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Academic literature on the topic 'Peptide effects'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Peptide effects"

1

NEVALAINEN, Leena T., Takashi AOYAMA, Mitsuhiko IKURA, Anna CRIVICI, Hong YAN, Nam-Hai CHUA, and Angus C. NAIRN. "Characterization of novel calmodulin-binding peptides with distinct inhibitory effects on calmodulin-dependent enzymes." Biochemical Journal 321, no. 1 (January 1, 1997): 107–15. http://dx.doi.org/10.1042/bj3210107.

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We describe the isolation and interaction with calmodulin (CaM) of two 10-amino-acid peptides (termed peptides 1 and 2; AWDTVRISFG and AWPSLQAIRG respectively) derived from a phage random peptide display library. Both peptides are shorter than previously described CaM-binding peptides and lack certain features found in the sequences of CaM-binding domains present in CaM-activated enzymes. However, 1H NMR spectroscopy and fluorimetry indicate that both peptides interact with CaM in the presence of Ca2+. The two peptides differentially inhibited CaM-dependent kinases I and II (CaM kinases I and II) but did not affect CaM-dependent phosphodiesterase. Peptide 1 inhibited CaM kinase I but not CaM kinase II, whereas peptide 2 inhibited CaM kinase II, but only partially inhibited CaM kinase I at a more than 10-fold higher concentration. Peptide 1 also inhibited a plant calcium-dependent protein kinase, whereas peptide 2 did not. The ability of peptides 1 and 2 to differentially inhibit CaM-dependent kinases and CaM-dependent phosphodiesterase suggests that they may bind to distinct regions of CaM that are specifically responsible for activation of different CaM-dependent enzymes.

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Srivastava, Mrinal Ranjan, Farzana Mahdi, Abbas Ali Mahdi, Sharique Ahmad, and Anu Chandra. "BIOLOGICAL EFFECTS OF C-PEPTIDE AND PROINSULIN: WE JIBE TOGETHER." Era's Journal of Medical Research 6, no. 1 (June 2019): 103–9. http://dx.doi.org/10.24041/ejmr2019.115.

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Lorenzón, E. N., G. F. Cespedes, E. F. Vicente, L. G. Nogueira, T. M. Bauab, M. S. Castro, and E. M. Cilli. "Effects of Dimerization on the Structure and Biological Activity of Antimicrobial Peptide Ctx-Ha." Antimicrobial Agents and Chemotherapy 56, no. 6 (March 5, 2012): 3004–10. http://dx.doi.org/10.1128/aac.06262-11.

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ABSTRACTIt is well known that cationic antimicrobial peptides (cAMPs) are potential microbicidal agents for the increasing problem of antimicrobial resistance. However, the physicochemical properties of each peptide need to be optimized for clinical use. To evaluate the effects of dimerization on the structure and biological activity of the antimicrobial peptide Ctx-Ha, we have synthesized the monomeric and three dimeric (Lys-branched) forms of the Ctx-Ha peptide by solid-phase peptide synthesis using a combination of 9-fluorenylmethyloxycarbonyl (Fmoc) andt-butoxycarbonyl (Boc) chemical approaches. The antimicrobial activity assay showed that dimerization decreases the ability of the peptide to inhibit growth of bacteria or fungi; however, the dimeric analogs displayed a higher level of bactericidal activity. In addition, a dramatic increase (50 times) in hemolytic activity was achieved with these analogs. Permeabilization studies showed that the rate of carboxyfluorescein release was higher for the dimeric peptides than for the monomeric peptide, especially in vesicles that contained sphingomyelin. Despite different biological activities, the secondary structure and pore diameter were not significantly altered by dimerization. In contrast to the case for other dimeric cAMPs, we have shown that dimerization selectively decreases the antimicrobial activity of this peptide and increases the hemolytic activity. The results also show that the interaction between dimeric peptides and the cell wall could be responsible for the decrease of the antimicrobial activity of these peptides.

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Wigle, D. A., B. M. Bennett, D. B. Jennings, I. R. Sarda, T. G. Flynn, and S. C. Pang. "Biological effects of rat iso-atrial natriuretic peptide and brain natriuretic peptide are indistinguishable from each other." Canadian Journal of Physiology and Pharmacology 70, no. 11 (November 1, 1992): 1525–28. http://dx.doi.org/10.1139/y92-218.

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Rat brain natriuretic peptide (rBNP) and iso-atrial natriuretic peptide (iso-rANP) were discovered independently by two research laboratories. They are considered to be members of the B-type natriuretic peptides. Except for the Gln/Leu substitution at position 44, the amino acid sequence of iso-rANP is identical with that of the C-terminal 45 amino acids of rat pro-BNP and with the 5-kDa cardiac peptide from rat atria. To determine whether this amino acid substitution can modify the known biological effects of rBNP and iso-rANP, the present investigation examined the cardiovascular and renal responses, vasorelaxant effect, receptor binding characteristics, and cyclic GMP production by the two peptides in relation to that of rat atrial natriuretic peptide (rANP). Results indicate that rBNP and iso-rANP are indistinguishable from each other in terms of these known biological activities of atrial natriuretic peptide. We therefore conclude that rBNP and iso-rANP are identical peptides and that the amino acid substitution at position 44 represents a polymorphic form of the rat B-type natriuretic peptide.Key words: atrial natriuretic peptide, brain natriuretic peptide, cardiovascular response, vasorelaxation, cyclic GMP, receptor binding.

