cooked D103 final

phosphate

changes mass and charge of amino acid/protein

Ca2+

second messenger, bonds to calmodulin
aCH —> IP3 —> ca2+ release —> Calmodulin —> NO —> guanylyl cyclase —> cAMP
low rate of diffusion

guanylyl cyclase (target for trimeric g proteins)

converts ATP to cAMP

phospholipase C (target for trimeric g proteins)

cleaves phospholipids to generate signaling molecules
pip2 cleaved into IP3 and DAG

cGMP phosphodiesterase [PDE5] (target for trimeric g proteins)

converts cGMP to GMP

viagra; breaks down cGMP; reverses vasodilation

K+ ion channel (target for trimeric g proteins)

allows efflux of potassium ions

SH2 domain

phosphorylated tyrosine
Cytokines, RTK

SH3

proline rich
Cytokines, RTK (cytoplasmic binding proteins)

MH

SMADs

PH

Phospholipase C
PIP2/PIP3

NO

arginine —> NOS (synthase) —> citrulline + NO

steroid hormones

rapid or slow cellular response
diffuse; NLS —> nuclear response
bound by chaperone proteins: inactivate in cytoplasm

signal transducers AND transcription factors

vit D/retinoid/thyroid hormones

inactive in cytoplasm; prevent transcription default

GPCR

—> g proteins —> modulate plasma membrane bound enzymes/ion channels
*can act as scaffold proteins for other pathway activation

GRKs (receptor specific kinases)

can desensitize GPCR responses

DAG

lipid (hydrophobic) second messanger

cGMP and cAMP

hydrophillic 2nd messanger
high rate of diffusion

IP3

second messanger for ca2+ release
fast rate of diffusion

TGFB (beta) Receptors

SMADs (transduce nuclear signals)

cytokine receptors

STATs (transduce nuclear signals)

RTKs

Via Ras and MAPK pathway(transduce nuclear signals)

CDKs

regulate gene expression, biochemical, and structural reorganization

Growth factors

(G1) stimulate cell mass and macromolecule synthesis

Mitogens

stimulate cell division by increasing Cyclin/CDK activity

Rb

inhibits E2F/inhibits cell cycle entry

S phase cyclin/CDK

controls initiation of DNA replication

CKI

regulate CDK activity via, phosphorylation, binding, or regulation of cyclins

M cyclin

key component of maturation promoting factor (MPF)

MPF activity is dependent on ….

cyclin B
must be degraded prior to mitosis
degraded by proteasome/ubiquination; regulated by UBE3 ligase/APC/C activity

CDH1

cofactor for APC/C to complete mitosis (anaphase through g1)

CDC20

cofactor for APC/C to trigger anaphase

Wee1

Regulated CDK activity by inhibitory phosphate groups to mitotic CDKs

CAK

directly activating Cyclin-Dependent Kinases (CDKs) through phosphorylation of a key threonine residue in their T-loop

APC/C

anaphase promoting complex/cyclosome
regulated M and S cyclin activity by polyubiquination and proteosome/Ub-E3 ligase activity

what is required for cytokinesis

decline in M-cdk activity

meikin

centrosome located protein that orients sister kinetochores

Rec8

meiosis specific cohesion ring closing molecule that is differentially degraded at anaphase I and II
allows for separase to separate sister chromatids

Scc1

mitosis; hold sister chromatids together after DNA replication, ensuring accurate chromosome division

caspases (protease family)

effects apoptosis
exist as pro-caspases, activated via extracellular or intracellular signaling pathways
brought into proximity via adaptor molecules (minimal protealytic activity)

BCL2/Fas proteins

control of intrinsic and extrinsic cell death pathways

Survival signals ____ the antiapoptic members

favor

absence of survival factors ___pro apoptotic BCL2 activity

enhances
survival factors inhibit apoptosis by binding to pro-apoptotic proteins, so their absence allows pro-apoptotic members (like BH3-only proteins) to activate effectors (Bax/Bak) and trigger cell death, essentially releasing the apoptotic machinery, making BCL2's inhibitory function less dominant, leading to cell death

Cytochrome c

cell death causes release of cytoc from mitochondria
both apoptosis and necrosis
apoptosis relying heavily on cyt c for caspase activation, while necrosis often involves massive mitochondrial rupture releasing cyt c and other damage signals (DAMPs)

survival moelcules

When survival molecules, often called anti-apoptotic factors, prevent apoptosis (programmed cell death), the result is an increase in the net number of cells

extracellular survival molecules

rate limiting in promoting cell survival
growth factors, nutrients, or extracellular matrix signals) are rate-limiting, it means their scarcity dictates how well cells can live, grow, or avoid apoptosis (programmed death)

extracellular signals

growth factors, cytokines, cell adhesion molecules
block apoptosis

what cycle does cancer cells use often

glycolysis
has presence of O2; produce NAD+ independent of oxidative phosphorylation