lecture 5 boyes Flashcards
give 3 advantages of regulation by TF activation
rapid response.
regulation in response to external factors
fine tuning of transcription level
how are nuclear hormone receptors activated
glucocorticoid binds
inactive receptor release
both move to nucleus
activate gene expression
what else does ligand binding do
conformational change
interact with co activators
describe how the E and M chain of the Notch receptor work
signal protein+ E chain
M chain dissociate
cleave M chain
Notch tail release
activate transcription
describe how HSF-1 is activated
HSF-1 + HSP90 = inactive
heat shock= dissociate
HSF-1 trimerize interacts with eEF1A
bind to heat shoch element on DNA
Phosphorylation
describe the JAK/STAT pathway
cytokines
signal
janus activated kinases
phosphorylate STAT transcription factors
STATS dimerisation
translocation
nucleus
bind target genes
what happens when ligand binds to receptor tyrosine kinase
signal cascade
auto phosphorylation
Ras activated
bind GTP
phosphorylated Raf
phosphorylates other kinases
what is the MAPK pathway
starve cell growth factor
ternary complex factor and serum response factor phosphorylated
interaction
bind to serum response elements
in early response genes
what can increase promoter activity
acetylation by HATs of TF
what does acetylation of GATA-1 do
GATA-1/DNA binding
GATA-1 dependent transcription
GATA-1 protein interactions
function in haematopoietic differentiation
how many K-48 linked ubiquitin molecules must be added to lead to degradation
4+
describe hoe E1,2,3 ligases are linked
E1 linked via lysine in target protein and glycine in c-terminus of ubiquitin
then linked to lysines in ubiquitin
how is GCN4 lost from promoters
Srb10 phosphorylates bound GCN4
recruit E3 SCFcdc34
ubiquitination
how is transcription factor degradation and PolII transcription linked
activator+ basal machinery
recruit ubiquitin for modification
recruit 26S proteasome
destroy activator
promote pol II elongation