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Ano, Yasuhisa, Yuka Yoshino, Kazuyuki Uchida, and Hiroyuki Nakayama. "Preventive Effects of Tryptophan–Methionine Dipeptide on Neural Inflammation and Alzheimer’s Pathology." International Journal of Molecular Sciences 20, no. 13 (June 29, 2019): 3206. http://dx.doi.org/10.3390/ijms20133206.

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Preventive approaches for age-related memory decline and dementia have become a high priority in the aging society because of the lack of therapeutic approaches. Recent epidemiological studies have reported that fermented dairy products can help prevent dementia. Previously, we identified tryptophan–tyrosine (WY) and tryptophan–methionine (WM) peptides as the suppressants of activation of the primary microglia and showed that WY peptide consumption suppresses inflammation in the brains of Alzheimer’s disease model mice. However, the effects of the WM peptide on inflammation in the brain and Alzheimer’s pathology have not been investigated. Here, we evaluated the effect of WM peptide consumption on Alzheimer’s disease model (5×FAD) mice. In 5×FAD mice, intake of WM peptide suppressed the production of inflammatory cytokines, activation of microglia, and infiltration of activated microglia around β amyloid (Aβ) depositions. WM peptide intake reduced Aβ deposition in the cortex and hippocampus and then improved the object recognition memory. Taken together with previous reports, the current findings indicate that ingestion of tryptophan-related peptides or food material rich in tryptophan-related peptides, thereby regulating microglial activity, represents a potential preventive approach for cognitive decline and dementia related to inflammation.

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Nongonierma, Alice B., and Richard J. FitzGerald. "Utilisation of the isobole methodology to study dietary peptide–drug and peptide–peptide interactive effects on dipeptidyl peptidase IV (DPP-IV) inhibition." Food & Function 6, no. 1 (2015): 312–19. http://dx.doi.org/10.1039/c4fo00883a.

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Chauhan, Sweeny, Sean O’Callaghan, Audrey Wall, Tomasz Pawlak, Ben Doyle, Alessandro Adelfio, Sanja Trajkovic, Mark Gaffney, and Nora Khaldi. "Using Peptidomics and Machine Learning to Assess Effects of Drying Processes on the Peptide Profile within a Functional Ingredient." Processes 9, no. 3 (February 26, 2021): 425. http://dx.doi.org/10.3390/pr9030425.

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Bioactive peptides are known to have many health benefits beyond nutrition; yet the peptide profile of high protein ingredients has been largely overlooked when considering the effects of different processing techniques. Therefore, to investigate whether drying conditions could affect the peptide profile and bioactivity within a functional ingredient, we examined the effects of spray (SD) and freeze (FD) drying on rice natural peptide network (NPN), a characterised functional ingredient sourced from the Oryza sativa proteome, which has previously been shown to effectively modulate circulating cytokines and improve physical performance in humans. In the manufacturing process, rice NPN was either FD or SD. Employing a peptidomic approach, we investigated the physicochemical characteristics of peptides common and unique to FD and SD preparations. We observed similar peptide profiles regarding peptide count, amino acid distribution, weight, charge, and hydrophobicity in each sample. Additionally, to evaluate the effects of drying processes on functionality, using machine learning, we examined constituent peptides with predicted anti-inflammatory activity within both groups and identified that the majority of anti-inflammatory peptides were common to both. Of note, key bioactive peptides validated within rice NPN were recorded in both SD and FD samples. The present study provides an important insight into the overall stability of the peptide profile and the use of machine learning in assessing predicted retention of bioactive peptides contributing to functionality during different types of processing.

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Hayes, Maria. "Bioactive Peptides in Preventative Healthcare: An Overview of Bioactivities and Suggested Methods to Assess Potential Applications." Current Pharmaceutical Design 27, no. 11 (April 27, 2021): 1332–41. http://dx.doi.org/10.2174/1381612827666210125155048.

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Food derived bioactive peptides can be generated from various protein sources and usually consist of between 2-30 amino acids with bulky, side-chain aromatic amino acids preferred in the ultimate and penultimate positions at the C-terminal end of the amino acid chain. They are reported to impart a myriad of preventative health beneficial effects to the consumer once ingested and these include heart health benefits through inhibition of enzymes including renin (EC 3.4.23.15) and angiotensin- I-converting enzyme (ACE-1; EC 3.4.15.1) within the renin angiotensin aldosterone system (RAAS) anti-inflammatory (due to inhibition of ACE-I and other enzymes) and anti-cancer benefits, prevention of type-2 diabetes through inhibition of dipeptidyl peptidase IV (DPP-IV), bone and dental strength, antimicrobial and immunomodulatory effects and several others. Peptides have also reported health benefits in the treatment of asthma, neuropathic pain, HIV and wound healing. However, the structure, amino acid composition and length of these peptides, along with the quantity of peptide that can pass through the gastrointestinal tract and often the blood-brain barrier (BBB), intact and reach the target organ, are important for the realisation of these health effects in an in vivo setting. This paper aims to collate recent important research concerning the generation and detection of peptides in the laboratory. It discusses products currently available as preventative healthcare peptide options and relevant legislation barriers to place a food peptide product on the market. The review also highlights useful in silico computer- based methods and analysis that may be used to generate specific peptide sequences from proteins whose amino acid sequences are known and also to determine if the peptides generated are unique and bioactive. The topic of food-derived bioactive peptides for health is of great interest to scientific research and industry due to evolving drivers in food product innovation, including health and wellness for the elderly, infant nutrition and optimum nutrition for sports athletes and the humanisation of pets. This paper provides an overview of what is required to generate bioactive peptide containing hydrolysates, what methods should be used in order to characterise the beneficial health effects of these hydrolysates and the active peptide sequences, potential applications of bioactive peptides and legislative requirements in Europe and the United States. It also highlights success stories and barriers to the development of peptide-containing food products that currently exist.

