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Relevant bibliographies by topics / Peptides; Protein kinase; Lipids

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Academic literature on the topic 'Peptides; Protein kinase; Lipids'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "Peptides; Protein kinase; Lipids"

1

Asokananthan, N., and M. H. Cake. "Stimulation of surfactant lipid secretion from fetal type II pneumocytes by gastrin-releasing peptide." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (March 1, 1996): L331—L337. http://dx.doi.org/10.1152/ajplung.1996.270.3.l331.

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Gastrin-releasing peptide (GRP) and bombesin apparently enhance the rate of secretion of surfactant lipids from cultured fetal rat type II pneumocytes. This effect, evident within 1h of addition of the peptide, is concentration-dependent, with a maximal response at 3.0 nM. When the effect of GRP was assessed in comparison with other known secretagogues, it was found that, whereas GRP and isoproterenol were additive in their effect, there was no response to GRP in the presence of saturating concentrations of A23187 or phorbol 12-myristate 13-acetate. This suggests that the secretory response to GRP is via activation of Ca2+/calmodulin-dependent protein kinase and/or protein kinase C and is independent of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase. This conclusion is supported by the observation that the GRP-induced secretion is inhibited by calphostin C, an inhibitor of protein kinase C, but not by H-89, an inhibitor of cAMP-dependent protein kinase. The fact that GRP regulates surfactant secretion from type II pneumocytes suggests that it and/or related peptides may play a significant role in the physiological maturation of the lung.

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McLaughlin, Stuart, Steven O. Smith, Michael J. Hayman, and Diana Murray. "An Electrostatic Engine Model for Autoinhibition and Activation of the Epidermal Growth Factor Receptor (EGFR/ErbB) Family." Journal of General Physiology 126, no. 1 (June 13, 2005): 41–53. http://dx.doi.org/10.1085/jgp.200509274.

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We propose a new mechanism to explain autoinhibition of the epidermal growth factor receptor (EGFR/ErbB) family of receptor tyrosine kinases based on a structural model that postulates both their juxtamembrane and protein tyrosine kinase domains bind electrostatically to acidic lipids in the plasma membrane, restricting access of the kinase domain to substrate tyrosines. Ligand-induced dimerization promotes partial trans autophosphorylation of ErbB1, leading to a rapid rise in intracellular [Ca2+] that can activate calmodulin. We postulate the Ca2+/calmodulin complex binds rapidly to residues 645–660 of the juxtamembrane domain, reversing its net charge from +8 to −8 and repelling it from the negatively charged inner leaflet of the membrane. The repulsion has two consequences: it releases electrostatically sequestered phosphatidylinositol 4,5-bisphosphate (PIP2), and it disengages the kinase domain from the membrane, allowing it to become fully active and phosphorylate an adjacent ErbB molecule or other substrate. We tested various aspects of the model by measuring ErbB juxtamembrane peptide binding to phospholipid vesicles using both a centrifugation assay and fluorescence correlation spectroscopy; analyzing the kinetics of interactions between ErbB peptides, membranes, and Ca2+/calmodulin using fluorescence stop flow; assessing ErbB1 activation in Cos1 cells; measuring fluorescence resonance energy transfer between ErbB peptides and PIP2; and making theoretical electrostatic calculations on atomic models of membranes and ErbB juxtamembrane and kinase domains.

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VINTON, B. Betsy, L. Stacey WERTZ, Jaison JACOB, Joanna STEERE, M. Charles GRISHAM, S. David CAFISO, and J. Julianne SANDO. "Influence of lipid on the structure and phosphorylation of protein kinase C α substrate peptides." Biochemical Journal 330, no. 3 (March 15, 1998): 1433–42. http://dx.doi.org/10.1042/bj3301433.

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The structure and phosphorylation of two protein kinase C (PKC) α substrate peptides were investigated in varying lipid systems using enzyme activity assays and circular dichroism (CD) spectroscopy. The α-peptide, which exhibits the typical PKC α substrate motif and is based on the pseudosubstrate region of PKC α, was phosphorylated to a similar extent in bovine brain phosphatidylserine vesicles or diheptanoylphosphatidylcholine (PC7) micelles (both with 5 mol % 1,2-dioleoyl-sn-glycerol), whereas neuromodulin (NM)-peptide, which does not exhibit this motif by virtue of its primary structure, was phosphorylated to a much lesser extent in the PC7 micellar system. CD spectra of the peptides indicated that NM-peptide underwent a dramatic structural change in the presence of dimyristoylphosphatidylserine (DMPS) vesicles, whereas spectra acquired in PC7 micelles were similar to those acquired in buffer alone. No significant structural change was observed in the α-peptide in the presence of either lipid. PKC activity assays conducted with a series of NM-peptides successively substituted with nitroxide spin labels at each residue position suggested that several residues distal to the phosphorylation site are necessary for substrate recognition. The effect of these substitutions is not consistent with the binding of the NM-peptide to PKC in an extended structure, but is consistent with the binding of this peptide in a helical conformation. Furthermore, the docking of a helical NM-peptide to the substrate binding site of PKC suggests that the interaction is energetically feasible. These results suggest that PKC may recognize some non-linear substrate motifs and that lipid binding may convert a protein into a better PKC substrate.

