Relevant bibliographies by topics / Peptidylprolyl isomerase

Academic literature on the topic 'Peptidylprolyl isomerase'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Peptidylprolyl isomerase"

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Gudavicius, Geoff, Heddy Soufari, Santosh Upadhyay, Cameron D. Mackereth, and Christopher J. Nelson. "Resolving the functions of peptidylprolyl isomerases: insights from the mutagenesis of the nuclear FKBP25 enzyme." Biochemical Society Transactions 41, no. 3 (May 23, 2013): 761–68. http://dx.doi.org/10.1042/bst20130013.

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Peptidylprolyl isomerases have been implicated in chromatin regulation through their association with histones, chromatin-modifying enzymes and DNA-binding transcription factors. As with other post-translational modifications to proteins, a mechanistic understanding of the regulation of biological processes is fostered by loss-of-function studies both in vitro and in vivo. For peptidylprolyl isomerases, this can be accomplished with small-molecule inhibitors with high affinity for the isomerase active site or by mutation of amino acid residues that contribute to catalysis. In the present article, we review caveats to each of these approaches, and place emphasis on the thorough characterization of loss-of-function mutations in FKBPs (FK506-binding proteins). Using a case study of mutagenesis of the nuclear FKBP25 peptidylprolyl isomerase enzyme, we demonstrate that certain mutations generate a loss-of-function phenotype because they induce a complete loss of the FKBP domain fold, whereas other mutations are ‘surgical’ in that they ablate catalytic isomerase activity, while maintaining domain structure. Peptidylprolyl isomerases are thought to have both catalytic and non-catalytic functions, but differentiating between these mechanisms has proved to be challenging. The domain-destabilizing and surgical mutants described will facilitate the characterization of these two reported functions of peptidylprolyl isomerases.
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Fujisaki, Hiroshi, Yasushige Yonezawa, Motoyuki Shiga, Luca Maragliano, and Shin-ichi Tate. "Exploring Reaction Pathways for Peptidylprolyl-Isomerase." Biophysical Journal 112, no. 3 (February 2017): 449a. http://dx.doi.org/10.1016/j.bpj.2016.11.2407.

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Norville, Isobel H., Katherine O'Shea, Mitali Sarkar-Tyson, Suxin Zheng, Richard W. Titball, Gabriele Varani, and Nicholas J. Harmer. "The structure of a Burkholderia pseudomallei immunophilin–inhibitor complex reveals new approaches to antimicrobial development." Biochemical Journal 437, no. 3 (July 13, 2011): 413–22. http://dx.doi.org/10.1042/bj20110345.

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Mips (macrophage infectivity potentiators) are a subset of immunophilins associated with virulence in a range of micro-organisms. These proteins possess peptidylprolyl isomerase activity and are inhibited by drugs including rapamycin and tacrolimus. We determined the structure of the Mip homologue [BpML1 (Burkholderia pseudomallei Mip-like protein 1)] from the human pathogen and biowarfare threat B. pseudomallei by NMR and X-ray crystallography. The crystal structure suggests that key catalytic residues in the BpML1 active site have unexpected conformational flexibility consistent with a role in catalysis. The structure further revealed BpML1 binding to a helical peptide, in a manner resembling the physiological interaction of human TGFβRI (transforming growth factor β receptor I) with the human immunophilin FKBP12 (FK506-binding protein 12). Furthermore, the structure of BpML1 bound to the class inhibitor cycloheximide N-ethylethanoate showed that this inhibitor mimics such a helical peptide, in contrast with the extended prolyl-peptide mimicking shown by inhibitors such as tacrolimus. We suggest that Mips, and potentially other bacterial immunophilins, participate in protein–protein interactions in addition to their peptidylprolyl isomerase activity, and that some roles of Mip proteins in virulence are independent of their peptidylprolyl isomerase activity.
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Mori, Tadashi, and Takafumi Uchida. "Small Molecule Inhibitors of Peptidylprolyl cis/trans Isomerase." Current Enzyme Inhibition 6, no. 1 (February 1, 2010): 46–53. http://dx.doi.org/10.2174/157340810790712005.

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Nagaoka, Akiko, Naohiro Takizawa, Ryohei Takeuchi, Yutaka Inaba, Izumi Saito, Yoji Nagashima, Tomoyuki Saito, and Ichiro Aoki. "Possible involvement of peptidylprolyl isomerase Pin1 in rheumatoid arthritis." Pathology International 61, no. 2 (December 28, 2010): 59–66. http://dx.doi.org/10.1111/j.1440-1827.2010.02618.x.