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Burkitt, William I., Anastassios E. Giannakopulos, Foteini Sideridou, Sajid Bashir, and Peter J. Derrick. "Discrimination Effects in MALDI-MS of Mixtures of Peptides—Analysis of the Proteome." Australian Journal of Chemistry 56, no. 5 (2003): 369. http://dx.doi.org/10.1071/ch02155.

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Peptide ion suppression in matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) can hinder the detection of site-specific post-translational protein modifications. Within a peptide mixture, the presence or absence of a particular peptide can affect the ion intensities of other peptides in the mixture. These effects have been studied using equimolar solutions of target peptides and observation of the increase or decrease in ion intensity of the peptides upon the removal or addition of individual peptides. Gas-phase basicities and hydrophobicity measures have been used to rationalize this behaviour. ZipTips have been used to remove impurities and reduce the number of peptides present at any moment in a solution, a procedure that results in a significant increase in the total percentage of the amino acid coverage of enzymatically digested proteins. The efficacy of this approach was demonstrated using specifically nitrated lysozyme and specifically nitrated myoglobin.

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Li, Mingjie, Eric Sanchez, Jennifer Li, Cathy S. Wang, Jing Shen, Mengyin Hu, Crystal Leung, et al. "TRAF6-Dominant Negative Peptides Show Potent Inhibitory Effects On Multiple Myeloma, Osteoclast Formation and Bone Resorption." Blood 114, no. 22 (November 20, 2009): 611. http://dx.doi.org/10.1182/blood.v114.22.611.611.

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Abstract Abstract 611 Tumor necrosis factor receptor-associated factor 6 (TRAF6) has been implicated in regulating NF-κB and JNK signal transduction pathway resulting in inhibition of tumor cell proliferation and osteoclast formation. The unique biological function of TRAF6 is largely determined within its TRAF-C domain which does not interact with peptide motifs that are recognized by other TRAFs including 1, 2, 3 or 5. We have recently reported inhibition of cell proliferation and increased apoptosis of multiple myeloma (MM) cells through regulation of the NF-κB and JNK pathways through silencing the TRAF6 C-domain mRNA. In this study, we determined the effects of TRAF6 dominant negative peptides on MM cells, osteoclast formation and bone resorption. We cloned a 167 amino acid (in residues 333 to 508) fragment to produce a TRAF6 negative dominant (TRAF6dn) construct and synthesized an inhibitory decoy peptide of the TRAF6 interaction domain with CD40 and another peptide interacting with the TRAF6-RANK binding domain as well as a control peptide. All peptides were synthesized with a 16 amino acid permeable peptide. Using the MM1s, RPMI8226, and U266, we evaluated the effects of these peptides on MM tumor cell growth using an MTS assay and apoptosis with an Annexin V assay. We found that TRAF6dn peptides significantly inhibited MM cell proliferation maximally at 72 hours whereas effects on induction of apoptosis in MM cells were most prominent at 48 hours. The decrease in cell proliferation and increase in cell apoptosis occurred in a concentration-dependent fashion. We found that TRAF6dn also markedly inhibited osteoclast cell formation from freshly derived human monocytes induced by RANKL and M-CSF in a concentration-dependent fashion comparing with cells exposed to control peptide. We further examined the effects on MM cell apoptosis of the TRAF6 decoy or CD40 decoy peptides alone and in cells exposed to the combination of both peptides. The results showed either decoy peptide alone slightly induced apoptosis of MM tumor cells whereas the combination of both peptides demonstrated marked apoptosis of MM cells. We also showed that although melphalan alone induced apoptotic cell death, this effect was markedly enhanced when this alkylating agent was combined with the TRAF6 decoy peptide. Although the CD40 peptide alone did not inhibit osteoclast formation, TRAF6 decoy peptide alone and the combination of both decoy peptides markedly inhibited formation of these bone resorbing cells. We also examined the effects of TRAF6dn on NF-κB and JNK by measuring JUN kinase kinase (JNKK), which activates the MAP kinase homologues SAPK and JNK in response to IL-1 receptor stimulation. Phospho-NF-κB protein levels and phosphorylation of JNKK are both markedly reduced when MM cells are exposed to TRAF6dn fragment or TRAF6 decoy peptide. These studies suggest that TRAF6dn or the combination of TRAF6 decoy and CD40 decoy peptides may be excellent targets to block both myeloma cell and osteoclast cell formation. The study has been extended to assess the effects of these peptides in vivo using our SCID-hu murine model of human myeloma. Disclosures: No relevant conflicts of interest to declare.

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Dissertations / Theses on the topic "Peptide effects"

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Ringstad, Lovisa. "Interaction Between Antimicrobial Peptides and Phospholipid Membranes Effects of Peptide Length and Composition /." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-101989.

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Singh, Shalini. "Amphiphilic Peptide Interactions with Complex Biological Membranes : Effect of peptide properties on antimicrobial and anti-inflammatory effects." Doctoral thesis, Uppsala universitet, Institutionen för farmaci, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-282781.

