Zeb1 encodes a transcription factor that activates expression of genes that help cells migrate (move to different parts of the body) during embryogenesis. Zeb1 is not expressed in most adult tissues, but can undergo a gain of function mutation in some tumors. Which change is likely to result from a gain of function mutation in Zeb1? a) sustaining proliferative signalling O b) activating invasion and metastasis O c) deregulating cellular energetics O d) resisting cell death

In the pathway below, normal signalling driving cell division requires a mitogen (ligand), an RTK, Ras and proteins X and Y. Which of the following statements is true about the genes that encode the mitogen and Ras in healthy cells? mitogen active Ras protein CYTOSOL GTP active signaling protein Y active receptor active signaling protein X tyrosine kinase CELL DIVISON

Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth.   a) What purpose does this forward…

What is a possible outcome of the addition of a transcription factor such as Myod to the nucleus of a cell?  Assume that there are no other factors to either activate or prevent the response of the cell. Group of answer choices A) Production of mRNA from genes that were previously not expresed B)adding methyl groups to DNA C)prevention of protein synthesis D)uncoiling of the chromatin to allow transcription

With protein kinase-mediated molecular switches, downstream target molecules are typically activated by ... a) being phosphorylated b) binding to ATP c) the action of a phosphataase d) hydrolysis of GTP e) binding to GTP

Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regions

Please give the answers only

For each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)

The p75 receptor differs from Trk receptors in that it a) can promote cell death. b) has high affinity for all neurotrophins. c) only binds a particular type of neurotrophin. d) can bind NGF to promote cell survival.

Cellular signaling follows a cascade of events and has multiple points of regulation. Which of the following could be a reason(s) why a signalling cascade is interrupted, or turned 'off', once it has been turned 'on'? A) a protein gets tagged with an ubiqutin group and gets degraded B) a chemical modification occurred on serine, threonine, or tyrosine side chains to turn on/off proteins C) allosteric regulation causes an active site to be hidden D) All of the other answers are correct E) The ligand is prevented from reaching the binding site