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Alag, Reema, Asha Manikkoth Balakrishna, Sreekanth Rajan, Insaf A. Qureshi, Joon Shin, Julien Lescar, Gerhard Grüber, and Ho Sup Yoon. "Structural Insights into Substrate Binding by Pv FKBP35, a Peptidylprolyl cis-trans Isomerase from the Human Malarial Parasite Plasmodium vivax." Eukaryotic Cell 12, no. 4 (February 22, 2013): 627–34. http://dx.doi.org/10.1128/ec.00016-13.

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ABSTRACT The immunosuppressive drug FK506 binding proteins (FKBPs), an immunophilin family with the immunosuppressive drug FK506 binding property, exhibit peptidylprolyl cis-trans isomerase (PPIase) activity. While the cyclophilin-catalyzed peptidylprolyl isomerization of X-Pro peptide bonds has been extensively studied, the mechanism of the FKBP-mediated peptidylprolyl isomerization remains uncharacterized. Thus, to investigate the binding of FKBP with its substrate and the underlying catalytic mechanism of the FKBP-mediated proline isomerization, here we employed the FK506 binding domain (FKBD) of the human malarial parasite Plasmodium vivax FK506 binding protein 35 ( Pv FKBP35) and examined the details of the molecular interaction between the isomerase and a peptide substrate. The crystallographic structures of apo Pv FKBD35 and its complex with the tetrapeptide substrate succinyl-Ala-Leu-Pro-Phe- p -nitroanilide (sALPFp) determined at 1.4 Å and 1.65 Å resolutions, respectively, showed that the substrate binds to Pv FKBD35 in a cis conformation. Nuclear magnetic resonance (NMR) studies demonstrated the chemical shift perturbations of D55, H67, V73, and I74 residues upon the substrate binding. In addition, the X-ray crystal structure, along with the mutational studies, shows that Y100 is a key residue for the catalytic activity. Taken together, our results provide insights into the catalytic mechanism of Pv FKBP35-mediated cis-trans isomerization of substrate and ultimately might aid designing substrate mimetic inhibitors targeting the malarial parasite FKBPs.
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Yu, Liang, Abdalla J. Mohamed, Leonardo Vargas, Anna Berglöf, Greg Finn, Kun Ping Lu, and C. I. Edvard Smith. "Regulation of Bruton Tyrosine Kinase by the Peptidylprolyl Isomerase Pin1." Journal of Biological Chemistry 281, no. 26 (April 27, 2006): 18201–7. http://dx.doi.org/10.1074/jbc.m603090200.

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Liu, Tao, Yu Liu, Hung-Ying Kao, and Dehua Pei. "Membrane Permeable Cyclic Peptidyl Inhibitors against Human Peptidylprolyl Isomerase Pin1." Journal of Medicinal Chemistry 53, no. 6 (March 25, 2010): 2494–501. http://dx.doi.org/10.1021/jm901778v.

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Mori, Tadashi, Seima Itami, Tomotaka Yanagi, Yota Tatara, Mari Takamiya, and Takafumi Uchida. "Use of a Real-Time Fluorescence Monitoring System for High-Throughput Screening for Prolyl Isomerase Inhibitors." Journal of Biomolecular Screening 14, no. 4 (April 2009): 419–24. http://dx.doi.org/10.1177/1087057109333979.

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Cyclophilin is a ubiquitous peptidyl prolyl cis/trans isomerase that plays critical roles in many biological processes. A number of cyclophilin inhibitors have been designed based on the structure of the immunosuppressant cyclosporin A. To discover inhibitors that have other structures, the authors established the high-throughput screening (HTS) method using FDSS6000 real-time fluorescence detector. The inhibitors identified with this HTS showed significant correlation with direct interaction as measured by surface plasmon resonance. This high-throughput assay system is a powerful tool for the discovery of peptidylprolyl isomerase inhibitors. ( Journal of Biomolecular Screening 2009:419-424)
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Riggs, Daniel L., Patricia J. Roberts, Samantha C. Chirillo, Joyce Cheung-Flynn, Viravan Prapapanich, Thomas Ratajczak, Richard Gaber, Didier Picard, and David F. Smith. "The Hsp90-binding peptidylprolyl isomerase FKBP52 potentiates glucocorticoid signaling in vivo." EMBO Journal 22, no. 5 (March 3, 2003): 1158–67. http://dx.doi.org/10.1093/emboj/cdg108.

