module 4 Flashcards
autocrine
target cell produces own signaling molecule
paracrine
signaling molecule produced by a cell adjacent to target cell
endocrine
signaling molecule from a cell that is related in remote location from target cell
sensor
histidine protein kinase
pathway bacteria use
effector
response regulator aspartic acid protein kinase
pathway bacteria use
kinase
protein which can transfer a phosphate anion to another protein
-changes conformation and makes active/inactive
phosphatase
proteins which remove phosphate from another protein
quorum sensing
bacteria transcribes a gene to make a protein
the protein creates and releases AI into host environment
as bacterial colony density increases the concentration of AI increases and diffuses back into the bacteria
one gene acting as regulator for own gene
auto inducer
allow bacteria to communicate both within and between different species
half life
time taken for something to undergo half of a process
mitogen
lead to immune cell activation/ stimulation
cAMP
cyclic AMP
type of secondary messenger
DAG
can activate Protein kinase C which is a serine- threonine kinase
G-Protein Coupled Receptor
membrane bound receptor , 7 membrane spanning regions
link G-protein to outside signals
have ligand binding domains on ectoplasmic face
have cytosolic domains that activate G-protein
G-protein
protein that binds to GTP(on) and GDP(off), responds rapidly
act as on/off switch
activate downstream proteins
arrestin
may bind to inhibit further signal transduction during G-protein coupled receptor
adenylyl cyclase
example of downstream effector protein
beta-aneregenic receptor
downstream effectors
type of g protein coupled receptor
Phosphatidylinositol
phosphorylated twice to produce PI, P2
Inositol Triphosphate
ligand for a calcium channel on smooth muscle
protein kinase C
activated by DAG
serine- threonine kinase
phospholipase
PI specific phospholipase cleaves phosphorylated inositol from lipid to produce 2 secondary messengers
receptor tyrosine kinase
auto phosphorylate themselves
auto-phosphorylation
phosphate added to protein kinase by itself
Receptor Tyrosine Linked Kinase
Receptors which lack kinase activity. These receptors rely on another molecule to phosphorylate and pass signal to cell effectors. Hence these receptors are Linked to a Tyrosine Kinase
Ras
on switch, signals mitogenic response
guanine exchange factor
replaces GDP with GTP to activate Ras
guanine dissociation inhibitor
inhibits the dissociation of GDP from Ras (guanine exchange factor)
GTPase activating protein
GAP
mediates ras
enables ras to hydrolyze gtp to gdp- ras inactive
mitogen activated protein
MAP
maturating promoting factor
MPF
factors present in cytoplasm cause cell cycle progression
ras activating factor
activated by ras
activates map kinase pathway to lead to cell proliferation
causes multi step phosphorylation cascade between downstream protein kinases
nuclear receptor
type 1-
bound to inactive form in cytoplasm or nucleus with HSP
ligand dependent (steroids)
type 2-
bound to gene and repressed, ligand dependent (thyroid)
orphan receptors
response element
orphan receptors
no identified ligand
in type 2 nuclear receptor
Raloxifene-HCl
agonist in bone tissue for osteoporosis
SERM
selective estrogen receptor modulators
Tamoxifen/Taxol
Tamoxifen is antagonist for breast cancer
agonist
target gene activation
binds to receptor inside a cell or on cell surface and causes same action as substance that normally binds
antagonist
target gene repression
stops action or effect of a substance
bleb
surface bleb formation due to apoptosis
death domain receptor
external initiation of apoptosis through receptor
BCl-2
interacts with bid
activated when stress signal detected by rer
Bad, bax, bak
when activated, causes changed in mitochondria permeability
procaspase
inactivated form of caspase
caspase
apoptosis involves the activation of these
executioner caspase
major is caspase 3
targets nucleus
apoptosome
APAF
apoptotic protease activating factor
caspase 8
cleaves procaspase 3 to activate procaspase 3
can target mitochondria
caspase 9
activates major executioner caspase (caspase-3) that targets the nucleus
Tumor Necrosis Factor (TNF)
bind to TNF receptor on plasma membrane
initiates receptor-mediated apoptosis pathway
external stress ligand
TNF receptor
receptor activates death domains and recruit adaptor proteins (FADD and TRADD)
adaptor death domain
granzyme
Molecules for natural killer cells that activate caspase 3
perforin
Caspase Activated DNase ??
CAD
interacts with inhibitor of CAD, which changes cell fate
convergance
multiple signals come to same effector, cell must base response on combination, timing, and strength of these signals
divergence
same ligand may signal through different pathways based upon tissue type, receptor makeup, other signals
crosstalk
different signaling cascades and pathways communicate with each other so multiple responses may occur from one signaling event causing multiple downstream events involving other pathways
cytochrome-C
when released, serves as messenger for apoptotic protease activating factor-1 to convert procaspase 9 to act caspase 9
SOS
GRB2
thyroid receptor
type II receptor
translocation to nucleus
remove compressor signal, activate gene transcription
sterorid receptor
type I receptor
conformational changes and released from carrier
translocation to nucleus
dimerization of receptor/ ligand complex
DNA interaction, gene transcription
g1 phase
normal growth and metabolism
s phase
synthesis phase for DNA, chromosome duplication
g2 phase
cell growth prior to mitosis, organelles replicate
m phase
mitosis
cell divides copied DNA and cytoplasm to make two new cells
cyclin a
regulate G2 and some of m phase activities
works with cdk 2
cyclin d
regulate G 1 activities
must pair with cdk4/6
cyclin e
regulate s phase activites
works with cdk2
cyclin b
works with cdk 1
master regulator for M phase
Cdk 4
works with cyclin d
Controls M ->G1 phase transition, highest concentration in g1
Cdk 6
works with cyclin d
Controls M ->G1 phase transition, highest concentration in g1
Cdk 2
works with cyclin a and cyclin e
controls s-> g2 phase transition, highest concentration in g2 (a)
Controls G1-> S phase transition, highest concentration in S (e)
Cdk 1
works with cyclin b
controls g2 -> m phase transition, highest concentration in m
26-S Proteasome
downregulates cyclin D in g1 phase?
proteolytic enzyme
cyclin taken to 26S proteasome after cyclin and CDK separate
temperature sensitive mutants
used in cell division cycle mutants
yeast grow at 25 C but not 35 C
ubiquitin
ubiquitin ligase
adds a polyubiquitin chain to cyclin
destruction box
specific targeting sequence recognized by proteins which bind ubiquitin to protein which needs to be destroyed
polyubiquitin isopeptidase
p21
stops cell from going through cell cycle
blocks cyclin/cyclin dependent kinase from being active
p53
TF for p21
expressed when cell conditions are good
MDM2
ubiquitin ligase
p53 expressed continually but gets degraded by ubiquitin proteosome pathway, done by interaction with MDM2
retino blastoma
inhibits gene transcription by binding to TF E2F
when phosphorylated it releases E2F which transcribes cyclin E and cdk 2
