Aberrant signaling through the EGF receptor signal transduction pathway drivesmany forms of breast cancer, while misregulation of PI3K drives many prostatecancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, andthere are several known activating mutations of PI3K.Would a small molecule that targets PI3K be an effective treatment for a breastcancer that is driven by aberrant signaling through the EGF receptor? Briefly explainyour choice.(THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY INABOUT EIGHT WORDS.)

Cell signaling is mediated by a ligand (usually a hormone but could be other molecules too) binding…

Answered: Aberrant signaling through the EGF…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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Practice ques tion 1A Mutations in the signalling pathways depicted above have been associated with an increased incidence of several types of cancer. Which of the below mutations (#1-5) could potentially cause cancer in an individual? Be sure to explain why. Info: In many mammalian species, including humans, there is a hormone (H) that acts as a key regulator of hexose (6 carbon sugar, eg - glucose) metabolism, cell cycle progression, and ultimately cell survival. Hormone H regulates these effects via its receptors which are found at both the cell surface (csRu) and within the cell (icRu). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRu). · The activated csBH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase…
You are studying a drug that affects a cAMP signalling pathway that is normally initiated when a signalling molecule binds to a G-protein coupled receptor. You determine that the drug prevents the hydrolysis of GTP bound to G-proteins in this pathway. Describe the impact, if any, that this drug would have on the G-protein coupled receptor (GPCR), assuming that the pathway has been activated by the presence of the signalling molecule (first messenger). Include an explanation for your response.
Hormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…
Briefly describe how inflammation can contribute to carcinogenesis and disease progression through heterotypic signaling.
GTP is an important high-energy molecule that facilitates the activation of many cellular sig- nal transduction pathways. Certain genetic dysfunctions can inhibit the ability of a cell to synthesize GTP. Which of the following describes the most direct result of GTP synthesis inhibition? A B с D The cell would be able to carry out reception and transduction but would not be able to produce the cellular response in the relevant signal transduction pathway. The G protein-coupled receptor will not be able to bind corresponding ligands, inhibiting the reception components of the relevant signal transduction pathway. The cell will use ATP instead of GTP to activate the G protein on the intracellular region of the G protein-coupled receptor. The cell would not be able to activate G proteins on the intracellular regions of G pro- tein-coupled receptors.
This is a tyrosine kinase receptor. a. Briefly describe the action of the receptor upon binding to the logand. b. There are several intracellular pathway possibilities for downstream responses. How might this receptor be able to selectively activate one particular pathway over another?
The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.
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
Some of the most common mutations associated with cancer are found in the small G protein Ras. Oncogenic mutants of Ras lead to constitutive signaling. Suggest several possible mechanisms for why these forms of Ras show constitutive signaling. Conversely, mutations of Ras have been isolated that have dominant-negative activity (that is, they block signaling by the normal, endogenous G protein). Suggest possible mechanisms for how these mutants block signaling.
RGS proteins accelerate the GAP activity of Gα subunits. What is the direct result of this GAP activity? - hydrolysis of GTP, resulting in a GDP-bound Gα - phosphorylation of GDP to GTP, resulting in a GTP-bound Gα - an exchange of GTP for GDP bound to Gα - an exchange of GDP for GTP bound to Gα
Binding of TGF-β to its receptors can elicit a variety of responses in different cell types. For example, TGF-β induces plasminogen activator inhibitor 1 in epithelial cells and specific immunoglobulins in B cells. In both cell types, Smad3 is activated. Given the conservation of the signaling pathway, what accounts for the diversity of the response to TGF-β in various cell types?
The output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK can lead to activation of a specific subset of proteins, leading to distinct effects in different cell types in response to the same growth signal.

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