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Dissertations / Theses on the topic "Peptidylprolyl isomerase"

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Pang, Wen-chi Roberta. "The role of Pin1 in the pathogenesis of human hepatocellular carcinoma." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36905847.

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Pang, Wen-chi Roberta, and 彭詠枝. "The role of Pin1 in the pathogenesis of human hepatocellularcarcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36905847.

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The Best PhD Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize,2005-2006
published_or_final_version
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Medicine
Doctoral
Doctor of Philosophy
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Cheng, Chi-wai, and 鄭智威. "Identification and characterization of PIN1 binding partners." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45199656.

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Chaturvedi, Vandana. "Structure and function relationship among the peptidyl prolyl cis/trans isomerases." Diss., Mississippi State : Mississippi State University, 2007. http://sun.library.msstate.edu/ETD-db/theses/available/etd-11062007-111918.

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Cluning, Carmel. "Steroid receptor-associated immunophilins : influence of targeted knockdown and altered expression on receptor signalling." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0215.

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[Truncated abstract] Steroid receptors belong to the superfamily of nuclear receptors, and include the androgen receptor (AR), estrogen receptors (ER[alpha] and ER[beta], glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and the progesterone receptors (PRA and PRB). Before binding ligand, the receptor undergoes biochemical and structural modifications through a series of interactions with molecular chaperones and cochaperones all within a receptor heterocomplex. The mature receptor complexes with the major chaperone Hsp90, the stabilising cochaperone p23, and one member of a group of cochaperones termed immunophilins. Steroid receptor-associated immunophilins include the cyclophilin, CyP40, two FK506-binding proteins, FKBP51 and FKBP52, and the protein phosphatase, PP5. Immunophilins are characterised by the presence of TPR domains which compete directly for the TPR-acceptor site within Hsp90. This leads to mutually exclusive, immunophilin-containing receptor complexes. While PP5 contains a C-terminal phosphatase domain, CyP40, FKBP51 and FKBP52 each contain an N-terminal peptidyl prolyl isomerase (PPIase) domain, which catalyses the cis/trans isomerisation of prolyl peptide bonds. FKBP52 has been demonstrated to potentiate the ligand-dependent activity of AR, GR and PR, but not ER[alpha]. Knowing that CyP40 is the preferred immunophilin associated with the ER[alpha] heterocomplex, it was hypothesised that this immunophilin plays a role in ER[alpha] function. ... As all mutants maintained this potentiating activity it was concluded that the five altered residues found within gpGR do not contribute to the altered interaction of FKBP52 and receptor. However, it cannot be discounted that FKBP51 is more competitive for gpGR. Immunophilins are hormonally regulated, with FKBP52 found to be essential for female fertility in mice. It was hypothesised that levels of immunophilins, associated with steroid receptors important in the menstrual cycle, would be regulated to reflect hormonal activity within cycling endometrium. Human pre-menopausal endometrial sections taken from different phases of the menstrual cycle were examined immunohistochemically for expression of CyP40, FKBP51, FKBP51 and PP5. Immunophilin levels peaked at the mid-secretory phase correlating with stromal decidualization, a process essential for eventual blastocyst implantation. The importance of immunophilins to steroid receptor action was therefore reinforced by the observation that immunophilins appear to be hormonally regulated in cycling pre-menopausal human endometrium. Further studies into the effects of immunophilin loss and knockdown on steroid receptor-mediated responses in specific mouse tissues, knockout-derived mouse embryo fibroblasts and cancer cell lines may contribute to our understanding of the receptor-selective and tissue-specific actions of the immunophilins. Elucidation of the mechanisms through which they modulate receptor function may provide opportunities for therapeutic intervention in steroid-related disease.
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Tapparo, Aurélie. "Purification de protéines de liaison du myo-inositol hexakisphosphate chez l'amibe Dictyostelium discoideum." Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10202.

