Relevant bibliographies by topics / Histidine peptide

Academic literature on the topic 'Histidine peptide'

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Published: 9 March 2023

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Journal articles on the topic "Histidine peptide"

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Gill, J. S., Y. Yiangou, D. J. Webb, L. Meleagros, N. Benjamin, B. J. Chrysanthou, J. R. Cockcroft, R. C. Causon, A. J. Camm, and S. R. Bloom. "Peptide histidine valine: Its haemodynamic actions and pharmacokinetics in man differ from those of vasoactive intestinal peptide and peptide histidine methionine." Clinical Science 78, no. 5 (May 1, 1990): 487–92. http://dx.doi.org/10.1042/cs0780487.

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1. The effects of intravenous and intra-arterial infusion of the peptides derived from prepro-vasoactive intestinal peptide, vasoactive intestinal peptide, peptide histidine methionine and peptide histidine valine, were examined in six healthy volunteers. 2. Vasoactive intestinal peptide given intravenously caused a significant increase in heart rate and a decrease in diastolic, but not systolic, blood presure, whereas peptide histidine valine caused an increase in heart rate alone, despite higher achieved circulating peptide concentrations. Peptide histidine methionine did not affect heart rate or blood pressure. Forearm blood flow was increased by vasoactive intestinal peptide and peptide histidine valine when infused locally intra-arterially, although vasoactive intestinal peptide was more potent than peptide histidine valine. 3. Plasma concentrations of cardiodilatin (the N-terminal peptide derived from pro-atrial natriuretic peptide) were increased by intravenous infusion of vasoactive intestinal peptide, but were unaffected by peptide histidine methionine or peptide histidine valine. Circulating plasma concentrations of adrenaline and noradrenaline did not change during infusion of vasoactive intestinal peptide, peptide histidine methionine or peptide histidine valine. 4. Peptide histidine valine had a long half-life when compared with peptide histidine methionine and vasoactive intestinal peptide. 5. We conclude that peptide histidine valine is active in the human cardiovascular system and has a similar, though less potent, vasodilating action to vasoactive intestinal peptide. The higher circulating levels of peptide histidine valine found in man suggest that it may be important in modulating vascular tone.
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Backwell, F. R. C., B. J. Bequette, L. A. Crompton, C. K. Reynolds, D. E. Beever, and J. C. MacRae. "Effect of intravenous histidine or histidine peptide infusion on milk protein yield in lactating goats with an induced histidine deficiency." Proceedings of the British Society of Animal Science 1996 (March 1996): 180. http://dx.doi.org/10.1017/s1752756200593752.

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Studies involving infusion of stable isotope labelled peptides have shown that the mammary gland has the ability to utilise peptide-derived AA for milk protein synthesis (Backwell et al., 1994a) and that peptides may be involved in the supply of phenylalanine to the mammary gland in vivo (Backwell et al., 1994b). The aim of the present experiment was to compare milk production responses to systemic (jugular vein) provision of histidine as free AA or as a peptide (glycyl-histidine) in lactating dairy goats with an induced histidine deficiency.
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Backwell, F. R. C., B. J. Bequette, L. A. Crompton, C. K. Reynolds, D. E. Beever, and J. C. MacRae. "Effect of intravenous histidine or histidine peptide infusion on milk protein yield in lactating goats with an induced histidine deficiency." Proceedings of the British Society of Animal Science 1996 (March 1996): 180. http://dx.doi.org/10.1017/s0308229600031469.

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Studies involving infusion of stable isotope labelled peptides have shown that the mammary gland has the ability to utilise peptide-derived AA for milk protein synthesis (Backwell et al., 1994a) and that peptides may be involved in the supply of phenylalanine to the mammary gland in vivo (Backwell et al., 1994b). The aim of the present experiment was to compare milk production responses to systemic (jugular vein) provision of histidine as free AA or as a peptide (glycyl-histidine) in lactating dairy goats with an induced histidine deficiency.
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Rigel, D. F. "Effects of neuropeptides on heart rate in dogs: comparison of VIP, PHI, NPY, CGRP, and NT." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 2 (August 1, 1988): H311—H317. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h311.

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This study was designed to evaluate the potential chronotropic actions of several cardiac neuropeptides in pentobarbital-anesthetized dogs. After bilateral vagotomy and stellectomy and muscarinic receptor blockade, I injected vasoactive intestinal polypeptide, peptide histidine isoleucine, neuropeptide Y, neurotensin, and calcitonin gene-related peptide into the intact sinus node artery. Neurotensin, calcitonin gene-related peptide, and neuropeptide Y exhibited no physiologically significant changes in heart rate. However, the structural homologues vasoactive intestinal polypeptide and peptide histidine isoleucine each augmented heart rate with maximal increases (approximately 120 beats/min) similar to those of norepinephrine. Vasoactive intestinal polypeptide and peptide histidine isoleucine were twice and 1/18, respectively, as potent as norepinephrine. The cardioacceleratory responses to vasoactive intestinal polypeptide and peptide histidine isoleucine were more slowly developing and longer lasting than those of norepinephrine. The responses to these two peptides were unchanged after beta-adrenergic blockade with propranolol in a dose sufficient to eliminate or greatly attenuate the norepinephrine tachycardia. These results indicate a potential role of endogenous vasoactive intestinal polypeptide and peptide histidine isoleucine in nonadrenergic, noncholinergic heart rate control in the dog.
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VANGURI, Vijay K., Shuxia WANG, Svetlana GODYNA, Sripriya RANGANATHAN, and Gene LIAU. "Thrombospondin-1 binds to polyhistidine with high affinity and specificity." Biochemical Journal 347, no. 2 (April 10, 2000): 469–73. http://dx.doi.org/10.1042/bj3470469.

