division Flashcards
what is cell cycle
cell growth and chromosome replication chromosome segregation division thus duplication division co ordination
what are cell cycle phases
m mitosis g1 s g2 (g1 s g2 =interphase) g0- non dividing like nuerones
where. are the check points in the cycle
g1 - g2- mitosis
what is checked per checkpoint
g1- environment (nutrients, growth factors)
g2- if dna has replicated
and if the damage has repaired /
m- are the chromosomes attache to the mitotic spindle
what happens when the cycle pauses
dna repair
undergo apoptosis
how cells leave g0
response from growth factors from g0 to g1
why are there multiple checkpoints
prevent disastrous progression
what happens when growth factor binds to gf receptor
lots of enzymes involved amplify signal protein synthesis increases protein degradation decreases so the cel can double in size
what is c-Myc
transciption factor
stimulates expression of cell cycle genes
function if c-Myc
promotes g0 to g1
overexpressed in many tumours
cdks
invloves into phosphyratlion and dephospharylation
involved in signalling
control cells
how cdks activated
only active when cyclin is bound
what does cell cyle entry require
Cdk 4/6:cyclin D complex
protien kinase cascade leads to
signal amplification
diversification - activate other pathways
opportunity for regulation
cdk cyclin dependent kinases activity is regulated by what
interaction and phosphyralytion
how cdk are activated
1) cylclin binds
multiple phosphyatlion reactions at both sites ( active and inhibotory)
phosphates removes inhibotory phosphate
is activated
what does active cdk do
drives cell cycle to progress to next step e.g. s cylin to s phase m cyclin to m phase gives timimng and direction to cycle
how are cdk inactivated
uniquiatyltion
ubiquitones are stuck to protiens that they want to degraded e.g. teh cyclin
they result in inactive cdk
retinoblastoma is what
a tumor supressor,
how it works
active rb sequesters a trasnciption factor in an inactive form
the tf can’t turn genes on for cell cycle prolliferation
how does proliferation occur
actiavtion of intracellular signalling leads to production of active cdk
these inactivate rb by phosphorylation
relaseing tf
target genes needed for dna sythesis are produced
what does p53 do
arrest cells with dna damage in g1
it activates protien kinase that can activate itself
if there is no dna damage what happens
p53 is made then degraded instantly
what does p53 induce
p21 by binding to the rehglutatory region on p21
casues transcition of p51 mrna
trasnlated to protien
it binds and sequesters the active cdk
what re the 2 tumor supressor
p53 and rb
