Medical Cell Biology
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| Signal Transduction | Intracellular processes that allows signals to be transduced from the outer cell membrane of cells to the nucleus
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| 4 Classes of Cell Surface Receptors | Catalytic, Noncatalytic, Steroid Hormones, and G-Protein Coupled Receptors
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| Catalytic Receptors | Tyrosine Kinases, Serine/threonine Kinases
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| Noncatalytic (non-kinase) | Wnts, Hedgehogs, and Notch
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| Steroid Hormone Receptors | Cytosol and Nucleus
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| G-Protein Coupled Receptors | cAMP-dependent, IP3-Ca2+ calmodulin dependent
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| Tyrosine Kinase Receptors Ligands | Insulin, Growth Factor, FGFs, VEGF, PDGF, EGF (Neuregulin), NGF
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| Tyrosine Kinase: Intracellular Signaling Pathway | PLC Pathway, Ras/MapK (Grb2/SOS), Phosphatidylinositol-3-kinase (PI3K) pathway
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| Tyrosine Kinase Receptor Pathway | Ligand binds, **dimerization, **autophosphorylation, ** and recruite SH2
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| RAS activation | Ligand binds, dimerization, phosphorylate tyrosine kinase recruits Grb2, Grb2 replace GDP w/ GTP on Ras, Ras GTP recruit Raf
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| 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
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| 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
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| Neuregulin acts through which receptors? | Erb Receptors
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| Loss of NRG1 | Leads to defective trabeculation of ventricles during heart development
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| Cytokine Receptor Signaling | Has tyrosine kinase tail
When these bind have crosslinked
Autophosphorylation = recruit SH2 domain
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| 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
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| Serine-Threonine Kinase Ligands | TGFB, BMP
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| Serine Threonine Kinase Receptors | TGFB Type 1, TGFB Type 2
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| Serine Threonine Kinase Intracellular Signaling | JAK1 pathway, Smad protein pathway
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| When is it useful for TGFB to inhibit cell proliferation? | Useful for bone formation and growth
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| 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!
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| 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
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| NODAL | Induced a left-right asymmetry in cardiac precursors: Position heart on left side, Formation of LT and RT ventricular chambers
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| Nodal Expressed on the Lt side of developing embryo by hedgehog signaling | Keeps **nodal expression on the left**
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| Lefty-1 binds to receptor competing with NODAL | Signals to determine Right
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| Normally: Nodal is not inhibited by lefty proteins | Will activate SMAD which activate PitX2 in the nucleus to determine leftness
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| When lefty proteins binds to receptor compete with nodal factor | No signals so no transcription so no leftness
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| Wnt | Blocking degradation of TS activator
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| Hedgehogs | Converts transcriptional repressor into activator
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| Notch | Transmitting cell-surface signals to the nucleus via proteolytic cleavage-activate Notch dependent gene TS by displacing TS repressor
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| 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
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| TCF | T Cell Factor
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| LEF | Leukemia enhancer factor
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