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Mosior, M., and S. McLaughlin. "Peptides that mimic the pseudosubstrate region of protein kinase C bind to acidic lipids in membranes." Biophysical Journal 60, no. 1 (July 1991): 149–59. http://dx.doi.org/10.1016/s0006-3495(91)82038-0.

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STOYANOVA, Stefka, Ginette BULGARELLI-LEVA, Cornelia KIRSCH, Theodor HANCK, Reinhard KLINGER, Reinhard WETZKER, and Matthias P. WYMANN. "Lipid kinase and protein kinase activities of G-protein-coupled phosphoinositide 3-kinase γ: structure–activity analysis and interactions with wortmannin." Biochemical Journal 324, no. 2 (June 1, 1997): 489–95. http://dx.doi.org/10.1042/bj3240489.

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Signalling via seven transmembrane helix receptors can lead to a massive increase in cellular PtdIns(3,4,5)P3, which is critical for the induction of various cell responses and is likely to be produced by a trimeric G-protein-sensitive phosphoinositide 3-kinase (PI3Kγ). We show here that PI3Kγ is a bifunctional lipid kinase and protein kinase, and that both activities are inhibited by wortmannin at concentrations equal to those affecting the p85/p110α heterodimeric PI3K (IC50 approx. 2 nM). The binding of wortmannin to PI3Kγ, as detected by anti-wortmannin antisera, closely followed the inhibition of the kinase activities. Truncation of more than the 98 N-terminal amino acid residues from PI3Kγ produced proteins that were inactive in wortmannin binding and kinase assays. This suggests that regions apart from the core catalytic domain are important in catalysis and inhibitor interaction. The covalent reaction of wortmannin with PI3Kγ was prevented by preincubation with phosphoinositides, ATP and its analogues adenine and 5′-(4-fluorosulphonylbenzoyl)adenine. Proteolytic analysis of wortmannin-prelabelled PI3Kγ revealed candidate wortmannin-binding peptides around Lys-799. Replacement of Lys-799 by Arg through site-directed mutagenesis aborted the covalent reaction with wortmannin and the lipid kinase and protein kinase activities completely. The above illustrates that Lys-799 is crucial to the phosphate transfer reaction and wortmannin reactivity. Parallel inhibition of the PI3Kγ-associated protein kinase and lipid kinase by wortmannin and by the Lys-799 → Arg mutation reveals that both activities are inherent in the PI3Kγ polypeptide.

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Hemmings, Hugh C., and Anna I. B. Adamo. "Activation of Endogenous Protein Kinase C by Halothane in Synaptosomes." Anesthesiology 84, no. 3 (March 1, 1996): 652–62. http://dx.doi.org/10.1097/00000542-199603000-00021.

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Background Protein kinase C is a signal transducing enzyme that is an important regulator of multiple physiologic processes and a potential molecular target for general anesthetic actions. However, the results of previous studies of the effects of general anesthetics on protein kinase C activation in vitro have been inconsistent. Methods The effects of halothane on endogenous brain protein kinase C activation were analyzed in isolated rat cerebrocortical nerve terminals (synaptosomes) and in synaptic membranes. Protein kinase C activation was monitored by the phosphorylation of MARCKS, a specific endogenous substrate. Results Halothane stimulated basal Ca2+ dependent phosphorylation of MARCKS (Mr = 83,000) in lysed synaptic membranes (2.1-fold; P< 0.01) and in intact synaptosomes (1.4-fold; P< 0.01). The EC50 for stimulation of MARCKS phosphorylation by halothene in synaptic membranes was 1.8 vol%. A selective peptide protein kinase C inhibitor, but not a protein phosphatase inhibitor (okadaic acid) or a peptide inhibitor of Ca2+/calmodulin-dependent protein kinase II, another Ca2+/-dependent signal transducing enzyme, blocked halothane-stimulated MARCKS phosphorylation in synaptic membranes. Halothane did not affect the phosphorylation of synapsin 1, a synaptic vesicle-associated protein substrate for Ca2+/calmodulin-dependent protein kinase II and AMP-dependent protein kinase, in synaptic membranes or intact synaptosomes subjected to KC1-evoked depolarization. However, halothane stimulated synapsin 1 phosphorylation evoked by ionomycin (a Ca2+ ionophore that permeabilizes membranes to Ca2+) in intact synaptosomes. Conclusions Halothane acutely stimulated basal protein kinase C activity in synaptosomes when assayed with endogenous nerve terminal substrates, lipids, and protein kinase C. This effect appeared to be selective for protein kinases C, because two other structurally similar second messenger-regulated protein kinases were not affected. Direct determinations of anesthetic effects on endogenous protein kinase C activation, translocation, and/or down-regulation are necessary to determine the ultimate effect of anesthetics on the protein kinase C signaling pathway in intact cells.

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Divecha, N., O. Truong, J. J. Hsuan, K. A. Hinchliffe, and R. F. Irvine. "The cloning and sequence of the C isoform of PtdIns4P 5-kinase." Biochemical Journal 309, no. 3 (August 1, 1995): 715–19. http://dx.doi.org/10.1042/bj3090715.

