In the RAD signaling pathway the EGF ligand binds the EGF receptor, this initiated a phosphorylation cascade that results in cell proliferation. Which of the following statements is correct: a. RAS protein is the sognal b. EGF ligand is the signal c. cell proliferation is the signal d. EGF receptor is the signal e. none of the above

In the RAD signaling pathway the EGF ligand binds the EGF receptor, this initiated a phosphorylation cascade that results in cell proliferation. Which of the following statements is correct: a. RAS protein is the sognal b. EGF ligand is the signal c. cell proliferation is the signal d. EGF receptor is the signal e. none of the above

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 13RQ: A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to...

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Use the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Sos Grb2 (Ras GEF) (adapter) Raf МАРКK Mek МАРКK Activation of target genes that stimulate proliferation Erk МАРК You have a skin cell in a dish and have added Neural Growth Factor (NGF) to the cell media (the liquid the cell needs to live).
Which of the following modifications of the Epithelial Growth Factor Receptor (EGFR) would be proliferative of epithelial cells? multiple answers A. Mutation of active site residue responsible for tyrosine phosphorylation. B. Deletion of extracellular ectodomain C. Mutation in ectodomain that prevents binding of EGF D. Cell expresses EGF E. Mutation in promoter that increases expression of EGF receptor F. Dimerization of receptor without growth factor G. Mutation in EGFR promoter that decreases expression of receptor
Aberrant signaling through the EGF receptor signal transduction pathway drives many forms of breast cancer, while misregulation of PI3K drives many prostate cancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, and there are several known activating mutations of PI3K. Would a small molecule that targets PI3K be an effective treatment for a breast cancer that is driven by aberrant signaling through the EGF receptor? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.)
Use the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Ras GEF ladapter) MAPIKK Mek MAPIK MAPK You have a skin cell that inject SGF protein directly into the cytoplasm but you do NOT put SGF in the media (the liquid the cell needs to live).
The figure below shows how normal signaling works with a Ras protein acting downstream of a receptor tyrosine kinase. CYTOSOL active receptor tyrosine kinase Taratas THERI signal molecule 00 active signaling Q Search active Ras protein GTP 99+ Į SIGNALING Il app.honorlock.com is sharing your screen. ✡ active signaling protein Y a
Which of the following statements regarding signaling in normal cells and cancer cells is false? a. In normal cells, RTK transphosphorylation is strictly dependent on ligand binding. Ligand binding promotes a conformational change in the RTKS that is required for dimerization, and dimerization is required for transphosphorylation. b. Cancers cells that over-express RTK's can respond to tiny amounts of ligand, and in some instances signaling can be ligand-independent. c. Cancer cells that have established several autocrine signaling loops have a poor prognosis, because these cells have enabled multiple independent mitogenic signal transduction pathways. 4 d. The extracellular ectodomains of all RTKS are highly conserved in primary sequence and structure. e. RTKS have a hydrophilic extracellular ectodomain, and hydrophobic transmembrane domain, and a hydrophilic cytoplasmic domain, which contains the catalytic portion of the protein.
Epidermal growth factor (EGF) signals through a receptor, tyrosine kinase. EGF signaling promotes cell division by increasing nuclear concentrations of CyclinD through both the MEK and AKT signaling pathways as shown in the diagram. Use the EGF Pathway passage to answer the questions. EGF signals by binding to cell surface EGF receptors. Which of these observations, if true, would BEST explain EGF’s mechanism of action? A. EGF is hydrophilic and can easily diffuse through the cell membrane. B. EGF is hydrophobic and can easily diffuse through the cell membrane. C. EGF is hydrophilic and cannot diffuse through the cell membrane. D. EGF is hydrophobic and cannot diffuse through the cell membrane. Which of these BEST describes how the signal is transduced from the EGF receptor to the Ras protein? A. Ras is phosphorylated. B. Ras is dephosphorylated. C. Ras binds to a GTP molecule. D. Ras hydrolyzes a GTP molecule. High concentrations of nuclear CyclinD is required for entry into S…
Glucocorticoids are sterojd hormones that are released into the circulation and will cause changes to gene expression in the cells that respond. Which of the following would be a factor that can determine whether a cell will respond to circulating glucocorticoids? Whether the cell expresses the lac repressor. O A. O B. Whether the cell expresses the CREB protein. Whether the cell expresses the glucocorticoid receptor. C. Whether CAMP is produced at high levels by adenylyl cyclase. D. O E. Whether adenylyl cyclase is activated or not.
A certain group of Brec-MUT cells expresses low levels of protein A, unlike the high expression levels of most Brec-MUT cells. Researchers determine that the cells have an excess of ATP and that there are no mutations in the gene encoding protein A. Describe a change in the Brec signaling pathway that would lead to the decreased expression of protein A even in the presence of Brec-MUT. Explain why B is able to bind to Brec but not to A.
Researchers have found that a certain signal transduction pathway, illustrated in the figure below, may be responsible for the development of cancer in pancreatic cells. In normal pancreatic cells, where the pathway remains inactive, a membrane-bound receptor called Ptc inhibits a downstream protein known as Smo. The inhibition of Smo blocks the activa- tion of a complex of proteins known as the HSC, which results in the cleaving of one of its proteins called Ci. The cleaving of Ci, in turn, prevents the pathway from initiating the syn- thesis of division-facilitating enzymes. A Ptc B Smo с inhibition D A model of a Ptc signal transduction pathway under normal conditions. HSC Ci cleavage A certain protein called the Hedgehog protein (Hh) is found to activate this signal transduction pathway and trigger uninterruptable cell division. cell division not initiated Which of the following describes the most plausible mechanism by which Hh triggers uninterruptable cell division? Hh binds to…
If a cell expresses a dominant-negative tyrosine-kinase-linked receptor (RTK) that lacks the kinase domain, which of the following will still happen in response to a growth factor that binds the RTK? A Receptor cross-phosphorylation. Activation of target proteins by Ras. C) Receptor dimerization. D) Binding of the growth factor to its receptor. Interaction of Ras with the activated receptor. B
Binding of a ligand (like TGFA) to a receptor tyrosine kinase (RTK) causes all of the following except (can use cell): OA. Dimerization of the receptor B. Auto-phosphorylation of the receptor O C. Activation of Ras through an interction with GRB2 (an adaptor) and SOS (a GEF) proteins. O D. Activation of heterotrimeric G proteins