BIO205

Myc,”translocation of c-myc gene from chromosome 8 to 14 places it under transcriptional control of a strong immunoglobulin gene transcriptional enhancer(don’t need growth factor, elevated expression…)overexpression of c-myc in these B cells causes Burkitt’s lymphomagoing to be self-sustaining b/c last step is activatedlast step in RTK signaling before activating Cyclin D (trips the cycle out of G0), transcription activated, make a proteindifficult to target(activate transcription of myc, RNA out of cytoplasm, comes back into nucleus, that activates Cyclin D–>once synthesis begins

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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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Proto-Oncogenes,”the cancer genesnormal genes that have normal proliferation but are going to go rogue and become oncogenespromote cell survival or proliferationex) HER2, Ras, Raf, Abl, Myceffect of mutation: gain-of-function mutations allow unregulated cell proliferation and survivalmutations genetically dominantarise by point mutation, chromosomal translocation

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Proto-Oncogenes,”the cancer genesnormal genes that[…]

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