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Thrombospondin-1 (TSP1) is a secreted trimeric glycoprotein of 450 kDa with demonstrated effects on cell growth, adhesion and migration. Its complex biological activity is attributed to its ability to bind to cell-surface receptors, growth factors and extracellular-matrix proteins. In this study, we used a 125I solid-phase binding assay to demonstrate that TSP1 binds specifically to proteins containing polyhistidine stretches. Based on studies with three different six-histidine-containing recombinant proteins, we derived an average dissociation constant of 5 nM. The binding of 125I-labelled TSP1 to these proteins was inhibited by peptides containing histidine residues, with the degree of competition being a function of the number of histidines within the peptide. Binding was not inhibited by excess histidine or imidazole, indicating that the imidazole ring is not sufficient for recognition by TSP1. Heparin was a potent inhibitor of binding with a Ki of 50 nM, suggesting that the heparin-binding domain of TSP1 may be involved in this interaction. This was confirmed by the ability of a recombinant heparin-binding domain of TSP1 to directly compete for TSP1 binding to polyhistidine-containing proteins. Affinity chromatography with a polyhistidine-containing peptide immobilized on agarose revealed that TSP1 in platelet releasates is the major polypeptide retained on the six-histidine-peptide column. We conclude that TSP1 contains a high-affinity binding site for polyhistidine and this is likely to be the molecular basis for the observed binding of TSP1 to histidine-rich glycoprotein. The possibility that other polyhistidine-containing proteins also interact with TSP1 warrants further study.
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Pogostin, Brett H., Anders Malmendal, Casey H. Londergan, and Karin S. Åkerfeldt. "pKa Determination of a Histidine Residue in a Short Peptide Using Raman Spectroscopy." Molecules 24, no. 3 (January 23, 2019): 405. http://dx.doi.org/10.3390/molecules24030405.

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Determining the pKa of key functional groups is critical to understanding the pH-dependent behavior of biological proteins and peptide-based biomaterials. Traditionally, 1H NMR spectroscopy has been used to determine the pKa of amino acids; however, for larger molecules and aggregating systems, this method can be practically impossible. Previous studies concluded that the C-D stretches in Raman are a useful alternative for determining the pKa of histidine residues. In this study, we report on the Raman application of the C2-D probe on histidine’s imidazole side chain to determining the pKa of histidine in a short peptide sequence. The pKa of the tripeptide was found via difference Raman spectroscopy to be 6.82, and this value was independently confirmed via 1H NMR spectroscopy on the same peptide. The C2-D probe was also compared to other Raman reporters of the protonation state of histidine and was determined to be more sensitive and reliable than other protonation-dependent signals. The C2-D Raman probe expands the tool box available to chemists interested in directly interrogating the pKa’s of histidine-containing peptide and protein systems.
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Liu, Yu, Huan-Huan Wan, Duo-Mei Tian, Xiao-Jun Xu, Chang-Long Bi, Xiao-Yong Zhan, Bi-Hui Huang, Yun-Sheng Xu, and Le-Ping Yan. "Development and Characterization of High Efficacy Cell-Penetrating Peptide via Modulation of the Histidine and Arginine Ratio for Gene Therapy." Materials 14, no. 16 (August 19, 2021): 4674. http://dx.doi.org/10.3390/ma14164674.

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Cell-penetrating peptides (CPPs), as non-viral gene delivery vectors, are considered with lower immunogenic response, and safer and higher gene capacity than viral systems. In our previous study, a CPP peptide called RALA (arginine rich) presented desirable transfection efficacy and owns a potential clinic use. It is believed that histidine could enhance the endosome escaping ability of CPPs, yet RALA peptide contains only one histidine in each chain. In order to develop novel superior CPPs, by using RALA as a model, we designed a series of peptides named HALA (increased histidine ratio). Both plasmid DNA (pDNA) and siRNA transfection results on three cell lines revealed that the transfection efficacy is better when histidine replacements were on the C-terminal instead of on the N-terminal, and two histidine replacements are superior to three. By investigating the mechanism of endocytosis of the pDNA nanocomplexes, we discovered that there were multiple pathways that led to the process and caveolae played the main role. During the screening, we discovered a novel peptide-HALA2 of high cellular transfection efficacy, which may act as an exciting gene delivery vector for gene therapy. Our findings also bring new insights on the development of novel robust CPPs.
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Zhang, Tong, Baoying Shen, and Xinghua Shi. "“Crawling” on the self-assembly system: A molecular simulation of peptide position adjusting over self-assembly block." MATEC Web of Conferences 189 (2018): 02002. http://dx.doi.org/10.1051/matecconf/201818902002.

