conf change makes alpha have a conf change and go for GTP
change conf again, lose beta and gamma sub units
adding phosphate is adding a slight negative charge
goes off to interact with other molecules after beta and gamma lost

23
Q

second messengers

A

signaling pathway molecs tht arent proteins, water soluble, not first receptor
Calcium, cAMP, cGMP

24
Q

amplification

A

when activated receptor turned on, it can interact wit LOTS of G proteins
G proteins interact with LOTS of adneyl cyclases
each of these catalyzes LOTS of transitions from ATP to cAMP,
activating protein kinase A
kinase A amplifies

25
Q

Termination of G protein Signal

A

dissociation of signal from receptor (adreniline in this case)
slow decay of GTP to GDP,
binds back to beta and gamma
not making cAMP
phosphdiesterase working on cAMP to make ATP back
no more cAMP, second messangers go away

26
Q

Phosphatases

A

remove phosphates from a molecule

turn molec off

27
Q

RAS Proteins

A

Rat Sarcoma (cancer)
Responsible for much cell signaling
turned on by presence of GTP bound to it
mutation in RAS: binds to GTP with too high affinity, it never turns off = CANCER
with ras on all the time, cells just continue to grow and divide

28
Q

Receptor Kinase Examples

A

limb formation, wound healing, insulin signaling,

mutation in pigmentations

29
Q

ACh

A

ligand gated ion channel
sodium ion floods through
muscle contraction
ACh originally released, conf change, sodium ions run in, change in membrane potential, contract

30
Q

Nitroglycerin and Angina

A

A:too much blockage in arteries, conflicted blood flow
N: can be rapidly made to nitric oxide, relaxes muscles, inc blood flow
NO: secondary messenger

31
Q

Viagra

A

new drug didnt work for angina…
circumvent first part of process
cGMP created: relaxed muscles.
NO is a secondary messenger
cGMP can be changed back to inactive GMP
drug works by blocking break down, allows cGMP to add up
but then you’ve stopped turning the signal off!!
Still make NO on your own
Viagra just keeps cGMP from being broken down
inhibits phosphodiesterase

32
Q

Cell Signaling and Cancer

A

1.increased number of receptors: More binding
excess cell division abnormal gene expression
2. over production or unnatural binding. Can cause binding to last too long (too tight). more chances of binding or abnormal gene expression
3. Ras mutations: 30% of all human cancers. Converting GTP to GDP, pathway is constantly on.

33
Q

Integration of signaling pathways

A

cells are receiving lots of signals on the surface, once in cytoplasm, they can cross talk, and you get complex things. Turning on lots of genes, turning on and off… so on