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True or False?
p21 inhibits the S-cyclin/S-Cdk complex.
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- Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.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…What inhibit CDK activity by bindingdirectly to the cyclin-CDK complex.
- 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.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.The protein AKT/PKB is a critical regulator of essential cellular processes, and dysregulation of AKT has been implicated in many diseases, including cancer. In the present study, we wanted to test if levels of protein AKT changed in in EGF-stimulated epithelial, human breast cancer cell line when treated with varying concentrations of a drug Chondramide (ChB; 30 nM or 100 nM) for different lengths of time (1 or 24 h). Cellular lysate was prepared for each experimental condition, and an equal concentration of protein was loaded into a single lane of the SDS-polyacrylamide gel for each sample. We used western blot to measure the total levels of AKT and the fraction of Akt that is phosphorylated on the serine residue at position 473 (p-AktS473) using a phosphorylation specific antibody. GAPDH was used a loading control. EGF 30 nM ChB 100 nM ChB P-Ak47 total Akt GAPDH 0 0 + 0 0 0 0 0 1h 24h 1h 24h 0 Why do you think the researchers included GAPDH in the figure? A. B. C. D. Control for…
- MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese woman in no…# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9The expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.
- Can I get help on drawing a mechanism for the paragraph below? p53 stabilization by IR The signal upstream of p53 stabilization and activation after IR exposure most likely originate from DNA DSBs. This is supported by the fact that the kinases implicated in the phosphorylation of p53 are also implicated in DSB repair. These include two kinases that belong to the PI-3 kinase family, DNA-PK and ATM (see above), and indirectly, the checkpoint kinase 2 (Chk2). Ser15 of p53 was identified as a substrate for DNA-PK in vitro (Lees-Miller et al., 1992). Since DNA-PK is required for DSB repair in mammalian cells after IR exposure and since this residue falls within the MDM2-binding domain of the protein, this was an attractive model of p53 stabilization after IR. However, several recent reports have shown that Ser15 of p53 is phosphorylated in cells deficient in DNA-PK and that p53 accumulation in these cells is capable of generating cell cycle arrest or apoptosis after IR (Abraham et al.,…You have two patients with pancreatic cancer. Patient 1 has a KRAS oncogenic mutation; a myc oncogenic mutation and has normal levels of P53. Patient 2 has normal KRAS expression: a myc oncogenic mutation and a tumor suppressor mutation in P53. You have the following therapeutics available Flavopiradol (a CDK inhibitor); CBP-93872 (a G2/M checkpoint inhibitor); Rigosertib; Oncorine; Nutlin a. Which patient would CBP-93872 be the most effective? Explain your answer. b. Which therapeutic(s) would not be expected to be effective in patient 2? For each, explain your answerSome studies have pointed that mutant p53 proteins have gained a novel function by inactivating p63/p73. Can you elaborate about this - thanks