CNBR cleaves PO lacz the peptide bond after methionine. B-Galactosidase Met - Insulin Met B-Galactosidase T A chain amp. A chain A chain Active insulin Transform into E. coli. Culture cells. Purify B-galactosidase- Treat with CNB.. Purify A and insulin fusion proteins. B chains. Refolding and disulfide bond Disulfide bond lacZ B-Galactosidase formation - Met - Insulin Met B-Galactosidase T. B chain ampe. B chain B chain FIGURE 22.1 The use of bacteria to make human insulin. In recent forms of manufactured insulin, slight changes have been made to the insulin amino acid sequence. These changes prevent insulin molecules from clumping together, and thereby improve the manufactured insulin's biological properties. Genes-Traits The synthesis of human insulin is not a trait that bacteria normally possess. However, genetic engineers can introduce the genetic sequences that en- code the A and B chains of human insulin via recombinant DNA technology, yielding bacteria that make these polypeptides as fusion proteins with B-galactosidase.

CNBR cleaves PO lacz the peptide bond after methionine. B-Galactosidase Met - Insulin Met B-Galactosidase T A chain amp. A chain A chain Active insulin Transform into E. coli. Culture cells. Purify B-galactosidase- Treat with CNB.. Purify A and insulin fusion proteins. B chains. Refolding and disulfide bond Disulfide bond lacZ B-Galactosidase formation - Met - Insulin Met B-Galactosidase T. B chain ampe. B chain B chain FIGURE 22.1 The use of bacteria to make human insulin. In recent forms of manufactured insulin, slight changes have been made to the insulin amino acid sequence. These changes prevent insulin molecules from clumping together, and thereby improve the manufactured insulin's biological properties. Genes-Traits The synthesis of human insulin is not a trait that bacteria normally possess. However, genetic engineers can introduce the genetic sequences that en- code the A and B chains of human insulin via recombinant DNA technology, yielding bacteria that make these polypeptides as fusion proteins with B-galactosidase.

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter27: Metabolic Integration And Organ Specialization

Section: Chapter Questions

Problem 18P

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PDGF 100 PI3K 740 751 PI3K 50 - GAP O771 O GAP PTP P 1009 O PTP protein P-site 1 12 4 5. 6. 7. PI3K 740, 751+ 1021 GAP 771 +] +] PTP 1009 PLC PLCy PLCT 1021 When activated by ligand binding, the PDGF (platelet-derived growth factor) receptor becomes phosphorylated on 5 tyrosine residues (left figure). These phosphorylated tyrosines serve as binding sites for proteins that contain SH2 domains (SH2 domains bind phosphorylated Y). These proteins include phospholipase C-gamma (PLC-gamma), a phosphotyrosine phosphatase (PTP), a Ras GTPase-Activating Protein (GAP), and a phosphotidylinositol 3-Kinase (PI3K). PDGF stimulates several changes in the target cell, one of which is DNA synthesis. To determine which effectors of the PDGF receptor is/are responsible for stimulating DNA synthesis, you construct several mutant forms of the receptor that retain individual or combinations of the phosphorylation sites. You express these in cells and monitor DNA synthesi The results are shown in the right…
valy All adrenoleukodystrophy patients carry the same mutation in the ABCD1 gene, however their clinical fates dramatically. Male patients, like Lorenzo from the film, have a 35-40% risk of developing the disease between 3 and 18 years of age whereas others develop it in adulthood. In adulthood, virtually all men and 80% of women with ALD develop a spinal cord disease. The disease caused by a mutation in ABCD1 leads to an increase in very long-chain fatty acids. These fatty acids cause stress to the endoplasmic reticulum of cells. This stress then leads to the destruction of myelin an important component in neural cells (we'll learn more about this later). Using a sheet of paper or electronically, draw a cell. (It doesn't have to be a specific type of cell any generic cell will do.) This cell is from a patient who suffers from adrenoleukodystrophy. Therefore, be sure to draw the following structures and make sure to label them: A. Plasma Membrane - doesn't need to be fancy B. Nucleus…
I. A protein, X, was Isolated from a pathogenlc mlcroorganism. The proteln Is a vlrulence factor whose path0genlclty lies In a heptapeptide of unknown sequence. After trypsin cleavage of the heptapeptide from protein X, the peptlde's compOsition and sequence was determined. The fOllowing were the results of the sequenclng process: 1. When the peptide was treated with dinitrofluorobenzene (DNFB), DNP-asp and a mixture of amino acids were produced. 2. When the same Intact peptide was treated with streptococcal protease, a pentapeptide of composition asp, asN, cys, gly and ser and 2 amlno acids were released. 3. When the heptapeptlde was also treated with hydrOxylamine HCI, a tripeptide and a tetrapeptide were obtained. The C-terminal amino acid of the tripeptide was asN. 1) What is the sequence of the heptapeptide if it is composed of cys, asp, lys, asN, gly and ser only? 2) What is the pl of the heptapeptide?
Explain the signifi cance of the observation that peptides such as fMet-Leu-Phe “activate” the phagocytotic (particle-engulfi ng) functions of mammalian leukocytes (white blood cells).
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.…
Need help Intaractions of FAK kinase which directly depend on the tyrosine residue 397 (Y397) are inhibbited by a chemical compound in cancercells. Intaraction of FAK kinase with what proteins are blocked by this inhibition? (please give a listt of them all, and that's it)
alpha 1 adrenergic receptor causes vasoconstriction through activation of Gq protein explain the mechanism of action for this receptorb starting from the ligand binding step untill final effectoe is activated
The distal histidine stabilises the iron in heme group of a deoxyhaemoglobin. T/F
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1 of 16 Data from an experiment is shown in the figure below. In the experiment, murine cells were treated with a specific a ligand that activates receptor R. In some cases, the cells were exposed to one of two drugs (X or Y) as well as the ligand or were left untreated (UT). After 30 minutes of treatment, the cells were lysed with a detergent-based buffer to release the soluble membrane, cyosolic and nuclear proteins. Samples from each cell extract were run (in duplicate) by SDS-PAGE (SDS-polyacrylamide gel electrophoresis) in order to separate the proteins by molecular mass (size). The separated proteins were then transferred to a nitrocellulose membrane which was then probed with different antibodies in a western blotting procedure to detect specific phosphorylated proteins or total proteins. If present in the cell extract, these proteins appear as a dark band in the relevant western blot image within the figure. Drug X Drug Y UT Ligand Ligand Ligand Western blotting antibodies…
ras GDP ras ras P.P P.P GTP raf Inactive Active raf Inside of cell Refer to the figure above. A portion of a signal transduction pathway is shown in the figure. The molecule raf is a protein kinase. This molecule becomes activated when a GTP-ras complex binds to it. Which equation describes how activated raf transmits the signal in this pathway? O ATP. --> CAMP +PPi O CAMP --> AMP Inactive enzyme + ATP --> active phosphorylated enzyme + ADP O Inactive phosphorylated enzyme + ADP --> inactive enzyme + ATP Inactive enzyme + ADP --> active phosphorylated enzyme + ATP Assessment Navigator Submit Questionmark Ondemand licensed to University of Dundee PPIP