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By combining non-equilibrium molecular dynamics(NEMD), umbrella sampling, and weighted histogram analysis method(WHAM), we calculated the potential of mean force of histidine peptide moving over a self-assembly structure. The reaction coordinate is along the main chain direction of the histidine peptide in the self-assembly structure. It is found that the energy needed for the histidine peptide with 3 and 5 residues while moving along the reaction coordinate is around -2.2 kCal/mol and -7.4 kCal/mol, respectively. And the histidine peptide crawls along the reaction coordinate, performing a snake-like movement. This result could illustrate how histidine peptide adjusts its position during self-assembly process.
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Lihi, Norbert, Daniele Sanna, István Bányai, Katalin Várnagy, and Imre Sóvágó. "Unusual binding modes in the copper(ii) and palladium(ii) complexes of peptides containing both histidyl and cysteinyl residues." New Journal of Chemistry 41, no. 3 (2017): 1372–79. http://dx.doi.org/10.1039/c6nj03735f.

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Tse, Dicky Lai-Yin, Ronald Ting-Kai Pang, Anderson On-Lam Wong, Siu-Ming Chan, Hubert Vaudry, and Billy Kwok-Chong Chow. "Identification of a Potential Receptor for Both Peptide Histidine Isoleucine and Peptide Histidine Valine." Endocrinology 143, no. 4 (April 1, 2002): 1327–36. http://dx.doi.org/10.1210/endo.143.4.8714.

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Abstract Peptide histidine isoleucine (PHI), peptide histidine valine (PHV), and vasoactive intestinal polypeptide (VIP) are cosynthesized from the same precursor and share high levels of structural similarities with overlapping biological functions. In this study, the first PHI/PHV receptor was isolated and characterized in goldfish. To study this receptor using homologous peptides, we have also characterized the goldfish prepro-PHI/VIP, and, surprisingly, a shorter transcript lacking the VIP coding region was isolated. A PHI/VIP precursor without the VIP coding sequence has never before been reported. Initial functional expression of the PHI/PHV receptor in Chinese hamster ovary cells revealed that it could be activated by human PHV [50% effective concentration (EC50): 43 nm] and to a lesser extent human PHI (EC50: 133 nm) and helodermin (EC50: 166 nm) but not fish and mammalian pituitary adenylate cyclase-activating polypeptides and VIPs. Subsequent studies indicated that, similar to the pituitary adenylate cyclase-activating polypeptide receptors (PAC1-R, VPAC1-R, and VPAC2-R), the receptor isolated in this study is able to interact with goldfish PHI and its C-terminally extended form, PHV with EC50 values 93 and 43 nm, respectively. Northern blot and RT-PCR/Southern blot analyses revealed that the PHI/VIP gene is expressed in the intestine, brain, and gall bladder and the PHI/PHV receptor gene is primarily expressed in the pituitary and to a lesser extend in the intestine and gall bladder, suggesting that PHI/PHV may play a role, notably in the regulation of pituitary function. In conclusion, our results demonstrate for the first time the existence of a PHI/PHV receptor, indicating that the functions of PHI and PHV could be mediated by their own receptor in addition to VIP receptors.
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Dissertations / Theses on the topic "Histidine peptide"

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Yiangou, Yiangos. "Studies on peptide-histidine isoleucine (PHI-27)-like peptides." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47318.

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Armstrong, Ellen Pauline. "Peptide histidine isoleucine : radioimmunoassay and immunohistochemical studies." Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335983.

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Zaramella, Simone. "Development of a novel methodology for the synthesis of oligonucleotide-peptide conjugates /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-919-6/.

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Letzien, Ulrike. "Effects of Carnosine and L-histidine on Viability and Expression of Pyruvate Dehydrogenase Kinase 4 in Human Glioblastoma Cells." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197285.

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Die Arbeit behandelt die Ergebnisse von Experimenten über die Wirkung des Dipeptides Carnosin (β Alanyl L Histidin) und der Aminosäuren L Histidin und β-Alanin auf Kulturen der humanen Zellreihen U87, T98G und LN405, welche von Zellen des malignen Hirntumors Glioblastoma multiforme abgeleitet sind. Die Vitalität der Zellen nach Inkubation mit Carnosin oder L Histidin wurde anhand der Adenosintriphosphatproduktion und der Dehydrohenaseaktivität für Inkubationszeiträume von 24, 48 und 72 Stunden bestimmt. Dabei zeigte sich eine signifikant niedrigere Vitalität der mit Carnosin oder L Histidin inkubierten Zellen gegenüber der unbehandelten Kontrolle. Dieser Effekt war bei L Histidin stärker ausgeprägt. Bei Messungen der Lakatdehydrogenaseaktivität im Medium der Zellen, welche als Indikator für Zellnekrosen diente, zeigten nur die mit L Histidin inkubierte Zellen Zeichen von Nekrose. Die gleichen Messungen wurden auch an humanen embryonalen Nierenzellen durchgeführt (HEK 293), wobei sich ein ähnliches Ergebnis feststellen ließ. In den drei Zellreihen wurde zudem mittels qRT-PCR die mRNA-Expression für die beiden Enzyme Carnosinase 1 und Carnosinase 2 bestimmt, welche L Histidin von Carnosin abspalten. Im Vergleich mit Proben aus normalem Hirngewebe war die Expression beider Enzyme in den Glioblastomzellen deutlich geringer, wenngleich nachweisbar. Nachdem vorhergehende Studien [8] einen Anstieg der Expression von mRNA der Pyruvatdehydrogenasekinase 4 (PDK4) in mit Carnosin inkubierten Glioblastomzellen gezeigt hatten, wurde dieser Effekt hier auch mittels qRT-PCR in mit L Histidin inkubierten Zellen nachgewiesen. Eine Wirkung von Carnosin oder L Histidin auf ein Reportergen des PDK4-Promoters wurde ebenfalls untersucht, wobei sich kein signifikanter Effekt nachweisen ließ.
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Garrett, Hannah Mary. "A study into the influence of amyloid-beta peptide oxidation on the rate of fibril formation, with a synthesis of 2-oxo-histidine." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8485.

