Gotowe bibliografie tematyczne / Calpain

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Calpain”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 25 lipca 2025

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Artykuły w czasopismach na temat "Calpain"

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Chhabra, A., H. Fernando, R. E. Mansel, and W. G. Jiang. "Pattern of expression of calpain subunits (large and small) in human breast cancer and the prognostic significance." Journal of Clinical Oncology 25, no. 18_suppl (2007): 21078. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21078.

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21078 Background: Calpains belongs to family of non-lysosomal calcium dependent cysteine proteases which are known to regulate cellular migration, apoptosis and cell cycle progression in normal and tumour cells. Calpain has also been indicated in the metastatic process of certain tumours like RCC and identified as a potential tumor suppressor for gastric cancer. Little is known about the expression pattern of calpain in human breast cancer. The current study investigated the expression pattern of the large (calpainL) and small (calpainS) subunits of calpain which are encoded by different genes
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Upla, Paula, Varpu Marjomäki, Liisa Nissinen, et al. "Calpain 1 and 2 Are Required for RNA Replication of Echovirus 1." Journal of Virology 82, no. 3 (2007): 1581–90. http://dx.doi.org/10.1128/jvi.01375-07.

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ABSTRACT Calpains are calcium-dependent cysteine proteases that degrade cytoskeletal and cytoplasmic proteins. We have studied the role of calpains in the life cycle of human echovirus 1 (EV1). The calpain inhibitors, including calpeptin, calpain inhibitor 1, and calpain inhibitor 2 as well as calpain 1 and calpain 2 short interfering RNAs, completely blocked EV1 infection in the host cells. The effect of the inhibitors was not specific for EV1, because they also inhibited infection by other picornaviruses, namely, human parechovirus 1 and coxsackievirus B3. The importance of the calpains in E
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Fontenele, Marcio, Bomyi Lim, Danielle Oliveira та ін. "Calpain A modulates Toll responses by limited Cactus/IκB proteolysis". Molecular Biology of the Cell 24, № 18 (2013): 2966–80. http://dx.doi.org/10.1091/mbc.e13-02-0113.

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Calcium-dependent cysteine proteases of the calpain family are modulatory proteases that cleave their substrates in a limited manner. Among their substrates, calpains target vertebrate and invertebrate IκB proteins. Because proteolysis by calpains potentially generates novel protein functions, it is important to understand how this affects NFκB activity. We investigate the action of Calpain A (CalpA) on the Drosophila melanogaster IκB homologue Cactus in vivo. CalpA alters the absolute amounts of Cactus protein. Our data indicate, however, that CalpA uses additional mechanisms to regulate NFκB
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SORIMACHI, Hiroyuki, Shoichi ISHIURA, and Koichi SUZUKI. "Structure and physiological function of calpains." Biochemical Journal 328, no. 3 (1997): 721–32. http://dx.doi.org/10.1042/bj3280721.

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For a long time now, two ubiquitously expressed mammalian calpain isoenzymes have been used to explore the structure and function of calpain. Although these two calpains, μ- and m-calpains, still attract intensive interest because of their unique characteristics, various distinct homologues to the protease domain of μ- and m-calpains have been identified in a variety of organisms. Some of these ‘novel’ calpain homologues are involved in important biological functions. For example, p94 (also called calpain 3), a mammalian calpain homologue predominantly expressed in skeletal muscle, is genetica
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Kizhakethil, Reshma V., Ashok K. Varma, Sagar H. Barage та ін. "Repercussions of the Calpain Cleavage-Related Missense Mutations in the Cytosolic Domains of Human Integrin-β Subunits on the Calpain–Integrin Signaling Axis". International Journal of Molecular Sciences 26, № 9 (2025): 4246. https://doi.org/10.3390/ijms26094246.

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Calpains, calcium-dependent cytosolic cysteine proteases, perform controlled proteolysis of their substrates for various cellular and physiological activities. In different cancers, missense mutations accumulate in the genes coding for the calpain cleavage sites in various calpain substrates termed as the calpain cleavage-related mutations (CCRMs). However, the impact of such CCRMs on the calpain–substrate interaction is yet to be explored. This study focuses on the interaction of wild-type and mutant β-integrins with calpain-1 and 2 in uterine corpus endometrial carcinoma (UCEC). A total of 4
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Murphy, Robyn M., Rodney J. Snow та Graham D. Lamb. "μ-Calpain and calpain-3 are not autolyzed with exhaustive exercise in humans". American Journal of Physiology-Cell Physiology 290, № 1 (2006): C116—C122. http://dx.doi.org/10.1152/ajpcell.00291.2005.

