Genetics: Gene Expression Flashcards Preview

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Flashcards in Genetics: Gene Expression Deck (30)
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1

Histone Structure

Octamer of two copies of each of 4 types of histones

2

Genomic Imprinting

Allele from either father or mother silenced so that only one is expressed

3

Mech of Genomic Imprinting

DNA methylases methylate the cytosine on CG islands

4

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

5

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

6

Coregulators (3)

Majority histone-modifying enzymes causing chromatin remodeling (coactivators releasing histones from DNA and corepressors causing condensation)

7

Histone Code Hypothesis

Modifications of histone residues (acetylation, methylation, phosphorylation, ubiquitylation) causes chromatin remodeling leading to either DNA condensation (inactivation) or relaxation (activation)

8

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

9

Attenuation of GPCR Response

PKA also activates phosphodiesterase (PDE) which hydrolyzes cAMP

10

Two Major Points from Wnt Canonical Pathway

Is classified as GPCR
Activates transcription via Beta-catenin

11

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

12

MAPK Pathway (4)

RTK activated by growth factors/mitogens, recruits GEFs to activate Ras which activates MAP kinase pathway which activates transcription factors

13

Crucial 2 Points of Growth Response Pathways

Kinases and G prots drive growth and their GAPs inhibit it

14

S6K1-HM

Crucial point of growth regulation, when AID region dissociates can stimulate transcription

15

Strongest Tumor Repressor

Phosphatase

16

Insulin R Pathway Notable Feature

Can activate both MAPK pathway and PI3K-mTOR Pathway

17

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

18

Starvation Response

LKB1/AMPK respond to low nutrient/energy by activating Rheb-GAP which downregulates mTOR

19

Oncogene

Gene that becomes cancer causing agent due to hyperactivation via mutation or overexpression. Usually in cell signaling pathways that drive cell growth

20

Stress Response

Stress activates kinase to phosphorylate eIF2/eEF2 which blocks translation

21

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

22

Opioid R Agonists (action, effect, 3 examples)

Stimulates GPCRs for pain relief/euphoria - morphine, codeine, oxycodone

23

Caffeine Mech

GPCR Purinergic R Antagonist, but that R antagonizes adrenergic R so it acts as a stimulant

24

Adrenergic R Agonists (action, effect, 3 examples)

GPCR agonists that mimic adrenaline, so stimulants (ephedrine, pseudoephedrine [sudafed], amphetamines)

25

Difference b/w Histamine H1 and H2 R Antagonists

H1s for allergies and H2 for stomach acid

26

Dopamine R Agonists (2 examples)

Cocaine and Thorazine (for schizophrenia)

27

3 Kinds of Steroid Medicines

Glucocorticoids (anti-inflammatory/immunosuppressants), anabolic steroids (bone/muscle growth), female needs like E&P

28

Gleevec

Turning point in cancer treatment, kinase inhibitor for leukemia

29

4 Kinds of Kinase Inhibitors for Cancer Treatment

BCR-Abl - leukemia
EGFR - lung/pancreatic
mTOR - immunosuppressant for transplants
JAK - antiinflammatory

30

Rapamune

mTOR inhibitor which acts as immunosuppressant so used for transplants