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The Amyloid Cascade Hypothesis states that fibrillation of the amyloid beta (Aβ) peptide is the primary cause of Alzheimer’s pathology. The trigger for the fibrillation is a subject of much debate, although it is clear, oxidative stress is a key feature of Alzheimer’s aetiology. This thesis explores a possible role of oxidation of Aβ, in particular the effect of histidine and methionine side-chain oxidation, on Aβ fibril growth rates. Within chapters 2 and 3 of this thesis is a discussion of various approaches to chemical synthesis of 2-oxo-histidine with a view to the incorporation of the oxidised amino acids into Aβ peptide using Fmoc approaches. Chapter 2 describes attempted chemical transformation of (protected) L-histidine into L-oxohistidine. Dimethyldioxirane oxidised Boc-His-OMe yielded products containing isopropylidene groups, while oxidation using a Cu(II)/ascorbate generated 2-oxo-histidine but gave very low yields. Within chapter 3, a successful synthesis of protected 2-oxo-histidine is described, via the known imidazolin-2-one-4-carboxylic. Chapter 4 analyses Aβ(1-40) fibrillation kinetics by treating the intact peptide with various oxidants. Contrary to previous reports, hydrogen peroxide alone did not slow fibrillation rates. Cu(II)/Cu(I)- catalysed oxidation increased the likelihood of amorphous aggregation over fibrillation. This thesis shows oxidation of Aβ has a profound influence on fibril growth and that incorporation of a stable oxidised histidine into Aβ is a realisable goal.
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GILARDONI, ETTORE. "AN INTEGRATED PROTEOMIC AND ANALYTICAL APPROACH FOR ELUCIDATING THE MECHANISM OF ACTION OF HISTIDINE DIPEPTIDES AND SYNTHETIC DERIVATES." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/797770.

