Identify which cartooned cell phenotype (A-C) would most likely be caused by the mutants described in the following questions. Mutant with a Cdk-activating kinase (CAK) that can NOT phosphorylate M-Cdk. A В C O picture A O picture B picture C No answer text provided.
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A: RTKs are the membrane-bound receptors present in the cells. The role of RTK is phosphorylating the…
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A: Cancer The continuous uncontrollable division of defective cell can leads to the cancer.
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Q: a. Cytoplasmic Receptor b. Transmembrane Receptor c. Intracellular Receptor d. Nuclear…
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A: Cell cycle It is a series of events in which cell duplicate it's organelles and divide.
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A:
Q: Metabolic syndrome is a clustering of various conditions including high blood pressure, high blood…
A: Answer :- Option (C) is correct. - Insulin receptor phosphorylation increases insulin secretion.
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Q: This inhibatory kinase phosphorylates an inactive M-Cdk. a) M-kinase b) Wee1 c) CAK d) Cdc25
A: CDKs are Cyclin Dependent kinases. CDKs work with cyclin to control cell cycle transition.
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Q: Increased stability of, would lead to low G1/S-Cdk activity. Select one: O a. Cdc20 O b. Wee1 О с.…
A: The G1/S transition is highly regulated by transcription factor p53 in order to halt the cell cycle…
Q: Which of the following could be classified as an oncogene? None are possible oncogenes A mutant of…
A: An oncogene is a mutated form of a proto-oncogene normally present in a cell and is involved in…
Q: In the pathway below, normal signalling driving cell division requires a mitogen (ligand), an RTK,…
A: Mutations are alterations in the DNA sequence of an organism. Small changes, such as adding or…
Q: Why do signals indicating damage to cells result in increase in the expression of p21Cip1?
A: P21cip1 is small 165 amino acid protein that mediates p53 dependent G1 growth arrest.
Q: Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related…
A: Consider the association between a protein 'P' and a ligand 'L'. P + L ⇌KDKB PL Here KB is the…
Q: Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related…
A: The dissociation constant is the equilibrium constant for the dissociation of a Protein-Ligand…
Q: egulate cell division and cell mass. the following effects of map kinase activation explains an…
A: MAPK pathways relay, amplify and integrate signals from a diverse range of stimuli and elicit an…
Q: CAMP (cyclic adenosine monophosphate) is a molecule that can activate kinase enzymes allosterically…
A: The cells are communicating with each other by the releasing of some signalling molecules that are…
Q: Which of the following is associated with a decrease in cell-cell interactions? Select one: a. loss…
A: Option e. is correct . Loss of E-cadherin is associated with a decrease in cell-cell interactions.
Q: I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis…
A: The TNF or Tumour Necrosis Factor receptors are Cysteine Rich Domain (CRD) containing Receptors. It…
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- Which of the following classes of oncogenes would likely be druggable with a small molecule (select all that apply)? A. Nuclear hormone receptor B. RAS C. Serine/Threoine Kinase D. Transcription Factor E. Receptor Tyrosine KinasePathway analysis: Link the protein names to the correct statements by interrogating the depicted pathway. Options: A. RTK Receptor Threonine Kinase B. GEF Guanidine Exchange Factor C. PLC Phospholipase C D. GAP GTPase Activating Protein E. Gαi F. Raf Rapidly Accelerated Fibrosarcoma G. PAK1 p21 Activated Kinase H. WASP Wiscott Aldrich syndrome protein I. RTK Receptor Tyrosine Kinase J. GPCR G-protein Coupled Receptor K. Steroid Receptor L. Phosphatase M. MEK1 (Mitogen-Activated Protein) Kinase/ERK (Extracellular Signal-Regulated Kinase) Kinase 1 N. AC Adenylyl cyclase O. IP3R IP3 Receptor P. ERK1/2 Extracellular Signal-Regulated KinaseFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
- I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.Which of the following would be expected to inhibit PKC activation by a GPCR ligand? phospholipase C inhibitor cAMP phosphodiesterase inhibitor Ras inhibitor MAP kinase inhibitorCell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
- i want the solution of this assingment please. 1- Typical N-terminal signal sequence ( include description, function, and how they work)2- list address codes for different parts of the cell3- Stop transfer sequence ( description, function, how they work)Which ONE of the following molecular abnormalities is associated with the POOREST prognosis in acute myleoid leukaemia? A. t(8;21) translocaton (RUNX1_RUNX1fusion) B. DNMT3A mutation C. TP53 deletion D. NPM1 mutation.What type of mutation might render the following proteins constitutively ac- tive: (a) Smad3, (b) MAP kinase, and (c) NF-κB?
- a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?Put the following steps in the correct orderedsequence.a. kinase cascadeb. activation of a transcription factorc. hormone binds transmembrane receptord. expression of target genes in the nucleuse. Ras molecular switchWhich of the following statements is true? Question 9 options: a) Executioner caspases are activated by cleavage. b) Initiator caspases are activated by cleavage. c) Executioner caspases are activated by dimerization. d) Executioner caspases trigger apoptosis but initiator caspases does not.