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With increasing problem of resistance development in bacteria against conventional antibiotics, as well as problems associated with diseases either triggered or enhanced by infection, there is an urgent need to identify new types of effective therapeutics for the treatment of infectious diseases and its consequences. Antimicrobial and anti-inflammatory peptides have attracted considerable interest as potential new antibiotics in this context. While antimicrobial function of such peptides is being increasingly understood demonstrated to be due to bacterial membrane disruption, the mechanisms of their anti-inflammatory function are poorly understood. Since bacterial membrane component lipopolysaccharide triggers inflammation, this thesis aims at clarifying importance of lipopolysaccharide (LPS)-peptide interactions while investigating possible modes of action of peptides exhibiting anti-inflammatory effect. Furthermore, effect of poly(ethylene)glycol (PEG)-conjugation was investigated to increase performance of such peptides. Results presented in this thesis demonstrate that peptide-induced LPS- and lipid A binding/scavenging is necessary but not sufficient criterium for anti-inflammatory effects of peptides. Furthermore, preferential binding to LPS over lipid membrane, as well as higher binding affinity to the lipid A moiety within LPS, are seen for these peptides. In addition, results demonstrate that apart from direct LPS scavenging, membrane-localized peptide-induced LPS scavenging seem to contribute partially to anti-inflammatory effect. Furthermore, fragmentation and densification of LPS aggregates, in turn dependent on the peptide secondary structure on LPS binding, as well as aromatic packing interactions, correlate to the anti-inflammatory effect, thus promoting peptide-induced packing transition in LPS aggregates as key for anti-inflammatory functionality. Thus, peptide-induced LPS aggregate disruption together with reduction of the negative charge of LPS suggests the importance of phagocytosis as an alternative to the inflammatory pathway, which needs to be further investigated. Furthermore, PEG conjugation of peptide results in strongly reduced toxicity at a cost of reduced antimicrobial activity but markedly retained anti-inflammatory effect. Taken together, the results obtained in this work have demonstrated several key issues which need to be taken into consideration in the development of effective and selective anti-inflammatory peptide therapeutics for the treatment of severe Gram-negative bacterial infections.

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Kerstetter, Dale R. "McLafferty rearrangement of peptides and substituent effects on peptide fragmentation: Theoretical and experimental investigation." Thesis, Wichita State University, 2009. http://hdl.handle.net/10057/2541.

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The research presented here details two studies that utilized theoretical analysis and experimentation to further the understading of peptide fragmentation. The first study was the McLafferty rearrangement, which involves transfer of a У-position hydrogen atom to a carbonyl oxygen atom through a cyclic intermediate, followed by the elimination of an alkene. The second study examined substituent effects on benzene ring terminated peptides.
Thesis (M.S.)--Wichita State University, College of Liberal Arts and Sciences, Dept. of Chemistry

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Matthews, Thomas. "The effects of environment on peptide stability." Thesis, Birkbeck (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406349.

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Ng, Ming Tak. "Effects of prominsulin C-peptide and other islet peptides on beta-cell function and insulin secretion." Thesis, University of Ulster, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.554231.

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Hyperglycaemia is a significant pathophysiological feature of diabetes mellitus. It has been considered to be a cause as well as a consequence of impaired pancreatic p-cell function and insulin action. The detrimental effects of a hyperglycaemic environment encourage the non-enzymatic glycation of regulatory and functional proteins. This thesis investigated the effects of pro insulin C-peptide and other important islet peptides such as insulin, somatostatin, islet amyloid polypeptide (IAPP) as well as the gut hormone gastric inhibitory polypeptide (GIP) in both native and glycated forms on insulin release and beta cell function in vitro using clonal pancreatic p-ce1ls and isolated mouse islets and in vivo, using Swiss TO lean mice. Pancreatic beta-cells not only secrete insulin into the bloodstream, but also release equimolar amounts of C-peptide. During the last decade, studies have provided definite evidence of C-peptide's active role in physiology and pathophysiology. However very little information currently exists on the direct effects of C-peptide on pancreatic beta cells. This study provides evidence that C-peptide is a biologically active endogenous peptide hormone that exerts tonic inhibitory effects on pancreatic beta cell function and these effects may be partially mediated through intracellular signalling pathways. Suppression of insulin secretion by C-peptide was observed at basal and stimulatory glucose concentrations and was shown to be concentration dependent. The ability of alanine and IBMX to potentiate glucose-induced insulin secretion was severely impaired in the pancreatic cell line and isolated islets in the presence of C-peptide. This inhibition of glucose stimulated insulin secretion may be associated with the mechanism by which cAMP and KATP channel potentiates insulin release. In vivo studies with the administration of C-peptide resulted in a decrease in plasma insulin levels and increase in plasma glucose concentrations. As proinsulin C-peptide clearly exhibited an inhibitory effect on insulin secretion, it was of interest to study the autocrine effect of the other important pancreatic p-cell peptide, insulin. Concentration dependent inhibitory effects of insulin on alanine- and IBMX-stimulated insulin secretion were observed in isolated islets. Validation of this result was confirmed in vivo using Swiss TO mice, where plasma C-peptide levels were decreased following insulin administration. In mechanistic studies, insulin not only inhibited cAMP production at stimulatory glucose concentration, but also decreased GLP-1 and forskolin-stimulated cAMP production in clonal pancreatic cells. Moreover, insulin exerted a negative effect on insulin biosynthesis by decreasing the alanine-stimulated insulin mRNA expression at basal and stimulatory glucose concentration. As expected, inhibitory effects on insulin secretion were also observed for the pancreatic peptides, somatostatin-14 and IAPP whilst the gut incretin hormone GIP exerted insulinotropic activity. Following incubation with glucose in vitro, glycated forms of C-peptide, insulin, somatostain-14 and GIP were all readily detectable by reverse-phase HPLC and MALDI- TOF mass spectrometry. The extent of glycation was shown to be time and glucose concentration dependent. G Iycated human C-peptide exerted an inhibitory effect on insulin secretion, but to a lesser extent than non-glycated C-peptide. Glycated human C- peptide in the presence of alanine, GIP and tolbutamide resulted in 22%, 12% and 27% inhibition, respectively compared to 50%, 52% and 42% inhibition with native human C- peptide. A similar trend was obtained when comparing glycated human insulin and non- glycated human insulin. Suppression of alanine- and IBMX-stimulated C-peptide release was observed with glycated insulin. Glycated insulin reduced cAMP production at stimulatory glucose concentration, GLP-l and forskolin-stimulated cAMP production. Both glycated C-peptide and glycated insulin exhibited a less potent inhibitory effect on insulin secretion. Contrastingly, glycation of somatostatin-14 increased its ability to inhibit insulin secretion. Likewise, glycated GIP was more insulinotropic than its native peptide. These studies indicate that C-peptide may be one of several players in the multifactorial regulation of the pancreatic beta cell. Insulin secretion is an important physiological process which is regulated by multiple regulatory mechanisms. C-peptide may have a compensatory regulatory effect through the fine control of insulin release. Collectively, these studies indicate the need for continuing investigation of the circulating levels of glycated peptides and their effects on the ability to modulate insulin secretion. Further investigations are thus necessary to find out the possible role of glycated peptides in the pathophysiology of type 2 diabetes.