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β-alanil-L-istidina (carnosina) è un peptide endogeno che possiede innumerevoli proprietà (chelante dei metalli, antiossidante, sequestrante delle specie reattive carboniliche). Diversi studi clinici hanno dimostrato un’attività farmacologica della carnosina in malattie su base ossidative, tuttavia il meccanismo dell’attività in vivo non è ancora noto. Questo progetto ha come scopo quello di comprendere il meccanismo in vivo della carnosina. Per far ciò, sono stati sviluppati nuovi metodi analitici di cromatografia liquida accoppiata a spettrometria di massa per la quantificazione in campioni biologici dei peptidi istidinici, loro derivati e gli addotti con le specie reattive carboniliche. Come prima cosa, un metodo analitico basato su una colonna ad interazione idrofiliche è stato sviluppato per l’analisi del carnosinolo in matrici biologiche di modelli animali di sindrome metabolica. La concentrazione di carnosinolo è stata determinata in diversi tessuti e, per la prima volta, l’addotto carnosinolo-acroleina è stato identificato in omogenato di fegato. Questo conferma l’attività del carnosinolo e dei peptidi istidinici come sequestranti delle specie reattive carboniliche in vivo. Tuttavia, è stata identificata l’instabilità metabolica dell’addotto carnosinolo-HNE in diversi tessuti. Saranno quindi necessari ulteriori studi per la caratterizzazione del metabolismo di questi addotti e l’identificazione della corretta entità chimica da ricercare nelle matrici biologiche come indice dell’attività sequestrante di carnosina e derivati. Il metodo basato su colonne ad interazioni idrofiliche è stato anche utilizzato per sviluppare un metodo a rivelazione diretta per determinare l’attività idrolitica del siero umano della carnosina. La carnosinasi serica è stata identificata come principale enzima impiegato nel metabolismo della carnosina. Rispetto ad altri metodi pubblicati in letteratura, quello sviluppato in questo elaborato si basa su una determinazione diretta della carnosina, senza dover effettuare processi complessi di preparazione del campione. I dati ottenuti sono stati convalidati con dati presenti in letteratura, dimostrando che il nostro metodo risulta essere affidabile ed accurato. È stato possibile anche condurre esperimenti di competizione fra substrati naturali e alcune molecole per valutare le principali interazioni substrato/enzima, con l’obiettivo di identificare inibitori della carnosinasi. I dati ottenuti sono stati condivisi con colleghi chimici computazionali che attraverso esperimenti di docking, virtual screening e dinamica molecolare hanno identificato dei possibili inibitori naturali della carnosinasi serica umana. Un nuovo meccanismo d’azione della carnosina è stato approfondito, in quanto recenti pubblicazioni hanno evidenziato un ruolo della carnosina nella prevenzione della formazione di addotti fra la 3,4-diidrofenilglicolaldeide (DOPEGAL), un metabolita intermedio del catabolismo della noradrenalina, e le proteine. La capacità della carnosina di legare covalentemente la DOPEGAL tramite la formazione di un prodotto di Amadori è stata determinata in vitro e in lisato cellulare dove la DOPEGAL è stata formata aggiungendo noradrenalina al lisato enzimaticamente attivo. Studi futuri dovranno caratterizzare la stabilità metabolica di quest’addotto e le caratteristiche della sua formazione in matrici biologiche in quanto risulta essere un interessante biomarcatore di tossicità noradrenalinergica. In fine è stata valutato l’impatto della carnosina e del carnosinolo sul proteoma di cellule endoteliali umane derivanti dalla vena ombelicale. È ormai noto che i farmaci non agiscono unicamente col meccanismo d’azione per il quale sono stati sviluppati, ma possono interferire con l’espressione delle proteine cellulari, aumentandone, o diminuendone l’espressione e di conseguenza attivando o disattivando vie biologiche. Carnosina e carnosinolo non inducono una variazione nell’espressione delle proteine in cellule sane. Questo conferma la sicurezza delle molecole, soprattutto prevedendone un uso come terapia cronica. In futuro l’effetto del trattamento andrà valutato su cellule in condizioni patologiche, per comprendere se, in queste condizioni, carnosina o carnosinolo riescono a influenzare vie metaboliche e risposte cellulari. Sebbene ci siano ancora diverse domande che sono rimaste senza risposta, i dati ottenuti in questo elaborato hanno portato all’aumento della conoscenza del meccanismo d’azione di carnosina e derivati e all’identificazione di composti inibitori della carnosinasi.
β-alanil-L-histidine (i.e. carnosine) is an endogenous peptide that have been extensively characterized for a number of in vitro properties (i.e. metal chelating, antioxidant, reactive carbonyl species quenching). Several clinical trials highlighted the potential benefits of carnosine in the treatment of oxidative stress-based diseases, although the in vivo mechanism of action is not known, yet. The research project herein tries to expand upon the in vivo mechanism of action of carnosine. New analytical methods have been developed by means of liquid chromatography – tandem mass spectrometry for the quantification of histidine dipeptides, their derivatives, and the adducts formed with reactive carbonyl species into biospecimens. A first step was the implementation of hydrophilic interaction chromatography to skip some sample preparation steps and to reduce the chance of systematic errors. The method allowed the quantification of carnosine and carnosinol (a carnosine derivative stable to carnosinase) in biospecimens. Carnosinol tissue distribution in animal models of metabolic syndrome was determined and carnosinol-acrolein adduct was detected for the first time in liver matrices. This finding experimentally confirmed the reactive carbonyl species (RCS quenching activity of histidine dipeptides and derivatives in vivo. However, the metabolic instability of carnosinolHNE adduct was proved and such an evidence requires further studies aiming at understanding the metabolic fate of RCS-adducts to characterize their disposal. Subsequently, a new method for the measurement of carnosine hydrolysis in serum was developed as well. Human serum carnosinase has been identified as the enzyme responsible for such an activity. Compared to other published assays, the method employs a direct detection of the substrate and the use of less sample. Competition experiments with either natural derivatives or other molecules were set to identify hit compounds acting as carnosinase inhibitors. The collected data were shared with computational chemists who identified putative hit compounds via docking, virtual screening, and molecular dynamic approaches. Furthermore, a novel carnosine mechanism of action was studied starting from the evidence that carnosine can prevent the formation of protein adducts with 3,4- dihydroxyphenylglycolaldehyde (DOPEGAL) (i.e. an aldehyde intermediate of norepinephrine metabolism). This could be relevant for the in vivo mode of action of carnosine since DOPEGAL can accumulate in cells because of oxidative stress and as it covalently binds proteins, it can alter their structures and functions. Carnosine quenching activity via the formation of an Amadori product with DOPEGAL was determined in vitro and in cell lysates producing DOPEGAL from enzymatic transformation of norepinephrine. Future studies should be done to characterize the metabolic stability of the adduct and its formation in biospecimens as potential biomarker of norepinephrine toxicity. Finally, the project included proteomics studies on human umbilical vein cells (HUVECs) to assess the impact of carnosine and carnosinol on protein expression. It is widely recognized that drugs exert their pharmacological effects also by an alteration of biological pathways by modifying protein expression. Carnosine and carnosinol have little or no impact on protein expression as detectable on proteome or secretome of healthy endothelial cells. In the future the impact on pathological cells should be carried out as well. These data support the hypothesis of a low toxicity for these molecules, making them suitable candidates for a chronic administration. Although a lot of questions are still unanswered, these data have given new insights in the mechanism of action of carnosine and in the discovery of molecules acting either as carnosine-like compounds or as carnosinase inhibitors.
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Dintner, Sebastian [Verfasser], and Susanne [Akademischer Betreuer] Gebhard. "Characterization of a sensory complex involved in antimicrobial peptide resistance : communication between a histidine kinase and an ABC transporter in Bacillus subtilis / Sebastian Dintner. Betreuer: Susanne Gebhard." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1062492692/34.

