Mammalian cells have a limitless replicative potential. During carcinogenesis, the cancer cell is not eradicated by the body's immune system. A breast cancer patient treated with Trastuzumab shows no benefits suggesting that the cancer is caused by HER- 2 receptors.
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- If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MIEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell’s behavior change?BIOC 384 Tumor Necrosis Factor Receptor Signaling Q8.2: What is the key activating signal in the TNF receptor signaling pathway that occurs downstream of TNF-alpha binding to the extracellular domain? What are the analogous activating signals downstream of receptor activation in the GPCR and RTK pathways.BIOC 384 Overview of Cell Signaling Pathways Q7.2: A first messenger molecule activates a receptor that stimulates Enzyme A, which synthesizes 100 second messenger molecules. In turn, each second messenger activates only one molecule of Enzyme B, which once activated, phosphorylates 100 molecules of Enzyme C that each phosphorylate 75 molecules of Enzyme D. In the last step, each Enzyme D phosphorylates 50 transcription factors. How many transcription factors are phosphorylated in response to the first messenger binding to the receptor? How many transcription factors would be phosphorylated if one copy of the Enzyme D gene were inactivated (heterozygous genotype) so that there were only half the number of functional Enzyme D molecules in the cell? Explain.
- BIOC 384 Receptor Tyrosine Kinase Signaling Q8.1: Explain why a glycine residue at position 12 of the G protein Ras is only active in the presence of growth factors but Ras with an aspartate residue at the same position is oncogenic (can cause cancer).EGF-R patho Discuss how the EGF-R becomes activeo How does the active receptor recruit substrate, and how does substrate hold ontoreceptor? When held, what “options” in regards to what the receptor does tobound substrate?o What proteins are involved in the recruitment of ras to the receptor, and how doesras become active – what does it do then? Make sure you include the G-proteinstory.o When active, ras triggers the MAPK cascade – what is the end result of this path.o Discuss the most common mutation in the ras gene found in cancer cells – how doesthis mutation play a role in the cancer cell story?How does PKC’s signaling role change in response to growth factor signaling versus an immune response? PKC interacts directly with signaling molecules in both cascades, but only exhibits kinase activity during growth factor signaling. PKC interacts directly with signaling molecules in growth factor cascades, but interacts with signaling inhibitors during immune signaling. PKC amplifies growth factor cascades, but turns off immune cascades. PKC is activated during growth factor cascades, but is inactivated during immune response cascades.
- In contrast to their similar brain abnormalities,newborn mice deficient in Apaf1 or caspase-9 have dis-tinctive abnormalities in their paws. Apaf1-deficient micefail to eliminate the webs between their developing digits,whereas caspase-9-deficient mice have normally formeddigits (Figure Q18–1). If Apaf1 and caspase-9 function inthe same apoptotic pathway, how is it possible for thesedeficient mice to differ in web-cell apoptosis?Q15. An enhancer facilitates the binding of a substrate to an enzyme, increasing the enzymes affinity for that substrate. How would adding an enhancer to a biochemical reaction affect the rate of that reaction? A. The Km would increase, the Vmax would stay the same. B. The Km would decrease, the Vmax would stay the same. C. The Km would increase, the Vmax would increase. D. The Km would decrease, the Vmax would increase.Targeted therapies are used in patients with a set gene expression pattern. A targeted therapy that prevents the activation of the estrogen receptor in breast cancer would be beneficial to which type of patient? patients who express the EGFR receptor in normal cells patients with a mutation that inactivates the estrogen receptor patients with lots of the estrogen receptor expressed in their tumor patients that have no estrogen receptor expressed in their tumor
- The affinity of integrins for matrix components canbe modulated by changes to their cytoplasmic domains:a process known as inside-out signaling. You have iden-tified a key region in the cytoplasmic domains of αIIbβ3integrin that seems to be required for inside-out signaling(Figure Q19–3). Substitution of alanine for either D723in the β chain or R995 in the α chain leads to a high levelof spontaneous activation, under conditions where thewild-type chains are inactive. Your advisor suggests thatyou convert the aspartate in the β chain to an arginine(D723R) and the arginine in the α chain to an aspartate(R995D). You compare all three α chains (R995, R995A,and R995D) against all three β chains (D723, D723A, andD723R). You find that all pairs have a high level of sponta-neous activation, except D723 vs R995 (the wild type) andD723R vs R995D, which have low levels. Based on theseresults, how do you think the αIIbβ3 integrin is held in itsinactive state?Q1 a) What is the difference between non-competitive or allosteric modes of inhibition for the compounds acting upon the caspases studied. b) How many caspase isozymes are known in humans? c) What is the reaction catalyzed by a caspase enzyme?More than 500 genes have been identified in the human genome that code for protein kinases. What does such identification imply regarding the role of protein kinases in cellular functions? Explain your answer.