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draw the p21 promoter in a cell with E2F
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- Chromosomal translocation can result in cells expressing a fusion protein with uncontrolled receptor tyrosine kinase activity due to inability to respond to growth factor ligamds . An example of this type of fusion is: Fos/Jun ErbB/Ras Tel/PDGFR Myc/MaxThe E132:GAL4 construct engineered into a fruit fly will causeExpression of S-phase genes is activated when O P16 inactive or absent P16 active Cdk4 inactive O Active Rb bind with E2F
- Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.Describe the nature of p53 reactivation as acancer-fighting strategyIn tumor cells obtained from patients with Burkittlymphoma, a cancer of the immune system’s B cells,the myc gene often appears close to one of the breakpoints of a reciprocal translocation between chromosomes 8 and 14. In this translocated position, myc is expressed at a higher-than-normal level. Scientists hypothesize that Myc protein overexpression in B cellscontributes to lymphoma formation.a. Explain how transgenic mice produced using pronuclear injection could be used to test this hypothesis. (Assume that you previously cloned a generegulatory region that is active specifically in Bcells throughout the life of the mouse.)b. Suppose you wanted to overexpress Myc only inthe immune cells of mice, starting at one week ofage. To restrict Myc transcription spatially, youwill use same promoter described in part (a). Torestrict Myc transcription temporally, you will usea cre transgene whose expression is controlled byheat shock (hs-cre). Describe the mouse you wouldcreate to accomplish…
- The following chromosomal aberration is found in nearly 90-95% of all patients who have chronic myelogenous leukemia. This is because the change brings the BCR and ABL genes in close proximity. BCR is responsible for cell growth, and ABL is a proto-oncogene... this favors uncontrolled growth. Which is the most accurate description of the aberration... chio moso me 9 Philad elphia chromosome chromosome 22 BCR ABL 22q11.2 (BCR) 9934 1 (ABL) Deletion Translocation Inversion Duplication DELL O O O CWhat is the abbreviated name of the human gene that contains the following sequence CAGATTGTGAAGAGGTCTCTTGA? ATR HBB XPA FGFR3 IDS XRCC1 p53 F8 APC ERCC323 of 41 Which of the following proteins is NOT encoded by a proto-onoogene? O Myc O Ras O E-cadherin Src O EGF receptor
- After a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.Can you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below? In addition to phosphorylation, the C-terminal domain of p53 can also be acetylated and sumolated in response to DNA damage. Acetylation and sumolation both result in an increase in the transactivation ability of p53 and may account for this finding. In vivo, IR induces the acetylation of p53 at Lys320 by PCAF and Lys382 by CBP/p300. Acetylation at these sites is dependent on N-terminal phosphorylation at Ser15 and to a lesser extent on phosphorylation at Ser6, Ser9, and Thr18 (Saito et al., 2002; Wahl and Carr, 2001). All of these phosphorylation events are ATM-dependent, although only Ser15 has been shown to be phosphorylated directly by ATM. Sumolation occurs at Lys386 after DNA damage (Muller et al., 2000). Sumolation refers to the covalent attachment of a small ubiquitin-like molecule (SUMO-1) to Lys residues, but in contrast to ubiquitination, does not result…// Which CDK and cyclin does p53 ultimately target in DNA damaged conditions? O CDK1/cyclin E O CDK2/cyclin E CDK1/cyclin B CDK2/cyclin B