Cell Cycle Flashcards
G1
growth phase before DNA synthesis
G2
second growth period that’s before cell division
M phase
cell division
G1/S checkpoint
start or restriction point. cell tells if conditions are faborable for division
G2/M chekcpoint
make sure all DNA has been replicated and the environment is still favorable for division
metaphase/anaphase transition point
all chromosomes are evalutated to ensure that they are attached to mitotic spindle
DNA damage checkpoint
functions throughout the cell cycle, detects damage ti DBA
CDKs
enzymes that help progress through the cell cycle
M phase Cyclin/CDK complexs
Cyclin A/CDK1
Cyclin B/CDK1
Mid G1 cyclin/CDK complexes
cyclin D/CDK4
Cyclin D/ CDK6
late G1 cyclin.CDK complexes
Cyclin E/CDK2
S cylin CDK compelx
cyclin A/CDK2
how are cyclins degraded
ubiquitin-dependent proteolysis
how is cyclin B ubiquinited
anaphase promoting complex
mitogenic signals
tissue-specific growth factors
required to stimulate cell growth and dvision
what phase are most differentiated cell in
G0
in general what do interactions between cell and ECM do
promote cell division
in general what do interactions between neighboring cells do
inhibit cell division
contract inhibition
two neighboring cells contact each other and inhibit cell dibision
early-response genes
genes transcribed within a few minutes of addition of gorwth factor to a cell in G0
what is a key player amoung the early-response genes
transcription factor c-FOs
function of c-fos
stimulate transcripition of delayed response genes
what do the recceptors for gorwth facotors contain
intrinsic tyrosine kinase activitry
what does ligand binding to receptors for growth factors tirgger
recpetor dimerixation, autophosphorylation of tyrosine residues within the recpetor
how do most growth factors stimulate transcription of the gene encording c-fos
MAP kinase cascade
how does MAP kinase cascade start
GRB2 binds to phosphotyrosine residues within the activated receptor.
what happesn after GRB2 bindws
binds to SOs, brining it into the cell membrane
what happens when Sos is in the cell membrane
activates Ras
what does active Ras do
activates Raf
what does activated Raf do
activate MAP kinase kinase
what does MAP kinase kinase do
activate MAP kinase
what does MAP kinase do
stimulate c-Fos transcirption
what happens after the cell passes the restrition point
it can go through the S, G2, M phases of cell cycle in the absense of growth factors
what is the key target for cycline D-CDK4/6 compelx
retinoblastoma protein (RB)
fucntion of Rb
binds to E2F proteins
functino of E2F proteins
transcription factors, stimulate transciriiption of cyclin E and cyclin A and CDK2.
when E2F is bound to Rb how does it function
as a repressor instead of activator
when cyclin E-CDK2 is present, Rb phosporylation because what
independt of cyclin D-CDK4.6
INK4
growth inhibitory factors taht compete with cyclin D for binding to CDK4/6
p27KIP1
small protein that forms a compelx with cyclin A-CDK2,
what is the most important driver of events leading up to mitosis
CDK1
when is cyclin A present
from early S phase
when does cyclin B synthesisi ahppen
late in S phase, incrases through G2
when is the peak levle of cyclin B
metaphase of mitosis
the cyclin/CDK1 complexes are held in an inactivate state until when
DNA replication is completed
what triggers activation of anaphase promoting complex
appropriate arrangement of chromosomes and attachment to mitotic spindle in metaphase
how does protein dephosphorylation affect the effects of cyclin/CDK1 actiity
reverse
ATM
detects replication forks, activates another kinase that preents dephosphorylation and activation of cyclin/CDK1 complexes needed to enter mitosis
when is ATM active
as long as replication forks are present
what is anaphase depend ont
association of all chromosomes with the spindle
what activates ATR
DNA damage caused by UV light and certain drugs
activation of ATM/ATR does what
inhbiits phosphateaases tha tnormally dephosphorylate and activate cycline/CDK2 and cyclin/CDK1 compelxes
activation of ATM/ATR results in phosphorylation of waht protein
p53
p53
transcritpion factor that is normally unsable
importnat traget of p53`
p21CIP1.
p21CIP1
inhbitior of cyclin-dpeendent kinases.
what specifically does p21CIP1 inhibit
cylin/CDK1 and cycline/CDK2
what caues ataxia-telangiectasisa
muations in protein kianse ATM
symptoms of ataxia telangeita
susceptivle to infection (especially chronic lung)
increases risk for leukemia, lymphoma, sensitive to radiation exposure
what produces TNF
macropahses
waht produces Fas ligands
natural killer cells, cytotoxic T lymphocytes
proapoptotic proteins
PUMA, BID, BAX (BCL-2 family)
BCL-2
antiapoptotic protein. inhibits BAX
BAX
can form a channel in the mitochondrial outer membran
function of PUMA and BID
stimulate BAX
when stimualtes BAX allows the release of waht
cytochrome c
what happens when cytochorome c enters cytoplasm
binds to Apaf-1
what happens after cytochrome c binds to Apaf-1
makes apoptosomes
function of apoptosome
recruite, activate caspase 9
functino of caspase 9
activates caspase 3 (excustioner caspases)
