MAPK,”Mitogen-activated Extracurricular signal-regulated Kinasedual-specificity Kinase (threonine, tyrosine)when activated, will rephosphorylate Rafcomes back and shuts Raf back off, goal is to not let proliferative pathway go any further than it already is(If MAPK can phosphorylate, it will shut off)when active, it forms homodimer sort of like PKA, it phosphorylates actual proteins in the cell, a huge number, only looking at a small subset necessary for the cell to proliferateand can come right to the nucleuswithin the nucleus, cohort of DNA transcription factors already there

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HW: How can normal HER2 promote cell proliferation even though it does not directly bind to any extracellular growth factors?,”Answer: None of the abovepromote tumor proliferation for 2 reasons: 1) Her2 can form heterodimers with any other Her family members (1, 3, 4). This is going to sensitize the cell to basically grow at very low extracellular concentrations of EGF that normally wouldn’t be enough to activate Her1 or Her4 homodimers. Her2 coming in and forming and activating a large number of other receptors that would normally be monomeric. The other thing that happens, new insight, when you overexpress Her2

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