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Dans la plupart des cellules eucaryotes, l'inositol hexakisphosphate (insp#6, acide phytique) est le phosphoinositol le plus abondant. Chez l'amibe dictyostelium discoideum, la concentration d'insp#6 est de 0,7 mm et se maintient lors du cycle de differenciation de l'amibe. La fonction intracellulaire de cet inositol polyphosphate n'est pas clairement elucidee, toutefois un role regulateur de l'insp#6 dans le processus d'endocytose a recepteurs a ete propose chez les mammiferes. Un test de liaison de l'insp#6 radioactif a ete tout d'abord mis au point afin de pouvoir suivre les proteines capables de lier ce phosphoinositide, lors de purifications a partir d'extraits solubles de d. Discoideum. En combinant cette methode avec un test immunologique permettant de detecter les chaines lourdes des adaptines (proteines impliquees dans l'endocytose a recepteurs), le protocole de purification a permis de mettre en evidence cette proteine chez l'amibe. L'adaptine chez d. Discoideum ne semble pas fixer l'insp#6 contrairement a la situation dans les cellules de mammiferes. Une purification des proteines cytosoliques de liaison de l'insp#6 a permis l'identification de trois proteines non decrites jusqu'a present chez l'amibe : une nouvelle isoforme de cyclophiline et les proteines ribosomales s4 et s10. Le clonage de leur gene respectif ainsi que l'etude de leur expression au cours du developpement de l'amibe ont ete entrepris. Les trois genes sont specifiques du stade vegetatif : leur niveau de transcription s'effondre apres le commencement de la differenciation. La cyclophiline b purifiee est capable de lier la ciclosporine a et possede une extension n-terminale qui est clivee apres traduction de la proteine. Cette sequence signal permet son adressage vers le reticulum endoplasmique : la cyclophiline peut se trouver dans ce compartiment ou dans une vesicule de la voie de secretion, en effet aucun signal de retention dans le reticulum n'a ete trouve dans sa sequence. Une autre isoforme de cyclophiline localisee dans la mitochondrie a ete obtenue par chromatographie par affinite pour la ciclosporine a.
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Edvardsson, Anna. "Peptidyl-prolyl cis-trans Isomerases in the Chloroplast Thylakoid Lumen." Doctoral thesis, Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med983s.pdf.

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Bilbeisi, Rana A. 1983. "Expedient synthesis of chiral poly-substituted morpholine and oxazepine derivatives for the preparation of cyclophilin A inhibitors." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111575.

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An efficient and expedient synthetic method was developed for the preparation of chiral poly-substituted morpholine and oxazepine derivatives. The method was designed in the objective of applying the synthesis to the preparation of Cyclophilin A inhibitors.
The stereo- and regioselective method involves the reaction of enantiopure beta-amino alcohols with alpha,beta-unsaturated aldehydes. The synthesis proceeds through three steps; i) Reductive amination, ii) N-alkylation/ N-tosylation and iii) intramolecular-haloetherification. Stereoselectivity of this last step was controlled by N-alkyl/ N-tosyl groups and substitution across the double bond, and was enhanced by the addition of Bronsted acids. Substitution across the double bond of the starting material controlled the regioselectivity of the method. Morpholines were obtained through 6- exo cyclization and oxazepines were obtained through 7-endo cyclization.
A small library of morpholine-based derivatives was designed in-silico. Affinity and binding modes to the Cyclophilin A were investigated through a docking-based virtual screening study.
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Pernollet, Martine. "Modification de l'antigène toxine tétanique par des radicaux libres oxygénés et par des protéines à activité peptidyl-prolyl cis-trans isomérase : influence sur sa présentation à des lymphocytes T spécifiques." Université Joseph Fourier (Grenoble ; 1971-2015), 1994. http://www.theses.fr/1994GRE10238.

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L'influence du radical libre oxygene, le radical hydroxyle (oh) et des proteines a activite peptidyl-prolyl cis-trans isomerase sur le traitement de l'antigene toxine tetanique par des cellules presentatrices d'antigenes (lymphocytes b) a ete etudiee. En ce qui concerne le radical hydroxyle, sa production par des cellules de type macrophagique a ete reproduite a l'aide d'un systeme chimique. La toxine tetanique traitee par le radical oh subit un changement de conformation, et des liaisons bityrosine intramoleculaires resistantes a la proteolyse sont formees. La toxine ainsi modifiee est plus resistante a la proteolyse in vitro par des fractions endosomales isolees des cellules presentatrices. Cette diminution de proteolyse est correlee a une meilleure presentation par des cellules presentatrices fixees, a des lymphocytes t lorsque cet antigene est pre-proteolyse in vitro par des fractions endosomales. Ainsi, le radical oh favorise la presentation des epitopes de la toxine en les protegeant contre une proteolyse trop importante. La production du radical oh par un autre systeme chimique a permis de montrer l'existence d'un site de fixation pour le zinc a l'interieur de la chaine legere de la toxine, au niveau d'un epitope t. En ce qui concerne les activites peptidyl-prolyl cis-trans isomerases (ppiase), celles-ci ont pu etre mises en evidence dans les fractions endosomales de cellules presentatrices. L'addition a ces fractions endosomales de proteines a activite ppiase telles que la cyclophiline ou la fkbp augmente la proteolyse de la toxine tetanique. Il reste a tester les consequences de cet effet sur la presentation de cette derniere a des lymphocytes t. Un autre point de ce travail a ete la mise en evidence de la phosphorylation in vitro de la cyclophiline par la proteine kinase c purifiee. L'etude des consequences de cette phosphorylation sur l'activite ppiase de la cyclophiline est en cours
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Ando-Roussel, Kunie. "Prolyl isomerase Pin1 et la maladie d'Alzheimer." Lille 2, 2007. http://www.theses.fr/2007LIL2S018.