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Nsereko, Victor Leonard Joseph. "Peptidase inhibitors as additives for ensilage : effects on silage characteristics with reference to peptide nitrogen." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU079015.

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Novel approaches to manipulating proteolysis in ensiled perennial ryegrass (PRG) were investigated. The effects of the following on nitrogen (N) distribution in silage were investigated: E- 64, a specific cysteine-peptidase inhibitor (CPI); pepstatin A a specific aspartic-peptidase inhibitor; cystamine dihyrochloride (CYS) and N-ethylmaleimide, general CPIs, and formic acid (FA). Treatment with FA or CPIs reduced total soluble N, as a result of reduced proteolysis, and FA and CYS treatments increased peptide N concentrations (determined using fluroescamine or ninhydrin assays, and by amino acid analysis) compared to the control. Pepstatin A had little or no effect on the N constituents of silage. Characterisation of silage peptides using Sephadex G-25 suggested that they were predominantly di and tripeptides, with a small proportion of longer peptides (>7 amino acid residues). Forty additional compounds were screened for their efficacy as inhibitors of proteolysis in aqueous extracts of PRG. Five selected compounds were applied to PRG at ensilage: TPCK, a non specific CPI; chelators, 1,10-phenanthroline and 8-hydroxyquinoline (8-HQ); bestatin, a metallo-peptidase inhibitor; and N-acetyl-L-tyrosine ethyl ester (ATEE), a serine-peptidase inhibitor. When compared to the control, TPCK and 1,10- phenanthroline reduced total soluble N and increased peptide N concentrations; 8-HQ increased only peptide N concentrations. These chelators also restricted fermentation. The effects of Trypticase (peptides produced by enzymic hydrolysis of casein), silage extracts and N fractions prepared from silage extracts by cation exchange chromatography, as sources of N, on the growth of rumen bacteria, Megasphaera elsdenii, Prevotella ruminicola and Selenomonas ruminantium, supplied with glucose as an energy substrate in vitro, were investigated. No growth was observed on media containing extracts from silages produced in the presence of chelators but all bacteria grew on purified N fractions. Increasing silage peptide N therefore did not enhance microbial growth but for some treatments, silage N supported faster growth than Trypticase.

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Milton, R. H. "The effects of beta-amyloid peptide on microglial function." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19221/.

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The role of microglia in Alzheimer’s Disease (AD) pathogenesis is widely acknowledged, and the beta-amyloid (Aβ) peptide which accumulates in AD brain is known to activate a range of microglial functions. In the present thesis, the acute induction of some of these processes is examined using live cell imaging techniques. Aβ causes activation of microglial NADPH oxidase, a membrane-localised enzyme system which produces reactive oxygen species (ROS) thereby engendering oxidative stress. The transfer of electrons across the membrane by this enzyme system to produce ROS generates a potential difference, which will limit enzyme function unless it is dissipated by a compensatory movement of charge. I show that chloride intracellular channel 1 (CLIC1), a protein enriched in microglia and implicated in Aβ- induced microglial-mediated neurotoxicity, mediates a chloride conductance which sustains NADPH oxidase activity. Thus, blockade or knockdown of CLIC1 limits Aβ- induced ROS production. Using a variety of imaging methods, I show that the fascinating CLIC1 protein achieves its functions following an Aβ-induced redoxdependent direct insertion into the plasma membrane from the cytosol. Acute Aβ-induced microglial calcium signalling is also examined. Aβ is shown to elicit rapid and complex changes in microglial cytosolic calcium concentration, although these changes are less frequently observed in microglia than in astrocytes. The changes are not linked to ROS damage nor to voltage-gated calcium channel (VGCC) activity, but may be dependent on CD36 receptor function. The effects of Aβ treatment on subsequent calcium signalling elicited by the neuronal damage signalling molecule adenosine triphosphate (ATP) are investigated, and found to be complex. Aβ causes disruption of microglial calcium homeostasis and a reduction in the response to ATP, despite the calcium levels in the endoplasmic reticulum required for the response being increased. This work suggests that Aβ has diverse and consequential effects on microglial function relevant to AD pathophysiology.