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μ-calpain and calpain-3 are Ca2+-dependent proteases found in skeletal muscle. Autolysis of calpains is observed using Western blot analysis as the cleaving of the full-length proteins to shorter products. Biochemical assays suggest that μ-calpain becomes proteolytically active in the presence of 2–200 μM Ca2+. Although calpain-3 is poorly understood, autolysis is thought to result in its activation, which is widely thought to occur at lower intracellular Ca2+ concentration levels ([Ca2+]i; ∼1 μM) than the levels at which μ-calpain activation occurs. We have demonstrated the Ca2+-dependent aut
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Theopold, U., M. Pintér, S. Daffre, et al. "CalpA, a Drosophila calpain homolog specifically expressed in a small set of nerve, midgut, and blood cells." Molecular and Cellular Biology 15, no. 2 (1995): 824–34. http://dx.doi.org/10.1128/mcb.15.2.824.

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Calpains are calcium-dependent proteases believed to participate in calcium-regulated signal pathways in cells. Ubiquitous calpains as well as tissue-specific calpains have been found in vertebrates. We isolated cDNA clones for a highly tissue-specific calpain gene from Drosophila melanogaster, CalpA, at 56C-D on the second chromosome. The expression of the CalpA gene product was monitored by using a specific antiserum directed against the product expressed by one cDNA clone. The encoded protein is found in a few neurons in the central nervous system, in scattered endocrine cells in the midgut
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Covington, Marisa D., David D. Arrington, and Rick G. Schnellmann. "Calpain 10 is required for cell viability and is decreased in the aging kidney." American Journal of Physiology-Renal Physiology 296, no. 3 (2009): F478—F486. http://dx.doi.org/10.1152/ajprenal.90477.2008.

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Aging is associated with abnormalities in kidney function, but the exact mechanisms are unknown. We examined calpains 1, 2, and 10 protein levels in kidneys from rats, mice, and humans of various ages and determined whether calpain 10 is required for cell viability. Calpain 10 protein expression decreased in the kidney, but not in the liver, of aging Fischer 344 rats, and this decrease was attenuated with caloric restriction. There was no change in calpains 1 or 2 levels in the kidney or liver in control and caloric-restricted aging rats. Aging mice also exhibited decreased calpain 10 protein
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Arora, A. S., P. de Groen, Y. Emori, and G. J. Gores. "A cascade of degradative hydrolase activity contributes to hepatocyte necrosis during anoxia." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (1996): G238—G245. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g238.

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Calpain proteases contribute to hepatocyte necrosis during anoxia. Our aim was to ascertain the mechanism causing calpain activation during anoxia. In rat hepatocytes, a twofold increase in calpain activity occurred despite the lack of an increase in cytosolic Ca2+ concentration ([Ca2+]i). The increase in calpain activity was not associated with an increase in calpain mRNA or a decrease in calpastatin mRNA expression. Because phospholipid degradation products generated by phospholipases can activate calpains at physiological [Ca2+]i, we determined the effect of phospholipase inhibitors and act
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Sultan, Karim R., Bernd T. Dittrich, and Dirk Pette. "Calpain activity in fast, slow, transforming, and regenerating skeletal muscles of rat." American Journal of Physiology-Cell Physiology 279, no. 3 (2000): C639—C647. http://dx.doi.org/10.1152/ajpcell.2000.279.3.c639.

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Fiber-type transitions in adult skeletal muscle induced by chronic low-frequency stimulation (CLFS) encompass coordinated exchanges of myofibrillar protein isoforms. CLFS-induced elevations in cytosolic Ca2+ could activate proteases, especially calpains, the major Ca2+-regulated cytosolic proteases. Calpain activity determined by a fluorogenic substrate in the presence of unaltered endogenous calpastatin activities increased twofold in low-frequency-stimulated extensor digitorum longus (EDL) muscle, reaching a level intermediate between normal fast- and slow-twitch muscles. μ- and m-calpains w
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Rozprawy doktorskie na temat "Calpain"

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Czerwinski, Eric Paul. "Two Proteins Containing Tandem DIII Domains, Calpain 10 and Dictyostelium Cpl, are Involved in Cytoskeletal Regulation." Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1193689816.

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Dissertation (Ph.D.)--University of Toledo, 2007.<br>"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 117-147.
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Janardhanan, Anitha C. "Gene expression of components of the calpain system m-calpain, [mu]-calpain and calpastatin in male and female broiler skeletal muscle /." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=895.