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In this study we describe the purification and sequencing of the C isoform of platelet PtdIns4P 5-kinase. Subsequently a cDNA was isolated from a human circulating-leucocyte library, which when sequenced was shown to contain all of the peptides identified in the purified protein. In addition, expression of this cDNA in bacteria led to the production of a protein which was recognized by specific monoclonal antibodies raised to the bovine brain enzyme [Brooksbank, Hutchings, Butcher, Irvine and Divecha (1993) Biochem. J. 291, 77-82] and also led to the appearance of PtdIns4P 5-kinase activity in the bacterial lysates. Interestingly, the cDNA showed no similarity to any of the previously cloned inositide kinases. A search of the DNA databases showed that two proteins from Saccharomyces cerevisiae shared close similarity to this enzyme, one of which, the mss4 gene product, has been implicated in the yeast inositol lipid pathway. These data suggest that the PtdIns4P 5-kinases are a new family of inositide kinases unrelated to the previously cloned phosphoinositide 3/4-kinases.

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Knopp, Michael, Arianne M. Babina, Jónína S. Gudmundsdóttir, Martin V. Douglass, M. Stephen Trent, and Dan I. Andersson. "A novel type of colistin resistance genes selected from random sequence space." PLOS Genetics 17, no. 1 (January 7, 2021): e1009227. http://dx.doi.org/10.1371/journal.pgen.1009227.

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Antibiotic resistance is a rapidly increasing medical problem that severely limits the success of antibiotic treatments, and the identification of resistance determinants is key for surveillance and control of resistance dissemination. Horizontal transfer is the dominant mechanism for spread of resistance genes between bacteria but little is known about the original emergence of resistance genes. Here, we examined experimentally if random sequences can generate novel antibiotic resistance determinants de novo. By utilizing highly diverse expression libraries encoding random sequences to select for open reading frames that confer resistance to the last-resort antibiotic colistin in Escherichia coli, six de novo colistin resistance conferring peptides (Dcr) were identified. The peptides act via direct interactions with the sensor kinase PmrB (also termed BasS in E. coli), causing an activation of the PmrAB two-component system (TCS), modification of the lipid A domain of lipopolysaccharide and subsequent colistin resistance. This kinase-activation was extended to other TCS by generation of chimeric sensor kinases. Our results demonstrate that peptides with novel activities mediated via specific peptide-protein interactions in the transmembrane domain of a sensory transducer can be selected de novo, suggesting that the origination of such peptides from non-coding regions is conceivable. In addition, we identified a novel class of resistance determinants for a key antibiotic that is used as a last resort treatment for several significant pathogens. The high-level resistance provided at low expression levels, absence of significant growth defects and the functionality of Dcr peptides across different genera suggest that this class of peptides could potentially evolve as bona fide resistance determinants in natura.

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Mozaffari, Saghar, Emira Bousoik, Farideh Amirrad, Robert Lamboy, Melissa Coyle, Ryley Hall, Abdulaziz Alasmari, Parvin Mahdipoor, Keykavous Parang, and Hamidreza Montazeri Aliabadi. "Amphiphilic Peptides for Efficient siRNA Delivery." Polymers 11, no. 4 (April 17, 2019): 703. http://dx.doi.org/10.3390/polym11040703.

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A number of amphiphilic cyclic peptides—[FR]4, [WR]5, and [WK]5—containing hydrophobic and positively-charged amino acids were synthesized by Fmoc/tBu solid-phase peptide methods and evaluated for their efficiency in intracellular delivery of siRNA to triple-negative breast cancer cell lines, MDA-MB-231 and MDA-MB-468, in the presence and absence of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE). Among the peptides, [WR]5, which contains alternate tryptophan (W) and arginine (R) residues, was found to be the most efficient in the delivery of siRNA by improving the delivery by more than 3-fold when compared to other synthesized cyclic peptides that were not efficient. The data also showed that co-formulation of [WR]5 with lipid DOPE significantly enhanced the efficiency of siRNA delivery by up to ~2-fold compared to peptide alone. Based on the data indicating the efficiency of [WR]5 in siRNA delivery, peptides containing arginine residues on the ring and tryptophan residues on the side chain, [R6K]W6 and [R5K]W5, were also evaluated, and demonstrated improved delivery of siRNA. The presence of DOPE again enhanced the siRNA delivery in most cases. [WR]5, [R5K]W5, and [R6K]W6 did not show any significant toxicity in MDA-MB-231, MDA-MB-468, and AU565 WT cells at N/P ratios of 20:1 or less, in the presence and absence of DOPE. Silencing of kinesin spindle protein (KSP) and Janus kinase 2 (JAK2) was evaluated in MDA-MB-231 cells in the presence of the peptides. The addition of DOPE significantly enhanced the silencing efficiency for all selected peptides. In conclusion, peptides containing tryptophan and arginine residues were found to enhance siRNA delivery and to generate silencing of targeted proteins in the presence of DOPE.

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Wei, Ying, Xiuwei Yang, Qiumei Liu, John A. Wilkins, and Harold A. Chapman. "A Role for Caveolin and the Urokinase Receptor in Integrin-mediated Adhesion and Signaling." Journal of Cell Biology 144, no. 6 (March 22, 1999): 1285–94. http://dx.doi.org/10.1083/jcb.144.6.1285.