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Strömstedt, Adam A. "Antimicrobial Peptide Interactions with Phospholipid Membranes : Effects of Peptide and Lipid Composition on Membrane Adsorption and Disruption." Doctoral thesis, Uppsala universitet, Institutionen för farmaci, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-100966.

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The interactions between antimicrobial peptides and phospholipid membranes were investigated, in terms of lipid headgroup variations and the role of cholesterol, as well as peptide composition and structure. Also strategies for increasing proteolytic stability were evaluated. The interactions were studied on model membranes in the form of liposomes and supported bilayers, through a combination of ellipsometry, fluorescence spectroscopy, circular dichroism, dynamic light scattering, electrophoresis, electron cryomicroscopy, and bacterial/cell culture experiments. The findings showed that membrane tolerance against the lytic activity of melittin, was increased on anionic membranes by electrostatic arrest in the headgroup region, and was reduced by hydration repulsion. The presence of cholesterol caused a reduction in melittin adsorption, while at the same time reducing membrane tolerance per adsorbed peptide. Differences in membrane leakage mechanisms were also attributed to cholesterol, where large scale structural effects contributed to the leakage, while other membranes followed the pore formation model. Substituting specific amino acids for tryptophan on an LL-37 derivative, was shown to increase stability against bacterial proteases, while at the same time significantly increasing antibacterial properties. These substitutions, as well as terminal modifications, increased adsorption and membrane lytic properties in a way that was less dependent on electrostatics. Furthermore, by comparing short cationic peptides with oligotryptophan end-tagged versions, the lytic mechanism of end-tagged peptides, and the different contributions of arginine and lysine to membrane adsorption and disruption were demonstrated. This thesis is a contribution to the development of antimicrobial peptides as therapeutic alternatives to conventional antibiotics.

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Chilumuri, Amrutha. "The effects of catalase and kisspeptin overexpression on amyloid peptide toxicity." Thesis, University of Westminster, 2014. https://westminsterresearch.westminster.ac.uk/item/8yq40/the-effects-of-catalase-and-kisspeptin-overexpression-on-amyloid-peptide-toxicity.

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Amyloid β (Aβ) is the major component of the senile plaques in Alzheimer’s disease (AD). The mechanism underlying cell death in AD includes oxidative stress, apoptosis, impaired mitochondrial function and receptor mediated effects. Compounds that specifically bind to Aβ are neuroprotective. Catalase is an antioxidant enzyme that specifically binds Aβ. Kisspeptin (KP) is a product of the KiSS-1 gene and contains an Aβ binding domain, which also interacts with Aβ. The localization of catalase, KP and Aβ in the AD brain plus the effects of catalase and KiSS-1 overexpression in neuronal cells were investigated in the present study. Tissue sections from the AD pons region were immunohistochemically stained to determine if catalase or KP colocalized with Aβ deposits. The immunohistochemistry results show that immunoreactive KP or immunoreactive catalase co-localizes with immunoreactive Aβ in AD pons sections. These results suggest that endogenous catalase and KP could play neuroprotective roles in AD. Catalase and KiSS-1 overexpressing gene models were created by stably transfecting human catalase and KiSS-1 constructs into SH-SY5Y cells and overexpression confirmed by RT-PCR, immunocytochemistry and Western blotting. The effects of Aβ and H2O2 on cell viability were determined by either MTT (3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) or trypan blue assay. Catalase overexpressing SH-SY5Y neurons showed a reduced susceptibility to Aβ and H2O2 toxicity compared to vector control cells. The catalase overexpression neuroprotection could by reduced by the catalase activity inhibitor 3-Amino-1,2,4-triazole and an inhibitor of catalase-Aβ interactions benzothiazole aniline-tetra (ethylene glycol). The KiSS-1 overexpressing SH-SY5Y neurons also showed a reduced susceptibility to Aβ and H2O2 toxicity compared to vector control cells. The KiSS-1 overexpression neuroprotection could by reduced by an anti-KP antibody, the oyxtocin antagonist atosiban and the cyclooxygenase inhibitor SC-560. In conclusion, both catalase and KP colocalize with Aβ in AD pons sections and overexpression of catalase or KiSS-1 is neuroprotective against Aβ toxicity.

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Demick, Kristen Ann. "Engineering Proteins via Peptide Backbone Mutagenesis: The Effects of Thioamide Linkages on the Folding and Stability of Short Peptides." Thesis, Boston College, 2009. http://hdl.handle.net/2345/724.