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Ng, Choi I.-teng Montserrat. "Solid-phase synthesis of 5-arylhistidine-containing peptides: from linear antimicrobial peptides to cyclic peptides derived from arylomycins and aciculitins." Doctoral thesis, Universitat de Girona, 2015. http://hdl.handle.net/10803/380739.

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The incorporation of unsymmetrical biaryl systems into peptide sequences is a strategy that can improve their biological activity. Due to the difficulty of arylating the 4(5}-position of the imidazole ring, this doctoral thesis was focused on the development of efficient methodologies for the solid-phase synthesis of 5-arylhistidine-containing antimicrobial undecapeptides through a Suzuki-Miyaura reaction under microwave irradiation. The extension of this protocol allowed the preparation of biaryl cyclic peptides of different ring sizes bearing a His-Phe or His-Tyr biaryl linkage. Then, it was developed a procedure for the total solid-phase synthesis of biaryl cyclic lipopeptides derived from arylomycins. These strategies were extended to the preparation of biaryl cyclic analogues of the marine bicyclic pptides aciculitins. In particular, it was achieved the synthesis of analogues of the northern and the southern hemispheres of aciculitins as well as biaryl bicyclic peptides incorporating a Phe-Phe, a Phe-Tyr, a His-Tyr or a Tyr-Tyr biaryl bridge
La incorporació de sistemes biarílics asimiètrics en seqüències peptídiques es considera un enfocament útil per a millorar l'activitat biològica de pèptids. Tenint en compte la dificultat d'arilar la posició 4 (5) de l'anell d'imidazole, aquesta tesi doctoral es centra en el desenvolupament de noves estratègies eficients per a la preparació en fase sòlida d'undecapèptids antimicrobians contenint una 5-arilhistidina a través d'una reacció de Suzuki-Miyaura sota irradiació microones. L'extensió d'aquesta metodologia ha permès la síntesi de pèptids biarílics cíclics de diferents mides que incorporen un enllaç His-Phe 0 His-Tyr. Posteriorment, s'ha desenvolupat un procediment per la síntesi total en fase sòlida de lipopèptids biarílics cíclics derivats de les arilomicines. Les estratègies anteriors s'han estès a la preparació de compostos biarílics anàlegs dels pèptids bicíclics marins aciculitines. Concretament, s'ha preparat anàlegs dels hemisferis nord i sud de las aciculitines així com pèptids biarílics bicíclics que incorporen un pont Phe-Phe, Phe-Tyr, Tyr-His 0 Tyr-Tyr.
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Hahn, Markus. "Chromatographische, NMR-spektroskopische und massenspektrometrische Untersuchungen der Reaktionen von histidin- und methioninhaltigen Peptiden mit [Pt(dien)(H2O)]2+, [Pt(en)(H2O)2)]2+ und cis-[PtCl2(NH3)2]." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960640940.

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Hoang, Huy Ngoc. "Metal clips for folding peptides : a study of palladium (II) binding to histidine residues in short peptides stabilize (sic) their a-Helical conformation in solutions /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17478.pdf.

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Book chapters on the topic "Histidine peptide"

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Harding, S. J., I. Heslop, J. H. Jones, and M. E. Wood. "The racemization of histidine in peptide synthesis: Further studies." In Peptides 1994, 189–90. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_77.

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Chelli, Mario, Mauro Ginanneschi, Anna Maria Papini, Daniela Pinzani, and Gianfranco Rapi. "Cyclization of histidine azide: A side reaction during peptide synthesis." In Peptides 1992, 255–56. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_103.

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Sieber, Peter, and Bernhard Riniker. "Protection of histidine in peptide synthesis: A reassessment of the trityl group." In Peptides, 270–72. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-010-9595-2_81.

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Flörsheimer, A. "Tct: A new trityl-derived histidine protecting group." In Peptides 1994, 145–46. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_55.

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Chang, Conway C., Jerry J. Pollock, and Anita L. Hong. "Synthesis and biological activity of histidine-rich peptides bonded to polylysine backbone." In Peptides 1990, 843–46. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_347.

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Kalbacher, Hubert, and Wolfgang Voelter. "Acid labile protection of histidine and arginine in SPPS using Adpoc derivatives." In Peptides 1990, 31–33. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_8.

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Gesquiere, Jean Claude, Eric Diesis, and André Tartar. "A new side reaction involving Nπ-Bom-protected histidine and N-terminal cysteine." In Peptides 1990, 82–83. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_31.

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Gesquière, J. C., J. Najib, E. Diesis, D. Barbry, and A. Tartar. "Investigations of the side reactions associated with the use of Bom and Bum groups for histidine protection." In Peptides, 641–42. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_257.