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Thesis (M.S.)--West Virginia University, 1999.<br>Title from document title page. Document formatted into pages; contains vii, 93 p. : ill. (some col.) Includes abstract. Includes bibliographical references (p. 72-80).
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Fernández-Montalván, Amaury Ernesto. "Structural requirements for activation and membrane binding of human m-calpain [mu-calpain]." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973390123.

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Schroeder, Ewald. "Structural studies of #mu#-calpain, a novel calpain substrate, and a papain-leupeptin complex." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386677.

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Huang, Xinhua. "DIII Domain of Calpain 10 and Cpl Towards an Understanding of Calpain 10 Function." University of Toledo Health Science Campus / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=mco1096641027.

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Huang, Xinhua. "DIII domain of calpain 10 and Cpl towards an understanding of calpain 10 function /." Connect to full-text via OhioLINK ETD Center, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1096641027.

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Thesis (Ph. D.)--Medical College of Ohio, 2003.<br>"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Ronald Mellgren. Includes abstract. Document formatted into pages: iv, 126 p. Title from title page of PDF document. Includes bibliographical references (p. 92-124).
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Rose, Robert Edward. "Calpain and lipopolysaccharide mediated hepatitis." Thesis, [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1806.

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Plammootil, Salma Martha. "Mutationen im Calpain-3-Gen." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973536306.

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Douillard, Aymeric. "Implication des calpaïnes lors d'un remodelage musculaire induit par un traitement chronique au clenbutérol." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON14001/document.

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Afin de lutter efficacement contre les malversations du dopage, il apparaît essentiel de comprendre les mécanismes conduisant au remodelage musculaire. Dans ce but nous avons analysé les effets d’un β2-agoniste, le clenbutérol, sur le remodelage musculaire et les différentes voies de signalisation qui y sont associées. Nous nous sommes particulièrement intéressés au système des calpaïnes qui a souvent été associé à des phénomènes de remodelage musculaire, principalement dans des modèles d’atrophie. Nous avons montré une sollicitation précoce du système des calpaïnes lors d’un traitement chroni
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Arthur, John Simon Campbell. "Regulation of m-calpain by phospholipids." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240569.

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Książki na temat "Calpain"

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Messer, Jeannette S., ed. Calpain. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1.

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Elce, John S. Calpain Methods and Protocols. Humana Press, 2000. http://dx.doi.org/10.1385/1592590500.

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S, Elce John, ed. Calpain methods and protocols. Humana Press, 2000.

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W, Wang Kevin K., and Yuen Po-Wai, eds. Calpain: Pharmacology and toxicology of calcium-dependent protease. Taylor & Francis, 1999.

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1946-, Mellgren Ronald L., and Murachi Takashi 1926-, eds. Intracellular calcium-dependent proteolysis. CRC Press, 1990.

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Public Service Commission of Wisconsin. and Wisconsin. Dept. of Natural Resources., eds. Calpine Fond du Lac Energy Center, LLC generation project. Public Service Commission of Wisconsin, 2002.

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Carnio, Leanne katherine. Direct association of integrin-linked kinase with a novel calponin homology domain-containing protein, CLINT. National Library of Canada, 2000.

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Suzuki, Koichi. Calpain. Chapman & Hall, 1997.

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Calpain Methods and Protocols. Humana Press, 2000.

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Elce, John S. Calpain Methods and Protocols. Humana Press, 2010.

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Części książek na temat "Calpain"

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Nimmrich, Volker, Anton Bespalov, and Achim Möller. "Calpain." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_23.

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Carragher, Neil O. "Calpain." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_782-2.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, et al. "Calpain." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_23.

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Carragher, Neil O. "Calpain." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_782.

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Carragher, Neil O. "Assaying Calpain Activity." In Adhesion Protein Protocols. Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-353-0_9.

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Ono, Yasuko, Hiroyuki Sorimachi, and Koichi Suzuki. "Calpains: structure and function of the calpain super family." In Proteases New Perspectives. Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8737-3_11.

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Nguyen, Anh T. H., Matthew Campbell, Paul F. Kenna, et al. "Calpain and Photoreceptor Apoptosis." In Retinal Degenerative Diseases. Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_69.

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Ryu, Morin, and Toru Nakazawa. "Calcium and Calpain Activation." In Neuroprotection and Neuroregeneration for Retinal Diseases. Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54965-9_2.