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The assembly of signaling molecules surrounding the integrin family of adhesion receptors remains poorly understood. Recently, the membrane protein caveolin was found in complexes with β1 integrins. Caveolin binds cholesterol and several signaling molecules potentially linked to integrin function, e.g., Src family kinases, although caveolin has not been directly implicated in integrin-dependent adhesion. Here we report that depletion of caveolin by antisense methodology in kidney 293 cells disrupts the association of Src kinases with β1 integrins resulting in loss of focal adhesion sites, ligand-induced focal adhesion kinase (FAK) phosphorylation, and adhesion. The nonintegrin urokinase receptor (uPAR) associates with and stabilizes β1 integrin/caveolin complexes. Depletion of caveolin in uPAR-expressing 293 cells also disrupts uPAR/integrin complexes and uPAR-dependent adhesion. Further, β1 integrin/caveolin complexes could be disassociated by uPAR-binding peptides in both uPAR-transfected 293 cells and human vascular smooth muscle cells. Disruption of complexes by peptides in intact smooth muscle cells blocks the association of Src family kinases with β1 integrins and markedly impairs their migration on fibronectin. We conclude that ligand-induced signaling necessary for normal β1 integrin function requires caveolin and is regulated by uPAR. Caveolin and uPAR may operate within adhesion sites to organize kinase-rich lipid domains in proximity to integrins, promoting efficient signal transduction.

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Dissertations / Theses on the topic "Peptides; Protein kinase; Lipids"

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Ahmed, Zareen. "Magnetic resonance spectroscopy of phospholamban and its interaction with Ca'2'+-ATPase." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343301.

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Zhao, Yue. "Synthetic probes for bacterial lipids and dimerizing proteins." Thesis, Boston College, 2015. http://hdl.handle.net/2345/bc-ir:104623.

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Thesis advisor: Eranthie Weerapana
This thesis includes two projects: “Bacteria-selective borono-peptides” and “A split ligand for lanthanide binding: facile evaluation of dimerizing proteins”. In both projects, de novo designed molecules were synthesized, optimized and incorporated into peptides. These synthetic molecular tools allow selective targeting of bacterial cell membranes and analyzing the dynamic associations of membrane-embedded proteins. 1. Bacteria-selective borono-peptides As the antibiotic resistance continues to grow, bacterial infection becomes one of the major threats to global public health. Currently, almost all the bacteria targeting strategies employ non-covalent driving forces, including charge-charge interactions, hydrophobic interactions and the formation of hydrogen bonds, to achieve bacterial selectivity. Towards novel bacteria targeting molecules, we have recruited reversible covalent chemistry in the development of bacteria-selective peptides. Targeting the diol-rich environment of a bacterial surface, we have designed and synthesized several unnatural amino acids that contain boronic acid moieties. Taking advantage of the boronic acid-diol reaction and multivalency effect, our borono-peptides are found to selectively recognize bacteria over mammalian cells. The sensitivity of the binding event to carbohydrate competitors gives a safe and facile approach to regulate molecular association with bacterial cells. This design may find applications in the fields of bacterial detection, imaging and antimicrobial drug delivery. 2. A split ligand for lanthanide binding: facile evaluation of dimerizing proteins Protein dimerization is a ubiquitous phenomenon in biology and plays a critical role in transcription regulations and various signaling processes. Methods that allow facile detection and quantification of protein dimers are highly desirable for evaluating protein dimerization in physiology and disease. Meanwhile, luminescence of lanthanides is attractive for biological applications due to its long lifetime and sharp emission profiles. We have developed a split lanthanide binding ligand that allows facile evaluation of dimerizing proteins. The fast lanthanide–ligand (dis)association allows us to monitor the dynamic behavior of dimerizing proteins. We have demonstrated the successful application of our assay on both soluble and transmembrane proteins in complex biological milieu. The split lanthanide ligand is cysteine reactive, and therefore should be readily applicable to a variety of proteins of interest
Thesis (PhD) — Boston College, 2015
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Chemistry

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Zheng, Hong. "Designing Peptides to Target Membrane Lipids and to Evaluate Fluorination of Proteins." Thesis, Boston College, 2012. http://hdl.handle.net/2345/3682.

