Cells require growth factors from other cells to proliferate B. Growth Factors must enter cell to signal cell growth C. Growth Factor Receptors can be oncogenes D. Protein Growth Factors can be Oncogenes E. Staurosporine is a potent inhibitor of Ser/Thr kinases and would be expected to inhibit Epidermal Growth Factor Receptor sig

Cells require growth factors from other cells to proliferate B. Growth Factors must enter cell to signal cell growth C. Growth Factor Receptors can be oncogenes D. Protein Growth Factors can be Oncogenes E. Staurosporine is a potent inhibitor of Ser/Thr kinases and would be expected to inhibit Epidermal Growth Factor Receptor sig

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter5: Membranes And Transport

Section: Chapter Questions

Problem 1ITD: Some cancer cells are insensitive to typical chemotherapy. Research into the mechanisms underlying...

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Cancer cells may be more susceptible than normal cells to mitotic catastrophe in response to chemotherapeutic drugs because of which of the following (select all that apply)? A. They express unique receptors for those drugs on their surface B. They may be resistant to apoptosis C. Cancer cells have more efficient DNA repair mechanism than normal cells. D. Only cancer cells are actively dividing E. They may lack key G2/M checkpoint controls
Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth. a) What purpose does this forward…
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Which of the following statements are correct about cytoplasmic signaling in cancer cells? Multiple answers. A. Only minor modifications of cell control machinery are required for normal cells to become highly proliferating cancer cells B. Immediate early genes are induced in the presence of protein synthesis inhibitors C. Many immediate -early genes are oncogenes D. Delayed early genes are highly expressed in the presence of protein synthesis inhibitors E. Delayed early genes are highly expressed in normal cells in the absence of growth factors
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
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	A.	Cells require growth factors from other cells to proliferate
	B.	Growth Factors must enter cell to signal cell growth
	C.	Growth Factor Receptors can be oncogenes
	D.	Protein Growth Factors can be Oncogenes
	E.	Staurosporine is a potent inhibitor of Ser/Thr kinases and would be expected to inhibit Epidermal Growth Factor Receptor signaling