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Juliano, L., I. Y. Hirata, P. Boschcov, M. A. Juliano, M. C. F. Oliveira, A. Miranda, and Y. Okada. "Synthesis of human (1–17)-angiotensinogen renin substrate and side reactions on arginine and histidine couplings." In Peptides 1990, 100–101. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_40.

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Li, G., L. W. Boteju, D. Patel, and V. J. Hruby. "A new method for the synthesis of the optically pure precursors to β-methyl derivatives of tryptophan, histidine, tyrosine and phenylalanine." In Peptides, 181–83. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_57.

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Conference papers on the topic "Histidine peptide"

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Garifullin, Ruslan, Rezeda Ishkaeva, and Diana Salakhieva. "Synthesis and characterization of multi-functional histidine-containing peptide amphiphiles." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-08538.

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Qin, Haifang, Yuqin Qin, Li Liu, Minli Fu, Lin Qiu, Yaqin Gu, Jianhao Wang, and Pengju Jiang. "In-capillary self-assembly of quantum dots and histidine containing peptide." In 2016 IEEE International Nanoelectronics Conference (INEC). IEEE, 2016. http://dx.doi.org/10.1109/inec.2016.7589389.

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Silva, Adriana F., Luiz H. F. Ferreira, Margareth L. Capurro, and Vani X. Oliveira Jr. "Influence of the Isoleucine and Histidine Residues in Anti-Plasmodium Activity of the Angiotensin II Analogs." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.074.

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Koide, T. "CHARACTERIZATION OF THE GENE FOR HUMAN HISTIDINE-RICH GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643599.

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Human histidine-rich glycoprotein (HRG) is a single-chain glycoprotein in plasma which is considered to modulate a coagulation and fibrinolysis system with the ability to bind to heparin, plasminogen, fibrinogen, thrombospondin, etc. Recently we have elucidated the primary structure of HRG by determining the nucleotide sequence of its cDNA, and showed that HRG is composed of several different types of internal repeats, each one of which shows considerable homology with the functional and/or structural domains of other proteins including high molecular weight kininogen, antithrombin III, cystatins, and proline-rich protein and peptide. Thus, the multifunctional property of HRG was suggested to be due to its multi-domain structure. In the present studies, a human genomic DNA library, cloned in the bacteriophage vector Charon 4A, was screened for HRG gene using a full-length cDNA coding for human IMI as a probe. A total of 7 clones were isolated from 6 × 105 phage and each was plaque purified. The entire HRG gene is represented in 3 genomic inserts with overlapping sequences that carry human DNA spanning 30 kb. Overlapping gene fragments were subcloned into pUC9 and characterized by Southern blot hybridization using 5’ and 3’ end probes isolated from human HRG cDNA and by DNA sequencing. These studies have shown that the gene for human HRG spans about 9 kb and consists of at least 5 exons and 4 introns. The putative histidine-rich region consisted of 12 tandemly repeated sequences of a 5 amino acid segment and 2 proline-rich regions contiguous to it are likely to be involved within one exon.
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Giannelli, B. F. "MOLECULAR GENETICS OF HAEMOPHILIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643981.

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Haemophilia B, an X-linked recessive disease with an incidence of 1/30,000 newborn males, is due to defects in the gene for coagulation factor IX, which is on the long am of the X chromosome at band Xq27.1. This gene consists of approximately 34 Kb and contains 8 exons which specify a mRtfc of 2803 residues coding for a protein of 415 aa preceded by a prepro signal peptide of 46 aa. Coripanson of the functional domains of the factor IX protein with the exon structure of the gene supports the exon/protein domain hypothesis of gene evolution. The factor IX gene seems to be formed by a number of functionally and evolutionally independent modules. The signal peptide and the gla (γcarboxy-glutamic) region encoded in the first three exons are homologous to those of factor X, protein C and prothrombin. Thevfourth and fifth exons which code for the connecting peptide are homologous to one another and to the epidermal growth factor, a module that has been used in the construction of a great variety of proteins including different members of the coagulation and fibrinolytic pathways. The sixth exon encodes the activation peptide region, while the catalytic region of factor IX is coded by the seventh and eighth exon. This is at variance with other serine protease genes that have different exons for the segments containing the cardinal ami no-acids of the active centre (histidine, aspartic acid and serine).Natural selection acts against detrimental mutations of the factor IX gene and at each generation a proportion of haemophilia B genes is eliminated, as a significant number of patients does not reproduce. There appears to be no selective advantage to the heterozygote and therefore haemophilia B is maintained in the population by new mutations. Consequently, a significant proportion of patients should be born to non-carrier mothers, and unrelated patients should carry different gene defects, as recently verified by detailed analysis of individual haemophilia B genes.The defects of factor IX described so far comprise both point mutations and gene deletions. The latter affect either part or the whole of the gene and are often associated with the development of antibodies against therapeutically adninistered factor IX (the inhibitor complication). Since gene deletions may result in the complete absenceof factor IX synthesis or in the production of an extremely abnormal product, it has been suggested that mutationspreventing the synthesis of a factor IX gene product capable of inducing immune tolerance to normal factor IX is important in predisposing to the inhibitor complication.Among the point mutations described so far, those affecting the signal peptide are of particular interest. Substitutions of the arginine at positions -4 and -1 cause failure of propeptide cleavage. Thus they indicate that the propeptide consists of 18 aa an(lthat lts excision is necessary for factor IX function. It appears also that the propeptide contains a signal for γcarboxylation which has been conserved during the evolution of different γcarboxylated proteins.In spite of coagulant treatment, haemophilia B is a serious disease and one for which genetic counselling is required. Paramount for this is the detection of carriers and the diagnosis ofaffected male fetuses. DNA probes derived from the cloned factor IX gene have been used for this purpose. Carrier and first or second trimester prenatal diagnoses have been done using factors IX gene markers to follow the transmission of haemophilia B genes. Six sequence variations causing restriction fragment length polymorphisms (RFLP) in the factor IX gene have been detected and used as markers for such indirect diagnoses The efficiency of the above markers is reduced by linkage disequilibrium but, nevertheless, they offer definite carrier and nremtal diagnoses in 75-80% of the relatives of familial cases of haemophilia B.The indirect detection of gene defects is of modest help in the counselling of individuals from the families of isolated patients, but new methods for the direct detection of gene mutations promise better results in such families and also the attainment of % diagnostic success in relatives of familial cases.Finally the successful expression of recombinant factor IX genes in tissue culture and transgenic mammals raises hopes of therapeutic advances.
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Reports on the topic "Histidine peptide"