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Thesis advisor: Jianmin Gao
My graduate research has used engineered peptides to perturb the non-covalent interactions in protein folding, protein-protein association and protein-membrane association. We have focused on understanding the fundamental principles of molecular recognition behind protein-protein and protein-membrane interactions, and further using these principles in protein engineering. This thesis includes three projects. I) Towards Small Molecule Receptors for Membrane Lipids: A Case Study on Phosphatidylserine The lipid composition and distribution of cell membranes play important roles in regulating the physiology of the cell. The lipid composition of plasma membranes is one characteristic feature that can be used to identify cell types and functions. Molecules that specifically recognize a particular lipid are useful as imaging probes for targeting cells or tissues of interest. Protein based lipid binding probes have intrinsic limitations due to their large size and poor pharmacokinetic properties such as slow clearance rate and poor in vivo stability. A plausible strategy to achieve a probe with small size and high binding affinity and selectivity is to use a peptide to mimic the protein lipid-binding domains. As a case study, a cyclic peptide that specifically targets phosphatidylserine containing membranes has been developed. This cyclic peptide is potentially capable of imaging apoptosis in vivo, and the strategy of developing this cyclic peptide can be generalized to the design of peptide-based probes for other lipid species. My research has pointed out a challenging but feasible way to design a peptide that achieves specificity and affinity similar to lipid-binding proteins. (II) Study of Apoptotic Cell Membrane (ACM) Permeant Molecules Noninvasive imaging of apoptosis is highly desirable for the diagnosis of a variety of diseases, as well as for the early prognosis of anticancer treatments. One characteristic feature of apoptotic cells that has been targeted for developing specific biomarkers is enhanced membrane permeability compared to that of healthy cells. Several unrelated molecules that are capable of selectively penetrating the apoptotic cell membrane (ACM) have recently been reported. However, the origin of the altered ACM permeability is poorly understood, as is the scope of molecular structures that can permeate through the ACM. Herein, we report a systematic investigation on the altered ACM permeability. Our results show that simple modifications of commonly used dyes (e.g. fluorescein) afford specific entry into cells at the early stages of apoptosis. The ACM appears to be permeable to molecules of various functional groups and charge, but does discriminate against molecules of large size. The new findings reported here greatly expand the pool of small molecules for imaging cell death, thus facilitating the development of noninvasive imaging agents for apoptosis. (III) Study of Aromatic-Fluorinated Aromatic Interactions in Peptide Systems Therapeutic proteins have been through a remarkable expansion in the last two decades. A general problem that they are facing is poor stability. Protein engineering focuses on solving this problem by incorporating unnatural amino acids into protein sequences to purposefully modify protein structures. Fluorinated aliphatic amino acids have been demonstrated to be effective in stabilizing protein structures and functioning as recognition motifs. In contrast, fluorinated aromatic amino acids are less studied. We investigated the effect of perturbation of fluorination on aromatic residues on the stability of protein model systems, as well as the influence on protein-protein association behavior. The results of this study provided a fundamental understanding of aromatic interactions in protein systems, and guidelines for protein engineering with fluorinated aromatics for stabilizing protein structures or directing specific protein-protein interactions
Thesis (PhD) — Boston College, 2012
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Chemistry

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Maitra, Sushmit. "The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase 2." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008r/maitra.pdf.

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Oldham, Alexis Jean. "Modulation of lipid domain formation in mixed model systems by proteins and peptides." View electronic thesis, 2008. http://dl.uncw.edu/etd/2008-1/r1/oldhama/alexisoldham.pdf.

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Danai, Laura V. "Role of Protein Kinase Map4k4 in Energy Metabolism: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/791.

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Systemic glucose regulation is essential for human survival as low or chronically high glucose levels can be detrimental to the health of an individual. Glucose levels are highly regulated via inter-organ communication networks that alter metabolic function to maintain euglycemia. For example, when nutrient levels are low, pancreatic α-cells secrete glucagon, which signals to the liver to promote glycogen breakdown and glucose production. In times of excess nutrient intake, pancreatic β-cells release insulin. Insulin signals to the liver to suppress hepatic glucose production, and signals to the adipose tissue and the skeletal muscle to take up excess glucose via insulin-regulated glucose transporters. Defects in this inter-organ communication network including insulin resistance can result in glucose deregulation and ultimately the onset of type-2 diabetes (T2D). To identify novel regulators of insulin-mediated glucose transport, our laboratory performed an siRNA-mediated gene-silencing screen in cultured adipocytes and measured insulin-mediated glucose transport. Gene silencing of Mitogen-activated protein kinase kinase kinase kinase 4 (Map4k4), a Sterile-20-related serine/threonine protein kinase, enhanced insulin-stimulated glucose transport, suggesting Map4k4 inhibits insulin action and glucose transport. Thus, for the first part of my thesis, I explore the role of Map4k4 in cultured adipose cells and show that Map4k4 also represses lipid synthesis independent of its effects on glucose transport. Map4k4 inhibits lipid synthesis in a Mechanistic target of rapamycin complex 1 (mTORC1)- and Sterol regulatory element-binding transcription factor 1 (Srebp-1)-dependent mechanism and not via a c-Jun NH2-terminal kinase (Jnk)-dependent mechanism. For the second part of my thesis, I explore the metabolic function of Map4k4 in vivo. Using mice with loxP sites flanking the Map4k4 allele and a ubiquitously expressed tamoxifen-activated Cre, we inducibly ablated Map4k4 expression in adult mice and found significant improvements in metabolic health indicated by improved fasting glucose and whole-body insulin action. To assess the role of Map4k4 in specific metabolic tissues responsible for systemic glucose regulation, we employed tissue-specific knockout mice to deplete Map4k4 in adipose tissue using an adiponectin-cre transgene, liver using an albumin-cre transgene, and skeletal muscle using a Myf5-cre transgene. Ablation of Map4k4 expression in adipose tissue or liver had no impact on whole body glucose homeostasis or insulin resistance. However, we surprisingly found that Map4k4 depletion in Myf5-positive tissues, which include skeletal muscles, largely recapitulates the metabolic phenotypes observed in systemic Map4k4 knockout mice, restoring obesity-induced glucose intolerance and insulin resistance. Furthermore these metabolic changes were associated with enhanced insulin signaling to Akt in the visceral adipose tissue, a tissue that is nearly devoid of Myf5-positive cells and does not display changes in Map4k4 expression. Thus, these results indicate that Map4k4 in Myf5-positive cells, most likely skeletal muscle cells, inhibits whole-body insulin action and these effects may be mediated via an indirect effect on the visceral adipose tissue. The results presented here provide evidence for Map4k4 as a potential therapeutic target for the treatment of insulin resistance and T2D.

