Explain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.
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Explain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.
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- Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.Explain the activation of the protein kinase, c-raf, in response to growth factor receptor activationTSC acts as a tumor suppressor by continually suppressing mTOR and must be inhibited in order for mTOR to be active. True or false, explain why
- Many malignant tumors are characterized by the activation of one or more growth-factor receptors. What is the catalytic activity associated with transmembrane growth factor receptors such as the EGF receptor?''In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.'' 'Is this statement true? Explain why or why not.Mutations that inactivate p53 have a recessive phenotype, whereas mutations affecting Ras are dominant. Explain the difference.
- The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.Briefly describe the following properties of the Ras GTPases: a) Size, structure and cellular localization (for structure I want to know if they are lipidated and any other unique features) , b) How are they activated and inactivated (i.e. include the GEFs and GAPs), c). Give an example of downstream effector proteins, d). Are they or could they be involved in human cancer.Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?