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La maladie d'Alzheimer (MA) est une démence neurodégénérative caractérisée neuropathologiquement par une Dégénérescence Neurofibrillaire (DNF) et des dépôts amyloïdes. La DNF est constituée de protéines Tau hyper- et anormalement phosphorylées, alors que dépôts amyloïdes sont constitués par des peptides Amyloid Beta qui sont les produits de clivages successifs du précurseur du peptide amyloïde (APP). Actuellement, les mécanismes qui conduisent à la DNF et aux dépôts amyloïdes sont encore mal connus. Récemment, Pin1 a été retrouvée dans les deux lésions de la MA. Pin1 est une peptidyl prolyl cis/trans isomérase qui régule ses cibles par isomérisation de sites phospho Serine / phospho Thréonine suivis d'une Proline (pSer/Thr-Pro). Pin1 elle-même est régulée par certaines modifications post-traductionnelles comme oxydation ou phosphorylation. De plus, des travaux récents sur un modèle de souris invalidées (KO) pour le gène PIN1 ont montré qu'une absence de Pin1 était associée au développement d'une DNF. Enfin, Pin1 KO et Pin1 KO en combinaison avec surexpression de APP mutée montraient une augmentation de Amyloid Beta insoluble dans les cerveaux de souris. Nous avons cherché à étudier la présence d'éventuelles variations des modifications post-traductionnelles de Pin1 qui seraient associées à la maladie d'Alzheimer en analysant des cerveaux de patients atteints de MA, de souris transgéniques pour tau et des cellules SY5Y qui surexpriment la tau humaine. Par ces travaux, nous mettons en évidence que la protéine Pin1 est régulée par phosphorylation. Il existe au moins 5 sites de phosphorylation comme cela est suggéré par nos analyses en électrophorèse bidimensionnelle. Par ailleurs, la progression de la pathologie tau peut moduler l'état de phosphorylation de Pin1. Notre étude, pour la première fois, montre la relation entre la pathologie tau et la phosphorylation de Pin1 dans la progression de la MA.
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Books on the topic "Peptidylprolyl isomerase"

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Sylvie, Rivière, ed. Peptidyl-prolyl cis/trans isomerases. Oxford: Oxford University Press, 1998.

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Foldase enzymes catalyzing protein folding. New York: Nova Science Publishers, 2008.

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Nagradova, N. K. Foldases catalyzing the formation and isomerization of disulfide bonds in proteins. New York: Nova Biomedical Books, 2009.

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Nagradova, N. K. Foldases catalyzing the formation and isomerization of disulfide bonds in proteins. New York: Nova Biomedical Books, 2009.

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1947-, Guzman Norberto A., ed. Prolyl hydroxylase, protein disulfide isomerase, and other structurally related proteins. New York: Marcel Dekker, 1998.

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Guzman. Prolyl Hydroxylase, Protein Disulfide Isomerase and Other Structurally Related Proteins. CRC, 1997.

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Christophe, Dugave, ed. Cis-trans isomerization in biochemistry. Weinheim: Wiley-VCH, 2006.

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Dugave, Christophe. Cis-Trans Isomerization in Biochemistry. Wiley & Sons, Limited, John, 2006.

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Dugave, Christophe. Cis-Trans Isomerization in Biochemistry. Wiley & Sons, Incorporated, John, 2006.

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Book chapters on the topic "Peptidylprolyl isomerase"

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Mattoo, Autar K. "[7] Peptidylprolyl cis-trans-isomerases from plant organelles." In Methods in Enzymology, 84–100. Elsevier, 1998. http://dx.doi.org/10.1016/s0076-6879(98)90009-x.

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Conference papers on the topic "Peptidylprolyl isomerase"

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Aluise, Christopher D., and Lawrence J. Marnett. "Abstract 2062: Peptidylprolyl cis/trans isomerase A1 (Pin1) is modified by lipid electrophiles generated during oxidative stress." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2062.

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