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Thesis advisor: Jianmin Gao
The development of proteins/peptides as therapeutic agents has emerged as a promising area for drug design. Due to increased antibiotic resistance, search for novel antibiotics has become a primary area of interest within the pharmaceutical industry. Antimicrobial peptides have been a significantly desirable model due to their innate cytolytic effects and favorable interaction with the membranes of bacterial cells within the host. Thioxylated analogues of biologically active peptides have shown increased enzymatic stability and increased selectivity and potency. Thioamide linkages have thus been installed in a variety of short peptides, replacing the backbone amide linkage, in order to study the effects on peptide conformation and stability. Several bioanalytical tools were used in the analysis including circular dichroism spectroscopy, NMR, size-exclusion high performance liquid chromatography, and fluorescence. The mutation was well-accommodated within several systems, including Trpzip 4 and gramicidin A, and proved to have comparable, and in several cases, enhanced stability in comparison to the wild-type peptides
Thesis (MS) — Boston College, 2009
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Chemistry

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Books on the topic "Peptide effects"

1

International Agency for Research on Cancer and World Health Organization, eds. Ingested nitrate and nitrite, and cyanobacterial peptide toxins. Lyon, France: International Agency for Research on Cancer, 2010.

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Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.

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International Symposium on Nonmammalian Peptides (1st 1985 Rome, Italy). First International Symposium on Nonmammalian Peptides: Held in Rome, Italy, May 11-15, 1985 at Accademia Nazionale dei Lincei, honorary president Vittorio Erspamer. Polifarma, Roma: Universitá degli Studi di Roma, 1985.

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International Symposium on VIP and Related Peptides (5th 1991 Shizuoka, Japan). Vasoactive intestinal peptide and related peptides: Proceedings of the Fifth International Symposium on VIP and Related Peptides, Shizuoka, Japan, November 12-15, 1991. Edited by Yanaihara Noboru. Tokyo: Biomedical Research Foundation, 1992.

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Chinese Peptide Symposium (4th 1996 Chengdu, China). Peptides: Biology and chemistry : proceedings of the 1996 Chinese Peptide Symposium, July 21-25, 1996, Chengdu, China. Dordrecht: Kluwer Academic, 1998.

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Khavinson, V. Kh. Peptides and ageing. Prague: Society of Integrated Sciences, 2002.

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Harding, Louise M. The effects of locusta peptides on mammalian calcium channels. Oxford: Oxford Brookes University, 1997.

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Hubert, Vaudry, and Laburthe Marc, eds. VIP, PACAP, and related peptides: From gene to therapy. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Adam, Rijnberk, Wimersma Greidanus, Tj. B. van., and Rijksuniversiteit te Utrecht. Vakgroep Geneeskunde van het Kleine Huisdier., eds. Comparative pathophysiology of regulatory peptides. Basel: Karger, 1987.

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NATO Advanced Research Workshop on the Role of Melatonin and Pineal Peptides in Neuroimmunomodulation (1990 Erice, Italy). Role of melatonin and pineal peptides in neuroimmunomodulation. New York: Plenum Press, 1991.

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Book chapters on the topic "Peptide effects"

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Goh, Shan, Jem Stach, and Liam Good. "Antisense Effects of PNAs in Bacteria." In Peptide Nucleic Acids, 223–36. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-553-8_18.

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Walcher, Daniel, and Nikolaus Marx. "Proatherogenic Effects of C-Peptide." In Diabetes & C-Peptide, 153–60. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-391-2_13.

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Sandow, Jürgen. "Effects on Different Peptide Hormones." In Drug Discovery and Evaluation: Pharmacological Assays, 1–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27728-3_84-1.

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Sandow, Jürgen. "Effects on Different Peptide Hormones." In Drug Discovery and Evaluation: Pharmacological Assays, 3691–745. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-05392-9_84.

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Brown, S. Lori, Sei Tokuda, Linda C. Saland, and Dennis E. Van Epps. "Opioid Peptide Effects on Leukocyte Migration." In Enkephalins and Endorphins, 367–86. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4899-0557-4_27.

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Nordquist, Lina, Åsa Kallas, Sara Stridh, Fredrik Palm, and John Wahren. "Renoprotective Effects of C-Peptide on Type 1 Diabetes." In Diabetes & C-Peptide, 67–77. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-391-2_7.

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Aoyagi, Takaaki. "Chapter 12. Small Molecular Protease Inhibitors and Their Biological Effects." In Biochemistry of Peptide Antibiotics, edited by Horst Kleinkauf and Hans von Döhren, 311–64. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110886139-013.

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Jew, J. Y., and N. E. Hynes. "Stress Effects on Central Autonomic Peptide Immunocytochemistry." In Histochemistry and Cell Biology of Autonomic Neurons and Paraganglia, 251–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72749-8_43.

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Kamiya, Hideki, Wei-Xian Zhang, and Anders A. F. Sima. "The Mechanisms Underlying the Effects of C-Peptide on Type 1 Diabetic Neuropathy." In Diabetes & C-Peptide, 79–92. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-391-2_8.

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Francke, Christof, Rosi Loyal, Itzhak Ohad, and Wolfgang Haehnel. "In Vitro Assembly of A “β2 Cytochrome b559” from Chemically Synthesised Peptide." In Photosynthesis: Mechanisms and Effects, 1085–88. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_258.

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Conference papers on the topic "Peptide effects"

1

Michailova, Silvia, Maya Georgieva, Thomas Bruckdorfer, and Tamara Pajpanova. "Influence of arginine mimetics on the biological effects of NT(8-13) analogues." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.257.