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Danai, Laura V. "Role of Protein Kinase Map4k4 in Energy Metabolism: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/791.

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Systemic glucose regulation is essential for human survival as low or chronically high glucose levels can be detrimental to the health of an individual. Glucose levels are highly regulated via inter-organ communication networks that alter metabolic function to maintain euglycemia. For example, when nutrient levels are low, pancreatic α-cells secrete glucagon, which signals to the liver to promote glycogen breakdown and glucose production. In times of excess nutrient intake, pancreatic β-cells release insulin. Insulin signals to the liver to suppress hepatic glucose production, and signals to the adipose tissue and the skeletal muscle to take up excess glucose via insulin-regulated glucose transporters. Defects in this inter-organ communication network including insulin resistance can result in glucose deregulation and ultimately the onset of type-2 diabetes (T2D). To identify novel regulators of insulin-mediated glucose transport, our laboratory performed an siRNA-mediated gene-silencing screen in cultured adipocytes and measured insulin-mediated glucose transport. Gene silencing of Mitogen-activated protein kinase kinase kinase kinase 4 (Map4k4), a Sterile-20-related serine/threonine protein kinase, enhanced insulin-stimulated glucose transport, suggesting Map4k4 inhibits insulin action and glucose transport. Thus, for the first part of my thesis, I explore the role of Map4k4 in cultured adipose cells and show that Map4k4 also represses lipid synthesis independent of its effects on glucose transport. Map4k4 inhibits lipid synthesis in a Mechanistic target of rapamycin complex 1 (mTORC1)- and Sterol regulatory element-binding transcription factor 1 (Srebp-1)-dependent mechanism and not via a c-Jun NH2-terminal kinase (Jnk)-dependent mechanism. For the second part of my thesis, I explore the metabolic function of Map4k4 in vivo. Using mice with loxP sites flanking the Map4k4 allele and a ubiquitously expressed tamoxifen-activated Cre, we inducibly ablated Map4k4 expression in adult mice and found significant improvements in metabolic health indicated by improved fasting glucose and whole-body insulin action. To assess the role of Map4k4 in specific metabolic tissues responsible for systemic glucose regulation, we employed tissue-specific knockout mice to deplete Map4k4 in adipose tissue using an adiponectin-cre transgene, liver using an albumin-cre transgene, and skeletal muscle using a Myf5-cre transgene. Ablation of Map4k4 expression in adipose tissue or liver had no impact on whole body glucose homeostasis or insulin resistance. However, we surprisingly found that Map4k4 depletion in Myf5-positive tissues, which include skeletal muscles, largely recapitulates the metabolic phenotypes observed in systemic Map4k4 knockout mice, restoring obesity-induced glucose intolerance and insulin resistance. Furthermore these metabolic changes were associated with enhanced insulin signaling to Akt in the visceral adipose tissue, a tissue that is nearly devoid of Myf5-positive cells and does not display changes in Map4k4 expression. Thus, these results indicate that Map4k4 in Myf5-positive cells, most likely skeletal muscle cells, inhibits whole-body insulin action and these effects may be mediated via an indirect effect on the visceral adipose tissue. The results presented here provide evidence for Map4k4 as a potential therapeutic target for the treatment of insulin resistance and T2D.

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Yamahara, Kenichi. "Significance and therapeutic potential of the natriuretic peptides/cGMP/cGMP-depnendent protein kinase pathway in vascular regeneration." Kyoto University, 2004. http://hdl.handle.net/2433/147491.

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Polozov, Ivan V. "Interactions of class A and class L amphipathic helical peptides with model membranes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0006/NQ30110.pdf.

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Yang, Chunhua. "Synthesis and Kinetic Mechanism Study of Phosphonopeptide as a Dead-End Inhibitor of cAMP-Dependent Protein Kinase." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc500671/.

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DL-2-Amino-4-phosphonobutyric acid, an isostere of phosphoserine, was incorporated into the heptapeptide sequence, Leu-Arg-Arg-Ala-(DL-2-amino-4-phosphonobutyric acid)-Leu-Gly, for kinetic mechanistic studies of the cAMP-dependent protein kinase. To block the phosphono hydroxyl groups, methyl, ethyl and 4nitrobenzyl esters were studied as possible protecting groups. The phosphono diethyl ester of the N-Fmoc-protected amino acid was utilized in the synthesis of the heptapeptide. Two configurational forms of the protected peptide were obtained and were separated by C18-reverse phase HPLC. Characterization of the two isomeric forms was accomplished by 3 1P NMR, 1H NMR, 13C% NMR and amino acid analysis. The protecting groups of the isomeric phsophonopeptides were removed by HBr/AcOH and purified by cation exchange HPLC. Both phosphonopeptides were found to be inhibitors of the cAMP-dependent protein kinase, having Ki values of 0.6 mM (peptide A) and 1.9 mM (peptide B).