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Chakraborti, Sajal, Mahasweta Ghosh, Dibyapriya Roy Chowdhury, Tapati Chakraborti, and Rajabrata Bhuyan. "Calpain, miRNA, and Cancer." In Handbook of Proteases in Cancer. CRC Press, 2024. http://dx.doi.org/10.1201/9781003394693-19.

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Biswas, Ashim Kumar, and Samarth Tandon. "Casein Zymography for Analysis of Calpain-1 and Calpain-2 Activity." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_3.

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Streszczenia konferencji na temat "Calpain"

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Colman, Robert W., Harlan Bradford, and Anjanayaki Annamalai. "FACTOR V IS ACTIVATED AND CLEAVED BY PLATELET CALPAIN: COMPARISON WITH THROMBIN PROTEOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643884.

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Platelets are known to process human and bovine factor V during secretion and/or membrane binding. We therefore studied the functional and structural changes produced in human factor V and Va by purified platelet calpain. A maximum increase in factor V coagulant activity of 2.5-fold over control incubations was observed for calpain (0.6 u/ml) at 25°C in comparison with a 10-fold increment for a thrombin (1 u/ml). Thrombin addition to reactions initiated by calpain resulted in further activation comparable to that of thrombin alone, while subsequent addition of calpain had no effect on the exte
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Kajiwara, Y., M. Sakon, T. Tsujinaka, J. Kambayashi, T. Mori, and T. Murachi. "STUDIES ON ROLE OF CALPAIN IN PLATELET REACTION, UTILIZING NEWLY SYNTHETIZED PEPTIDE ANTAGONISTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642823.

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The system of calpain (Ca2+-activated protease) and its inhibitor calpastatin in platelets have been well characterized in our laboratory but the role of the system has not been fully elucidated yet, though various endogenous substrates have been identified. Employing SH inhibitors as calpain antagonists, We have proposed a possible role of platelet calpain in myosin light chain (20K) phosphorylation (Biochem.Int. 6,767,1986) but more specific calpain antagonists were required to draw conclusion. Recentry, series of peptide calpain antagonists(PCAs) were syn-thetized such as Ac-Leu-Leu-Nle.al(
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verhallen, P. F. J., E. M. Bevers, P. Comfurius, W. M. A. Linkskens, and R. F. A. Zwaal. "CALPAIN-MEDIATED CYTOSKELETAL DEGRADATION CORRELATES WITH STIMULATION OF PLATELET PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642821.

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We have shown earlier that the negatively charged phospholipid phosphatidylserine (PS), which becomes translocated from the inner surface to the outer surface of the plasma membrane upon platelet activation, is responsible for platelet procoagulant activity. Studies with erythrocytes have suggested a role for cytoskeletal proteins in the regulation of transmembrane asymmetry of PS. The possibility that platelet cytoskeletal proteins are involved in the loss of transmembrane asymmetry of PS, was explored by correlative investigations of both platelet prooagulant activity and activity of calpain
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Puri, R. N., F. Zhou, H. Bradford, E. J. Gustafson, R. F. Colman, and R. W. Colman. "HIGH MOLECULAR WEIGHT KININOGEN SPECIFICALLY BLOCKS THROMBIN-INDUCED AGGREGATION BY INHIBITING PLATELET CALPAIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643860.

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We have previously shown that platelet-aggregation induced by alpha-thrombin (1.7 nM) involves complete cleavage of the surface membrane polypeptide, Mr = 100 kDa (MP 100) labeled by FSBA in intact platelets. The failure to cleave MP100 in membrane preparations or in platelets treated with metabolic inhibitors or leupeptin, suggested that thrombin was acting by activating platelet calpain. Since high molecular weight kininogen (HMWK) is the most potent plasma inhibitor of calpain(s), we now report that HMWK inhibited thrombin-induced aggregation in a dose-dependent manner over a range of plasm
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duVERLE, DAVID, ICHIGAKU TAKIGAWA, YASUKO ONO, HIROYUKI SORIMACHI, and HIROSHI MAMITSUKA. "CaMPDB: A RESOURCE FOR CALPAIN AND MODULATORY PROTEOLYSIS." In Proceedings of the 9th Annual International Workshop on Bioinformatics and Systems Biology (IBSB 2009). IMPERIAL COLLEGE PRESS, 2010. http://dx.doi.org/10.1142/9781848165786_0017.

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Okita, J. R., M. M. Frojmovic, S. Kristopeit, T. Wong, and T. J. Kunicki. "MONTREAL PLATELET SYNDROME: DECREASED ACTIVITY OF PLATELET CALPAINS ASSOCIATED WITH AGGREGATION ABNORMALITIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642822.

