Which change is most likely to directly interfere with cytokinesis in a dividing animal cell? The loss of a lysine residue in a histone protein A mutation that affects the G2–M cyclin-CDK complex A mutation in the gene that encodes actin A mutation that affects the S cyclin–CDK complex A mutation in the RB gene
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- Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP What effect would this have on downstream cellular events?We have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPaseThe destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сокThe cell enters g1 and cyclin D binds with CDK4/6 Increases in cyclin D expression prevent p21/p27 from inhibiting cyclin E/CDK2 Rb is hypo-phosphorylated E2F is no longer repressed and induces expression of E2F and cyclin E The cell enters S phase and cyclin A binds to CDK2 cyclin A binds to CDC 2 > Cell enters G2 and cyclin B binds CDC 2 Cell enters M phase and proliferates Rb is hyperphosphorylated Upsteam signaling pathways lead to increase of expression of Cyclin D put in correct order from 1-10The cell enters g1 and cyclin D binds with CDK4/6 Increases in cyclin D expression prevent p21/p27 from inhibiting cyclin E/CDK2 Rb is hypo-phosphorylated E2F is no longer repressed and induces expression of E2F and cyclin E The cell enters S phase and cyclin A binds to CDK2 cyclin A binds to CDC 2 > Cell enters G2 and cyclin B binds CDC 2 Cell enters M phase and proliferates Put these in the correct order from 1-8
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.13 of 16 STAT proteins signal in a manner that is uncommon for signaling proteins that carry out similar functions in cell signaling because STAT proteins O are transcriptional regulators that are regulated by second messengers are transcriptional regulators that are directly activated by binding the primary signal molecule are transcriptional regulators that are activated at the plasma membrane of the cell are transcriptional regulators that also are heterotrimeric G-proteins O are transcription regulators that function entirely at the plasma membrane of the cellWilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…
- Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophataseCan 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.,…A growth factor Fsh3 stimulates the proliferation of culture fish cells. The receptor that binds Fsh3 is a receptor tyrosine kinase (RTK) and there are numerous fish tumor cell lines that have a mutation for the gen for this receptor. Which of the following mutations would be expected to promote uncontrolled cell proliferation. a mutation that inactivates the protein tyrosine phosphatase that acts on the receptor a mutation that prevents the binding of the normal extracellular signal to the receptor a mutation that inhibits the Ras GEF a mutation that destroys the kinase activity of the receptor a mutation that prevents dimerization of the receptor