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Books on the topic "Peptides; Protein kinase; Lipids"

1

Miguel A. R. B. Castanho. Membrane-active peptides: Methods and results on structure and function. La Jolla, Calif: International University Line, 2009.

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Membrane-active peptides: Methods and results on structure and function. La Jolla, Calif: International University Line, 2009.

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Proteins: Membrane binding and pore formation. New York: Springer Science+Business Media, 2010.

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M, Bergfors Terese, ed. Protein crystallization. La Jolla, Calif: International University Line, 2008.

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N, Fain John, ed. Lipid metabolism in signalling systems. San Diego: Academic Press, Inc., 1993.

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Methods in Neurosciences: Lipid Metabolism in Signaling Systems (Methods in Neurosciences). Academic Press, 1993.

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N, Fain John, ed. Lipid metabolism in signaling systems. San Diego: Academic Press, 1993.

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Book chapters on the topic "Peptides; Protein kinase; Lipids"

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Flinn, N., M. R. Munday, C. Van der Walle, C. Toomey, and I. Toth. "Investigation of protein kinase substrate recognition." In Peptides, 938–39. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_315.

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Williams, R. E., B. R. Chakravarthy, M. Sikorska, J. F. Whitfield, and J. P. Durkin. "A protein kinase C substrate peptide derived from MARCKS protein." In Peptides, 923–24. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_374.

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Eller, Marika, Jaak Järv, Ulf Ragnarsson, Reet Toomik, Pia Ekman, and Lorentz Engström. "Substrate specificity studies on protein kinase C." In Peptides 1992, 794–95. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_365.

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de Bont, H. B. A., J. H. van Boom, and R. M. J. Liskamp. "Synthesis of lipopeptides: Preparation of inhibitors of protein kinase C." In Peptides, 185–87. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_65.

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Yarger, Ronald G., Rolf H. Berg, Susan A. Rotenberg, and James P. Tam. "Substrates of tyrosine-specific protein kinase: Synthetic peptides derived from lipocortins." In Peptides, 587–89. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-010-9595-2_176.

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Gordon, H., W. Neugebauer, R. Rixon, R. Somorjai, W. Sung, H. Jouishomme, W. Surewicz, J. Whitfield, and G. Willick. "Parathyroid hormone domain for protein kinase C stimulation located within amphiphilic helix." In Peptides, 37–39. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_8.

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Hannun, Y. A. "Regulation of Protein Kinase C." In Eicosanoids and Other Bioactive Lipids in Cancer and Radiation Injury, 275–83. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3874-5_42.

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Williams, R. E., B. R. Chakravarthy, and J. P. Durkin. "Minimum structural requirements of myristoylated protein kinase C (PKC) inhibitory peptides: Minimizing the structure of a MARCKS protein derived peptide." In Peptides 1994, 662–63. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_303.

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Neugebauer, Witold, and Gordon Willick. "Lactam analogues of a human parathyroid hormone (hPTH) domain for protein kinase C (PKC) stimulation." In Peptides 1992, 395–96. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_172.

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Borek, C., and A. H. Merrill. "Sphingolipids Inhibit Protein Kinase C and Multistep Transformation." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 431–34. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_85.

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Conference papers on the topic "Peptides; Protein kinase; Lipids"

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Tuháčková, Zdena, Eva Šloncová, Jan Hlaváček, Vlasta Sovová, and Jiří Velek. "Activation of the protein kinase B and glycogen synthase kinase-3 signalling pathway during transient differentiation of human colon cancer HT-29 cells." In VIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199903019.

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Caffrey, Martin. "Lipid Phase Behavior: Databases, Rational Design and Membrane Protein Crystallization." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192724.

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The relationship that exists between structure and function is a unifying theme in my varied biomembrane-based research activities. It applies equally well to the lipid as to the protein component of membranes. With a view to exploiting information that has been and that is currently being generated in my laboratory, as well as that which exists in the literature, a number of web-accessible, relational databases have been established over the years. These include databases dealing with lipids, detergents and membrane proteins. Those catering to lipids include i) LIPIDAT, a database of thermodynamic information on lipid phases and phase transitions, ii) LIPIDAG, a database of phase diagrams concerning lipid miscibility, and iii) LMSD, a lipid molecular structures database. CMCD is the detergent-based database. It houses critical micelle concentration information on a wide assortment of surfactants under different conditions. The membrane protein data bank (MPDB) was established to provide convenient access to the 3-D structure and related properties of membrane proteins and peptides. The utility and current status of these assorted databases will be described and recommendations will be made for extending their range and usefulness.

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Mohbeddin, Abeer, Nawar Haj Ahmed, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Innate Immunity on Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0224.

