Signal Transduction Flashcards
Beta Adrenergic Rs
GPCR that when bound, activates AC -> cAMP -> PKA which can enter nucleus and activate transcription factors/DNA synth/cell division
Galphaq
When stimulated, activates PLC which cleaves PIP2 into IP3 and DAG. DAG and Ca from IP3-Ca channels on ER activate PKC, which enters nuc to stimulate cell cycle progression
RTKs
Dimerized and activated by GFs to autophospho themselves. Then bind adapter prots and GEFs that activate Ras
Ras
Activates kinase cascade which can change shit in cytosol, or end in ERK which goes to nucleus and activates transcription factors
Multiple Roles of PIP2
Cleaved by PLC to form IP3 and DAG
Phospho’d by PI3K into PIP3
PTEN Phosphatase
Reverses PI3K action, serving as important tumor suppressor. Lots breast cancers shut down
PIP3 Roles
Activate PLC to cleave PIP2 into IP3 and DAG as well
Activate PKB/AKT which activates Bcl-2, which inhibits apoptosis
PKB/AKT also inactivates TSC complex, so can’t inhibit Rheb->mTOR -> cell synth/growth
2 Ligands on mTOR
GBetaL and Raptor
Integrin-based cell-matrix junctions
Can activate ras pathway. In absence of integrin junctions w/ BL, cells will apoptose
B-catenin
Usually in epithelial cytoplasm to anchor E-cadherin cell-cell junction filaments. Any unbound destroyed by APC complex. When WNT binds its R, APC inhibited, and B-catenin enters nucleus and promotes cell cycle
Hyperactive WNT Pathway
Also promotes epithelial-mesenchymal transition (EMT) which can lead to mets of epithelial tumors (by activating SNAI1-2 TFs in nuc)
TGF-Beta Rs
Dimerize and inhibit division in normal epithelial cells via Smads and are thus tumor suppressor
However can stimulate EMT in localized tumor cells, aiding metastasis
JAKs
Cytokine Rs activate JAKs which phospho receptor tyrosines. STATs then bind phosphates and also activated by JAKs. Activated STAT dimers turn on a lot of genes, including some involved w/ growth
