оооооA. EGF YIYV would bind SrcB. PDGF-YLIP would bind SrcC. PDGF YLIP would bind ShcD. Adding EGF to cells expressing EGF YIYV receptor would activate the PLC-gamma signaling pathwayE. Adding EGF to cells expressing EGF-YIYV receptor would activate Shc signaling pathway Which of the following would you expect to happen if amino acids 579 to 582 (YIYV) in the PDGF-Beta receptor wereexchanged with amino acids 992 to 995 (YLIP) from the EGF receptor to give PDGF (YLIP) and EGF (YIYV) (Select allthat apply)?(A)PDGF-BreceptorSrcINCK-BSHP2PLC-yP 579P 581YIYVPI3KYP 740 YMDMNCK-a P 751 YVPMP 771 YMAPGAPP 1009 YTAVP 1021 YIIP(B)POE845 YHAE992 YLIP1045 YSSD1068 YINQ1086 YHNK1148 YQQD1173 YLRVPPPPPPPEGFreceptorSTAT3/5PLC-yShcCblJAK2Grb2STAT3/5ShcSHP1PTP1

PGDF beta-receptor contain multiple domains that activate the various pathways inside the cell. The…

Answered: ооооо A. EGF YIYV would bind Src B.…

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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Would the following alterations to Src be oncogenic? Explain. (a) The deletion or inactivation of the SH3 domain. (b) The mutation of Tyr 416 to Phe.
Many enzymes can hydrolyze GTP between the β and γ phosphates. The GTP analog β,γ-imidoguanosine 5′-triphosphate (Gpp(NH)p), shown below, cannot be hydrolyzed between the β and γ phosphates. Predict the effect of microinjection of Gpp(NH)p into a myocyte on the cell’s response to β-adrenergic stimulation.
Mutation in the fibroblast growth factor receptor (FGFR) gene results in achondroplasia (dwarfism), which is a dominant condition caused by a single base substitution (GGG>AGG) that changes the amino acid glycine at position 480 to arginine (G480R) in the FGFR protein. FGFR is normally active when FGF binds to it, but the mutant FGFR is always on to stimulate signaling that inhibits excessive bone growth. How can gene therapy be used to treat achondroplasia? Select all that apply. RNAi that knocks down the mutant FGFR expression Adeno-associated viral (AAV) vector that carries the wild-type FGFR Retroviral vector that carries the wild-type FGFR CRISPR with the wild-type FGFR donor DNA
Some strains of bacteria or microorganisms have developed toxins that can modify the activity of the alpha subunit of G proteins which results in disease. For ex. cholera toxin, produced by Vibrio cholerae, causes ADP ribosylation of the stimulatory Gαs subunit of G proteins. This modification abolishes the GTPase of Gαs, and results in an αs subunit that is always in the “on” or active state. It results in continuous stimulation of adenylyl cyclase (AC). The main cells affected by this are the epithelial cell in gastrointestinal tract. Knowing this altered activity of AC, explain why patients affected by this toxin experience severe diarrhea and dehydration that may result in death.
RTKs are receptors made of an extracellular ligand binding domain and an intracellular kinase domain (see image). Insulin binds to its RTK Insulin receptor, causing an increase in glucose absorption and storage in liver cells. EGF binds to its own RTK, EGFR and promotes cell growth through the Ras pathway. a) Explain why the same type of tyrosine kinase in two RTKs can lead to very different cellular responses. Give an example of potential cellular outputs for each of these two RTKs.
In contrast to their similar brain abnormalities,newborn mice deficient in Apaf1 or caspase-9 have dis-tinctive abnormalities in their paws. Apaf1-deficient micefail to eliminate the webs between their developing digits,whereas caspase-9-deficient mice have normally formeddigits (Figure Q18–1). If Apaf1 and caspase-9 function inthe same apoptotic pathway, how is it possible for thesedeficient mice to differ in web-cell apoptosis?
Psilocybin is rapidly de-phosphorylated in the body into psilocin, which is anagonist For the 5-HT 2A Serotonin receptor, which binds the neurotransmitter serotonin as its natural ligand, and acts as a ligand-gated ion channel in the central nervous system. HO. Serotonin (a) Part of the sequence of the 5-HT 24 Receptor is NH₂ ...RQKACKVIGIVFFLFVVMWLAFFITNICDES... Identify the trans-membrane region within this sequence. Do you predict this sequence will Be transmembrane a-Helix or ß sheet? Why? (b) What is the distance spanned by this transmembrane region?
Using molecular cloning, a hybrid receptoer is produced that consists of the extracellular domain of the B-adrenergic receptor (B-AR) and the transmembrane and intracellular domains of the EGF receptor (EGFR). Question: What is the stoichiometric ratio of epinephrine to the hybrid receptor (B-AR-EGFR)? 1:1 O 1:4 O 1:2 2:1 O O O
The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.
Two GPCR mutations (Mutant A and Mutant B) were tested for activity. One was confirmed as being a constitutively activating, gain of function GPCR mutation and one was confirmed as being a loss of function GPCR mutation. Which is which? Explain your answer.
It is not an easy matter to assign particular func-tions to specific components of the basal lamina, sincethe overall structure is a complicated composite materialwith both mechanical and signaling properties. Nidogen,for example, cross-links two central components of thebasal lamina by binding to the laminin γ-1 chain and totype IV collagen. Given such a key role, it was surprisingthat mice with a homozygous knockout of the gene fornidogen-1 were entirely healthy, with no abnormal phe-notype. Similarly, mice homozygous for a knockout of thegene for nidogen-2 also appeared completely normal. Bycontrast, mice that were homozygous for a defined muta-tion in the gene for laminin γ-1, which eliminated just thebinding site for nidogen, died at birth with severe defectsin lung and kidney formation. The mutant portion of thelaminin γ-1 chain is thought to have no other functionthan to bind nidogen, and does not affect laminin struc-ture or its ability to assemble into the basal lamina.…
What is the structural difference between normal EGFR and oncogenic receptor, e.g. ERbB? How does it affect its activity?

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