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The Montreal platelet syndrome (MPS) is an inherited disorder of platelet function characterized by a) severe thrombocytopenia, b) formation of "giant" platelets upon physical or biochemical stimulation, c) spontaneous aggregation (stir-induced microaggregate formation) and d) a lack of aggregation in response to thrombin. The Bernard-Soulier syndrome (BSS) is similar to MPS in that both syndromes are characterized by "giant" platelets and an abnormal aggregation response to thrombin. BSS patients have a deficiency of specific platelet glycoproteins (GPs). From our investigations we conclude M
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Supinski, Gerald S., Lin Wang, Alexander Alimov, Xiao-Hong Song, and Leigh Ann P. Callahan. "CPLA2 Modulates Cytokine Induced Superoxide Generation And Calpain Activation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2715.

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Ryan, Dorothy M., Emer P. Reeves, Noel G. McElvaney, and Shane J. O'Neill. "Secretory Leukoprotease Inhibitor Regulates Neutrophil Chemotaxis Via Calpain Inhibition." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2804.

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Berkowitz, S. D., H. Nozaki, K. Titani, T. Murachi, and T. S. Zimmerman. "CALPAIN AND ELASTASE ARE NOT RESPONSIBLE FOR THE VON WILLEBRAND FACTOR FRAGMENTS IN NORMAL PLASMA AND IIA VON WILLEBRAND DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644103.

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Recent evidence suggests that proteolysis plays an important role in some forms of inherited and acquired von Willebrand disease (vWD). Using monoclonal epitope mapping, we have examined the proteolysis of the von Willebrand factor (vWF) subunit with platelet calcium activated neutral protease (CANP) and human leukocyte elastase and found that they are not responsible for the proteolytic cleavage sejen in normal individuals and IIA vWD. Previously we have shown that in vivo proteolysis of vWF is a normal event with a small but consistent proportion of plasma vWF being composed of 189, 176, and
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Ma, J., J. A. Voynow, A. Kummarapurugu, S. Ghosh, and A. Hawkridge. "Neutrophil Elastase Mediates Macrophage Phagocytic Failure Via Increased Calpain Activity." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7447.

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Raporty organizacyjne na temat "Calpain"

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Mudryj, Maria. Calpain-Dependent Proteolysis of the Androgen Receptor. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada517269.

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Kim, Yuan, Edward M. Steadham, Steven M. Lonergan, and Elisabeth J. Huff-Lonergan. Antioxidant Capacity of Calcium Lactate on m-Calpain Activity In Vitro. Iowa State University, 2009. http://dx.doi.org/10.31274/ans_air-180814-1237.

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Tagliarino, Collen, and David A. Boothman. Exploiting an NQ01-Directed, Calpain-Medicated Apoptotic Pathway for Breast Cancer Therapy. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada398218.

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Maddock, K. R., Elisabeth J. Huff-Lonergan, and Steven M. Lonergan. The Effect of pH on µ-calpain Activity and Implications in Meat Tenderness. Iowa State University, 2005. http://dx.doi.org/10.31274/ans_air-180814-1109.

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Anderson, Mark J., Kathy T. Y. Mou, Cassie Gregorich, Edward M; Steadham, Steven M. Lonergan, and Elisabeth J. Huff-Lonergan. Proteolysis, Calpastatin Activity, and µ-Calpain Autolysis in Specific Muscles from the Beef Round. Iowa State University, 2008. http://dx.doi.org/10.31274/ans_air-180814-1234.

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Herradón, Bernardo. Calpaína y sus inhibidores. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), 2011. http://dx.doi.org/10.18567/sebbmdiv_anc.2011.07.1.

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Dettling, Mark, Diana Humple, Michael Mahoney, Mark Dettling, Diana Humple, and Michael Mahoney. Riparian landbird monitoring in Golden Gate National Recreation Area and Point Reyes National Seashore: Progress report for 2021?2023. National Park Service, 2024. http://dx.doi.org/10.36967/2305750.

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Point Blue Conservation Science (hereafter Point Blue) conducted landbird monitoring from 16 August 2021 through 15 August 2023 in predominantly riparian habitat found in Point Reyes National Seashore and Golden Gate National Recreation Area. This monitoring was on behalf of the National Park Service?s (NPS) Inventory and Monitoring (I&amp;M) Program. Progress reports, like this one, are intended to document the survey efforts and to provide a basic summary of the data collected. This progress report deviates slightly from the structure of previous progress reports by summarizing two years of
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