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Balacheva, Anelia, Momchil Lambev, Roumyana Detcheva, Thomas Bruckdorfer, and Tamara Paypanova. "In vitro assessment of the cytotoxic effects of novel RGD analogues and conjugates." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.259.

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Newberry, Robert W., and Ronald T. Raines. "The Main-Chain Oxygen: Unappreciated Effects on Peptide and Protein Structure." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.020.

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Drieu la Rochelle, Armand, Karel Guillemyn, Maria Dumitrascuta, Simon Gonzalez, Charlotte Martin, Valérie Utard, Raphaëlle Quillet, et al. "A Bifunctional Biased Mu Opioid Agonist - Neuropeptide Ff Receptor Antagonist as Analgesic with Improved Acute and Chronic Side Effects." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.276.

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Lee, Yeon Sun, Sara M. Hall, Cyf Ramos-Colon, Michael Remesic, Alexander Kuzmin, David Rankin, Todd W. Vanderah, Frank Porreca, Josephine Lai, and Victor J. Hruby. "Amphipathic Non-opioid Dynorphin A Analogs to Inhibit Neuroexcitatory Effects at Central Bradykinin Receptors." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.080.

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Lipscombe, Christina, Israel Benjamin, Devon Stutzman, Amelie Bottex, Chinyere Ebo, William Chau, Harsh Patel, et al. "Protein Kinase C Beta II (PKCβII) Peptide Inhibitor Exerts Cardioprotective Effects in Myocardial Ischemia/Reperfusion Injury." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.165.

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Rajbhandary, Annada, and Bradley L. Nilsson. "Investigating the Effects of Aromatic Amino Acids on Amphipathic Peptide Self-Assembly and Emergent Hydrogel Viscoelasticity." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.228.

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Kairane, Ceslava, Riina Mahlapuu, Rando Porosk, Mihkel Zilmer, and Ursel Soomets. "The effects of glutathione analogues on Na,K-ATPase activity in the kidneys of the wildtype and the Wfs1 gene mutated mice in vitro and in vivo." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.223.

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Bertolet, Matthew L., Michael Minni, Tyler Galbreath, Robert Barsotti, Lindon H. Young, and Qian Chen. "Effects of Mitochondrial-Targeted Antioxidants on Real-Time Blood Nitric Oxide and Hydrogen Peroxide Release in Acute Hyperglycemic Rats." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.158.

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Giri, Aswini Kumar, C. R. Apostol, P. Davis, D. Rankin, G. Molnar, T. W. Vanderah, F. Porreca, and V. J. Hruby. "Effects of Methyl and Halogens in Analgesic Peptide Molecules for Their Potent Agonist Activities at MOR/DOR and Antagonist Activity at NK1R." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.069.

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Reports on the topic "Peptide effects"

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Bumpers, Harvey L. Effects of a Viral Peptide (Nef) on Growth and Metastasis of Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada512002.

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Matthew, Gray. Data from "Winter is Coming – Temperature Affects Immune Defenses and Susceptibility to Batrachochytrium salamandrivorans". University of Tennessee, Knoxville Libraries, January 2021. http://dx.doi.org/10.7290/t7sallfxxe.

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Environmental temperature is a key factor driving various biological processes, including immune defenses and host-pathogen interactions. Here, we evaluated the effects of environmental temperature on the pathogenicity of the emerging fungus, Batrachochytrium salamandrivorans (Bsal), using controlled laboratory experiments, and measured components of host immune defense to identify regulating mechanisms. We found that adult and juvenile Notophthalmus viridescens died faster due to Bsal chytridiomycosis at 14 ºC than at 6 and 22 ºC. Pathogen replication rates, total available proteins on the skin, and microbiome composition likely drove these relationships. Temperature-dependent skin microbiome composition in our laboratory experiments matched seasonal trends in wild N. viridescens, adding validity to these results. We also found that hydrophobic peptide production after two months post-exposure to Bsal was reduced in infected animals compared to controls, perhaps due to peptide release earlier in infection or impaired granular gland function in diseased animals. Using our temperature-dependent infection results, we performed a geographic analysis that suggested that N. viridescens populations in the northeastern United States and southeastern Canada are at greatest risk for Bsal invasion. Our results indicate that environmental temperature will play a key role in the epidemiology of Bsal and provide evidence that temperature manipulations may be a viable Bsal management strategy.

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Underhill, Charles B., and Lurong Zhang. Therapeutic Effect of Targeted Hyaluronan Binding Peptide on Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada431642.

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Zhang, Lurong. Therapeutic Effect of Targeted Hyaluronan Binding Peptide on Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412140.

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Underhill, Charles B., and Lurong Zhang. Therapeutic Effect on Targeted Hyaluronan Binding Peptide on Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada507414.

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Zhang, Lurong. Therapeutic Effect of Targeted Hyaluronan Binding Peptide on Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada420850.

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Greenfield, Edward. Inhibition of Orthopaedic Implant Infections by Immunomodulatory Effects of Host Defense Peptides. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada575574.

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Greenfield, Edward. Inhibition of Orthopaedic Implant Infections by Immunomodulatory Effects of Host Defense Peptides. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada594031.

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Greenfield, Edward. Inhibition of Orthopaedic Implant Infections by Immunomodulatory Effects of Host Defense Peptides. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555797.

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Jaradat, Ihab, Sarah Al Sharie, Raed Ennab, and Sohaib Al-Omari. Seasonal Variation Effects on Perforated Peptic Ulcer - A systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0096.

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