Genetics: Gene Expression Flashcards
Histone Structure
Octamer of two copies of each of 4 types of histones
Genomic Imprinting
Allele from either father or mother silenced so that only one is expressed
Mech of Genomic Imprinting
DNA methylases methylate the cytosine on CG islands
Differences b/w Type I and II Nuclear Rs (3)
I: binds R in cyt, II: binds R in nuc
I: releases repressor prots, II: releases corepressor prots
I: forms homodimers, II: most often forms heterodimers, requiring two different signalling molecules
Examples of Type I (4) and Type II (3) Nuclear R Signalling Molecules
Type I: E, P, androgen, glucocorticoid
Type II: Vit A, Vit D, thyroid hormones
Coregulators (3)
Majority histone-modifying enzymes causing chromatin remodeling (coactivators releasing histones from DNA and corepressors causing condensation)
Histone Code Hypothesis
Modifications of histone residues (acetylation, methylation, phosphorylation, ubiquitylation) causes chromatin remodeling leading to either DNA condensation (inactivation) or relaxation (activation)
Process of GPCR (5)
Ligand binds GPCR which acts as GEF on Galpha which activates adenylyl cyclase which forms cAMP which activates PKA to activate regulators of transcription
Attenuation of GPCR Response
PKA also activates phosphodiesterase (PDE) which hydrolyzes cAMP
Two Major Points from Wnt Canonical Pathway
Is classified as GPCR
Activates transcription via Beta-catenin
JAK-STAT Pathway (4)
Cytokine binds cytokine R, causing neighboring Jak to phosphorylate Tyrs on R, read by SH2 domain of Stat which dimerizes to activate transcription
MAPK Pathway (4)
RTK activated by growth factors/mitogens, recruits GEFs to activate Ras which activates MAP kinase pathway which activates transcription factors
Crucial 2 Points of Growth Response Pathways
Kinases and G prots drive growth and their GAPs inhibit it
S6K1-HM
Crucial point of growth regulation, when AID region dissociates can stimulate transcription
Strongest Tumor Repressor
Phosphatase