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Apart from its traditional role in disease control, recent body of evidence has implicated a role of the immune system in regulating metabolic homeostasis. Owing to the importance of this “immune-metabolic alignment” in dictating a state of health or disease, a proper mechanistic understanding of this alignment is crucial in opening up for promising therapeutic approaches against a broad range of chronic, metabolic, and inflammatory disorders like obesity, diabetes, and inflammatory bowel syndrome. In this project, we addressed the role of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) innate immune pathway in regulating different metabolic parameters using the Drosophila melanogaster (DM) fruit fly model organism. Mutant JAK/STAT pathway flies with a systemic knockdown of either Domeless (Dome) [domeG0282], the receptor that activates JAK/STAT signaling, or the signal-transducer and activator of transcription protein at 92E (Stat92E) [stat92EEY10528], were used. The results of the study revealed that blocking JAK/STAT signaling alters the metabolic profile of mutant flies. Both domeG0282 and stat92EEY10528 mutants had an increase in body weight, lipid deprivation from their fat body (lipid storage organ in flies), irregular accumulation of lipid droplets in the gut, systemic elevation of glucose and triglyceride levels, and differential down-regulation in the relative gene expression of different peptide hormones (Tachykinin, Allatostatin C, and Diuretic hormone 31) known to regulate metabolic homeostasis in flies. Because the JAK/STAT pathway is evolutionary conserved between invertebrates and vertebrates, our potential findings in the fruit fly serves as a platform for further immune-metabolic translational studies in more complex mammalian systems including humans.

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Katayama, Yoshiki, Hirotaro Kitazaki, Jeong-Hun Kang, Xiaoming Han, Takeshi Mori, and Takuro Niidome. "High-throughput Detection of Protein Kinase Activities in Cell Lysate Based on the Aggregation of Gold Nanoparticles with Peptides." In 2009 MRS Spring Meet. Materials Research Society, 2009. http://dx.doi.org/10.1557/proc-1241-xx08-08.

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Timmons, Sheila, and Jack Hawiger. "REGULATION OF PLATELET RECEPTORS FOR FIBRINOGEN AND VON WILLEBRAND FACTOR BY PROTEIN KINASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644674.

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Positive and negative regulation of platelet receptors for adhesive proteins, fibrinogen (F) and von Willebrand Factor (vWF) determines whether binding of these ligands will or will not take place. We have shown previously that ADP stimulates and cyclic AMP inhibits binding of F and vWF to human platelets. Now we show that positive regulation of F and vWF binding to platelets via the glycoprotein 11b/1111a complex is dependent on platelet Protein Kinase C, a calcium- and phospholipid-dependent enzyme. A potent activator of Protein Kinase C, phorbol-12-myristoyl-13-acetate (PMA) induced saturable and specific binding of F and vWF which was inhibited by synthetic peptides, gamma chain .dodecapeptide (gamma 400-411) and RGDS. The phosphorylation of 47kDa protein (P47), a marker of Protein Kinase C activation in platelets, preceded binding of F and vWF induced with PMA as well as with ADP and thrombin. Sphingosine, an inhibitor of Protein Kinase C, blocked binding of F and vWF to platelets stimulated with PMA, ADP, and thrombin. Inhibition of binding was concentration-dependent and it was accompanied by inhibition of platelet aggregation. Thus, stimulation of Protein Kinase C is required for exposure of platelet receptors for adhesive proteins whereas inhibition of Protein Kinase C prevents receptorexposure. Protein Kinase C fulfills the role of an intraplatelet signal transducer, regulating receptors for adhesive proteins, and constitutes a target for pharmacologic modulation of the adhesive interactions of platelets.

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Koutouzov, S., A. Remmal, P. Marche, and P. Meyer. "IMPAIRMENT OF PLATELET PHOSPHOINOSITIDE METABOLISM IN PRIMARY HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643812.

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Blood platelets from hypertensive patients and spontaneously hypertensive rats (SHR) display multiple abnormalities when compared with cells from normotensive controls. The major features of the modified platelet profile are an enhanced rate of adhesion/aggregation in response to many stimuli, a greater sensitivity for thrombin and adrenaline to produce increases in cytoplasmic free Ca2+, and an exaggerated release reaction. Furthermore, the resting levels of cytosolic free Ca2+ ions are specifically and constantly increased. Since phosphoinositides are involved in the stimulus-response coupling mediated by intracellular Ca2+ mobilization, the metabolism of these lipids was investigated in platelets of SHR and compared with those of normotensive Wistar-Kyoto rats (WKY). Following 32P-labelling of quiescent platelets, labeled lipids were analyzed both in platelets at rest and after thrombin stimulation. In resting platelets, the 32P associated with each of the phosphoinositides and phosphatidic acid (PA) was similar in SHR and WKY indicating that both the pool size of the various lipids and their basal turnover did not differ between the two strains. By contrast, within the first seconds after thrombin stimulation (10-60 sec), the dose-response and time-course curves of agonist-induced increase in 32P-PA were markedly shifted to the left and reached higher equilibrium levels in SHR. Since thrombin-induced 32P-PA formation is held as the most sensitive index of phospholipase C activity, our results indicate that this enzyme displays hyperreactivity in SHR (vs WKY). It is therefore likely that in SHR, the enhanced physiological responses (serotonin secretion, aggregation) that we observed under the same experimental conditions may be related to an increased formation of Phospholipase C products (inosi-toltriphosphate and diacylglycerol) which are the two second messengers responsible for internal Ca2+ mobilization and activation of protein kinase C, respectively. Therefore, these data suggest that the hypersensitivity of Phospholipase C may be involved in the overall alteration of cell calcium handling and hence in the SHR platelet responses.

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