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Cell Signaling Part

Medical Cell Biology

Signal Transduction Intracellular processes that allows signals to be transduced from the outer cell membrane of cells to the nucleus
4 Classes of Cell Surface Receptors Catalytic, Noncatalytic, Steroid Hormones, and G-Protein Coupled Receptors
Catalytic Receptors Tyrosine Kinases, Serine/threonine Kinases
Noncatalytic (non-kinase) Wnts, Hedgehogs, and Notch
Steroid Hormone Receptors Cytosol and Nucleus
G-Protein Coupled Receptors cAMP-dependent, IP3-Ca2+ calmodulin dependent
Tyrosine Kinase Receptors Ligands Insulin, Growth Factor, FGFs, VEGF, PDGF, EGF (Neuregulin), NGF
Tyrosine Kinase: Intracellular Signaling Pathway PLC Pathway, Ras/MapK (Grb2/SOS), Phosphatidylinositol-3-kinase (PI3K) pathway
Tyrosine Kinase Receptor Pathway Ligand binds, **dimerization, **autophosphorylation, ** and recruite SH2
RAS activation Ligand binds, dimerization, phosphorylate tyrosine kinase recruits Grb2, Grb2 replace GDP w/ GTP on Ras, Ras GTP recruit Raf
MAPK pathway through RTK Ras binds activated Raf, Ras-GTP hydrolyze to GDP release Raf, Raf activates MEK, MEK activates ERK, ERK translocates to nucleus activates TS factors
FGF pathway FRS2alpha activates GRB2 GRB2 activates SOS SOS convert Ras-GDP  Ras-GTP Ras-GTP activates Rac and Raf Raf activates MAPKK (MEK) MEK activates ERK ERK phosphorylates transcription factors, turn genes on or off
Neuregulin acts through which receptors? Erb Receptors
Loss of NRG1 Leads to defective trabeculation of ventricles during heart development
Cytokine Receptor Signaling Has tyrosine kinase tail When these bind have crosslinked Autophosphorylation = recruit SH2 domain
Cytokine Receptors and JAK/STAT pathway When cytokine binds to its receptor Which phosphorylate Jak In term recruit STAT STAT proteins kinase got phosphorylated and dimerized Then will translocate into nucleus and activate transcription factor
Serine-Threonine Kinase Ligands TGFB, BMP
Serine Threonine Kinase Receptors TGFB Type 1, TGFB Type 2
Serine Threonine Kinase Intracellular Signaling JAK1 pathway, Smad protein pathway
When is it useful for TGFB to inhibit cell proliferation? Useful for bone formation and growth
TGFB signaling Pathway Ligand binds to receptor, direct phosphorylation of serine/threonine kinase, Activated TGFB phosphorylates SMAD 3 (R-SMAD) expose NLS, Phosphorylated R-smad interacts with Co-SMAD (SMAD 4) and IMPORTIN, SMAD complex translocates to nucleus, TFE3!
Bone Morphogenic Proteins Pathway BMP binds to receptor, Phosphorylated receptors 1) Activate TAK1-activate MKK3/6 and then p38 JNK 2)Activate SMAD 1/4 3) P38 and SMAD 1/4 – activate transcription factor ATF-2 inside the nucleus 4) ATF-2 activate/upregulate cardiac TFs that cause ca
NODAL Induced a left-right asymmetry in cardiac precursors: Position heart on left side, Formation of LT and RT ventricular chambers
Nodal Expressed on the Lt side of developing embryo by hedgehog signaling Keeps **nodal expression on the left**
Lefty-1 binds to receptor competing with NODAL Signals to determine Right
Normally: Nodal is not inhibited by lefty proteins Will activate SMAD which activate PitX2 in the nucleus to determine leftness
When lefty proteins binds to receptor compete with nodal factor No signals so no transcription so no leftness
Wnt Blocking degradation of TS activator
Hedgehogs Converts transcriptional repressor into activator
Notch Transmitting cell-surface signals to the nucleus via proteolytic cleavage-activate Notch dependent gene TS by displacing TS repressor
Wnt Signaling pathway complex Wnt bind to receptor, blocking the degradation of B-cateninin (TS activator), B-catenin enter nucleus form complex w/TCF/LEF activating TS of genes = cell proliferation/transformation
TCF T Cell Factor
LEF Leukemia enhancer factor
Created by: jsabangan