Cell Signaling Flashcards
What does absence of signaling cause
Apoptosis
5 types of signaling
Endocrine- hormonal, long range. Blood stream
Paracrine- nearby, diffusion
Neuronal- very close, synapses
Contact dependent- cells linked by signal
Autocrine- cell signals self
Signal components
Ligand, receptor, intracellular signal proteins, target proteins
Is ligand concentration high or low
Low, and affinity is very high
Two types of receptor
Cell surface and intracellular. Intra requires small hydrophobic signal like a steroid
Domains of intracellular signal protein
Dna binding, ligand binding, transcription activation, inhibitory or promoter
Types of cell surface receptors
Ion channel linked(bind to allow ions in), G protein linked (7 pass), and enzyme linked (single pass)
Secondary signal protein uses
Turn signal on or off, amplify signal, or split signal
Can response proteins do different things with same signal, or same with different?
Yes
Which is slower: dna pathway or altered protein pathway
DNA pathway
G protein receptor pathway
Receptor binds signal, causing protein to bind G protein. Makes gtp, and splitting trimer into two. Alpha unit activates target and makes gdp, rebinding to trimer
cAMP pathway
G protein. Activates a protein that makes cAMP, activates protein kinase A, which goes to nucleus to phosphorylate.
Ca signaling pathway
G protein activated. Activates phospholipase C, which releases inositol, opening Ca channel in ER, activating Protein kinase c
Enzyme pathways
Generally receptor tyrosine kinase. Involve dimer signals. Which dimerize tyrosine kinase, P itself to make signal complex
What do phosphorylation sites on RTKs do?
Serve as protein docking sites
What are signal transduction switches and what types?
Turn signal on or off. Kinase type and gtpase type.
SRC domains and functions
N and C lobe- ATP between SH1- kinase SH2- phosphotyrosine binding SH3- protein binding SH4- binds membrane
SRC pathway
Nonreceptor TKR. Tail Dephosphorylated to open, then loop is phosphorylated, opening catalytic cleft. Three states
RAS basics
RTK linked to GTPase. Tethered to membrane.
RAS pathway
Activated by GEF, forcing in GTP. Then signals, and GAP induces GTP hydrolysis inactivation, turning off. Activates MAP kinase cascade.
JAK-STAT pathway
RTK. Cytokine binds, binding JaK to itself. Then it phosphorylates itself twice, where STAT binds and dimerizes
NF-kB path
Activates inhibitor kinase, which degrades inhibitor of NF-kB
TGF- b pathway
Type 2 receptor binds signal(BMP), which binds and phosphorylates type 1. Activates smads
Wnt pathway
Frizzled binds receptor, activating disheveled, which prevents GSK from degrading beta catenin
Hedgehog pathway
Sonic binds, preventing patched from inhibiting smoothened, which prevents GLI from being cut. Normally repressor, now inducer.
Cell contact path (Notch)
Delta binds notch, connecting cells. Pulls up notch, allowing cleavage. Lowers notch, further cleavage. Bit inside goes to nucleus. Differentiation.
Types of combinatorial action
Integration, divergence, cross talk, specialization.