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
Insulin R Pathway Notable Feature
Can activate both MAPK pathway and PI3K-mTOR Pathway
Insulin R non-MAPK Pathway (7)
Insulin binds, causing autophosphorylation, activating PI3K which activates PDK1 which activates PKB which inhibits Rheb GAP so Rheb G prot can activate mTOR protein kinase to stimulate transcription
Starvation Response
LKB1/AMPK respond to low nutrient/energy by activating Rheb-GAP which downregulates mTOR
Oncogene
Gene that becomes cancer causing agent due to hyperactivation via mutation or overexpression. Usually in cell signaling pathways that drive cell growth
Stress Response
Stress activates kinase to phosphorylate eIF2/eEF2 which blocks translation
RNAi
miRNA binds w/ Argonaut to form RISC which can directly cleave or block specific RNA sequences, so can be used to block specific genes
Opioid R Agonists (action, effect, 3 examples)
Stimulates GPCRs for pain relief/euphoria - morphine, codeine, oxycodone
Caffeine Mech
GPCR Purinergic R Antagonist, but that R antagonizes adrenergic R so it acts as a stimulant
Adrenergic R Agonists (action, effect, 3 examples)
GPCR agonists that mimic adrenaline, so stimulants (ephedrine, pseudoephedrine [sudafed], amphetamines)
Difference b/w Histamine H1 and H2 R Antagonists
H1s for allergies and H2 for stomach acid
Dopamine R Agonists (2 examples)
Cocaine and Thorazine (for schizophrenia)
3 Kinds of Steroid Medicines
Glucocorticoids (anti-inflammatory/immunosuppressants), anabolic steroids (bone/muscle growth), female needs like E&P
Gleevec
Turning point in cancer treatment, kinase inhibitor for leukemia
4 Kinds of Kinase Inhibitors for Cancer Treatment
BCR-Abl - leukemia
EGFR - lung/pancreatic
mTOR - immunosuppressant for transplants
JAK - antiinflammatory
Rapamune
mTOR inhibitor which acts as immunosuppressant so used for transplants