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Barefoot, Susan F., Bonita A. Glatz, Nathan Gollop, and Thomas A. Hughes. Bacteriocin Markers for Propionibacteria Gene Transfer Systems. United States Department of Agriculture, June 2000. http://dx.doi.org/10.32747/2000.7573993.bard.

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The antibotulinal baceriocins, propionicin PLG-1 and jenseniin G., were the first to be identified, purified and characterized for the dairy propionibaceria and are produced by Propionibacterium thoenii P127 and P. thoenii/jensenii P126, respectively. Objectives of this project were to (a) produce polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1; (b) identify, clone and characterize the propionicin PLG-1 (plg-1) and jenseniin G (jnG) genes; and (3) develop gene transfer systems for dairy propionibacteria using them as models. Polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1 were produced in rabbits. Anti-PLG-1 antiserum had high titers (256,000 to 512,000), neutralized PLG-1 activity, and detected purified PLG-1 at 0.10 mg/ml (indirect ELISA) and 0.033 mg/ml (competitive indirect ELISA). Thirty-nine of 158 strains (most P. thoenii or P. jensenii) yielded cross-reacting material; four strains of P. thoenii, including two previously unidentified bacteriocin producers, showed biological activity. Eight propionicin-negative P127 mutants produced neither ELISA response nor biological activity. Western blot analyses of supernates detected a PLG-1 band at 9.1 kDa and two additional protein bands with apparent molecular weights of 16.2 and 27.5 kDa. PLG-1 polyclonal antibodies were used for detection of jenseniin G. PLG-1 antibodies neutralized jenseniin G activity and detected a jenseniin G-sized, 3.5 kDa peptide. Preliminary immunoprecipitation of crude preparations with PLG-1 antibodies yielded three proteins including an active 3-4 kDa band. Propionicin PLG-1 antibodies were used to screen a P. jensenii/thoenii P126 genomic expression library. Complete sequencing of a cloned insert identified by PLG-1 antibodies revealed a putative response regulator, transport protein, transmembrane protein and an open reading frame (ORF) potentially encoding jenseniin G. PCR cloning of the putative plg-1 gene yielded a 1,100 bp fragment with a 355 bp ORF encoding 118 amino acids; the deduced N-terminus was similar to the known PLG-1 N-terminus. The 118 amino acid sequence deduced from the putative plg-1 gene was larger than PLG-1 possibly due to post-translational processing. The product of the putative plg-1 gene had a calculated molecular weight of 12.8 kDa, a pI of 11.7, 14 negatively charged residues (Asp+Glu) and 24 positively charged residues (Arg+Lys). The putative plg-1 gene was expressed as an inducible fusion protein with a six-histidine residue tag. Metal affinity chromatography of the fused protein yielded a homogeneous product. The fused purified protein sequence matched the deduced putative plg-1 gene sequence. The data preliminarily suggest that both the plg-1 and jnG genes have been identified and cloned. Demonstrating that antibodies can be produced for propionicin PLG-1 and that those antibodies can be used to detect, monitor and compare activity throughout growth and purification was an important step towards monitoring PLG-1 concentrations in food systems. The unexpected but fortunate cross-reactivity of PLG-1 antibodies with jenseniin G led to selective recovery of jenseniin G by immunoprecipitation. Further refinement of this separation technique could lead to powerful affinity methods for rapid, specific separation of the two bacteriocins and thus facilitate their availability for industrial or pharmaceutical uses. Preliminary identification of genes encoding the two dairy propionibacteria bacteriocins must be confirmed; further analysis will provide means for understanding how they work, for increasing their production and for manipulating the peptides to increase their target species. Further development of these systems would contribute to basic knowledge about dairy propionibacteria and has potential for improving other industrially significant characteristics.
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