All but which of the following best explains the advantage of cancer cells expressing PKM2 over PKM1? OPKM1 has lower activity PKM2 allows for accumulation of glycolytic intermediates Serine is a more potent allosteric effector of PKM2 Higher serine levels lead to increased activity of PKM2
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- Notch signaling orchestrates transition from G1 to S phase of cell cycle by multiple other interactions that target the G1/S checkpoint machinery. This is a highly conserved pathway that is seen across multiple kingdoms of life and the ligands involved in notch signaling are typically membrane-bound proteins. This suggests that: -This pathway relies on hormone interactions via endocrine pathways -This pathway relies on signal propagation via paracrine molecules -This pathway relies on direct signaling across gap junctions -This pathway relies on cell binding via autocrine signalingYou established two cell lines (Cell line X and Cell line Y) from colon cancer patients and both of them can proliferate without the Wnt ligand. When you analyze the tumor suppressor APC (Adenomatous Polyposis Coli) protein in these lines, X does not express functional APC but Y expresses functional APC. How can Y keep proliferating without Wnt? Which function (protein) within the Wnt signaling pathway might be defective in Y?please help
- The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode: A protein that induces degradation of MARCH-1 A protein that mimics MARCH-1 and functions similarly A protein that binds to MARCH-1 and inhibits its function A protein that is induced by IL-10 in macrophages and dendritic cells A protein that induces degradation of CD861) Explain what is the role of PTEN in the regulation of cell cycle/growth and how does it lead to cancer and gove one example of a cancer caused by mutation in the gene of PTEN protein and how doctors detected pten gene mutation in that cancer?Imagine that you created a cell that over-expresses a truncated version of its extrinsic pathway initiator caspase. This protein contains the caspase's DED, but none of the caspase's protease domains. This truncated version is present as an extra copy in addition to the WT copy. In 1-2 sentences, explain what the outcome would be on extrinsic apoptosis (i.e. would it be a positive/negative regulator/have no effect) and why.
- Which of the following types of mutations would be most likely to cause cells to undergo apoptosis (programmed cell death)? One that increases the affinity of p21 for Cdks One that decreases the affinity of Rb for the transcription factor E2F One that decreases the ability of p53 to bind to DNA One that causes p53 to be constitutively phosphorylatedThe 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 1-8The product of the human papillomavirous oncogene E7promotes cancer by emhancing expression of telomere inhibiting DNA damage repair pathways binding to Rb protein and preventing itd function ubiquitinating the tumor suppressor p53