Gotowa bibliografia na temat „Calpain 1”
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Artykuły w czasopismach na temat "Calpain 1"
Upla, Paula, Varpu Marjomäki, Liisa Nissinen, Camilla Nylund, Matti Waris, Timo Hyypiä i Jyrki Heino. "Calpain 1 and 2 Are Required for RNA Replication of Echovirus 1". Journal of Virology 82, nr 3 (21.11.2007): 1581–90. http://dx.doi.org/10.1128/jvi.01375-07.
Pełny tekst źródłaWeber, Jonasz J., Eva Haas, Yacine Maringer, Stefan Hauser, Nicolas L. P. Casadei, Athar H. Chishti, Olaf Riess i Jeannette Hübener-Schmid. "Calpain-1 ablation partially rescues disease-associated hallmarks in models of Machado-Joseph disease". Human Molecular Genetics 29, nr 6 (21.01.2020): 892–906. http://dx.doi.org/10.1093/hmg/ddaa010.
Pełny tekst źródłaBen-Aharon, Irit, Paula R. Brown, Nir Etkovitz, Edward M. Eddy i Ruth Shalgi. "The expression of calpain 1 and calpain 2 in spermatogenic cells and spermatozoa of the mouse". Reproduction 129, nr 4 (kwiecień 2005): 435–42. http://dx.doi.org/10.1530/rep.1.00255.
Pełny tekst źródłaBaudry, Michel. "Calpain-1 and Calpain-2 in the Brain: Dr. Jekill and Mr Hyde?" Current Neuropharmacology 17, nr 9 (22.08.2019): 823–29. http://dx.doi.org/10.2174/1570159x17666190228112451.
Pełny tekst źródłaMurphy, Robyn M., Rodney J. Snow i Graham D. Lamb. "μ-Calpain and calpain-3 are not autolyzed with exhaustive exercise in humans". American Journal of Physiology-Cell Physiology 290, nr 1 (styczeń 2006): C116—C122. http://dx.doi.org/10.1152/ajpcell.00291.2005.
Pełny tekst źródłaMcCartney, Christian-Scott E., Qilu Ye, Robert L. Campbell i Peter L. Davies. "Insertion sequence 1 from calpain-3 is functional in calpain-2 as an internal propeptide". Journal of Biological Chemistry 293, nr 46 (25.09.2018): 17716–30. http://dx.doi.org/10.1074/jbc.ra118.004803.
Pełny tekst źródłaCovington, Marisa D., David D. Arrington i Rick G. Schnellmann. "Calpain 10 is required for cell viability and is decreased in the aging kidney". American Journal of Physiology-Renal Physiology 296, nr 3 (marzec 2009): F478—F486. http://dx.doi.org/10.1152/ajprenal.90477.2008.
Pełny tekst źródłaPiper, Ann-Katrin, Reece A. Sophocleous, Samuel E. Ross, Frances J. Evesson, Omar Saleh, Adam Bournazos, Joe Yasa i in. "Loss of calpains-1 and -2 prevents repair of plasma membrane scrape injuries, but not small pores, and induces a severe muscular dystrophy". American Journal of Physiology-Cell Physiology 318, nr 6 (1.06.2020): C1226—C1237. http://dx.doi.org/10.1152/ajpcell.00408.2019.
Pełny tekst źródłaPánico, Pablo, Marcia Hiriart, Patricia Ostrosky-Wegman i Ana María Salazar. "TUG is a calpain-10 substrate involved in the translocation of GLUT4 in adipocytes". Journal of Molecular Endocrinology 65, nr 3 (październik 2020): 45–57. http://dx.doi.org/10.1530/jme-19-0253.
Pełny tekst źródłaOu, B. R., i N. E. Forsberg. "Determination of skeletal muscle calpain and calpastatin activities during maturation". American Journal of Physiology-Endocrinology and Metabolism 261, nr 6 (1.12.1991): E677—E683. http://dx.doi.org/10.1152/ajpendo.1991.261.6.e677.
Pełny tekst źródłaRozprawy doktorskie na temat "Calpain 1"
Ishak, Reezal. "Calpain-1 : investigating its role in murine neutrophils". Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/37448/.
Pełny tekst źródłaHanouna, Guillaume. "Rôle des calpaïnes dans le vieillissement et la réponse anti-tumorale". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066385/document.
Pełny tekst źródłaCalpain 1 and 2 are cysteine proteases and calpastatin is their natural inhibitor. Calpains and calpastatin are ubiquitous. Calpains are involved in inflammatory response development via activation by partial proteolysis of several substrates (NF-kappaB activation by I-kappaBalpha cleavage, remodeling of inflammatory cells cytoskeleton, cleavage of chaperone protein HSP90 ... ). It has been previously shown that calpains promote neuronal aging. We have shown in a mouse model that inhibition of calpain by calpastatin overexpression limits renal and vascular aging. The inflammation associated with aging or "inflammaging" is considerably reduced by specific inhibition of calpain. This is due, at least in part, to calpain effect on production of pro-inflammatory cytokines and in maturation of interleukin-1 alpha. If intracellular calpains are pro-inflammatory, secreted calpains have an anti-inflammatory effect via cleavage of TLR2. Calpains can indeed be excreted out of the cells via the transporter ABCA1. In the context of a mouse model of melanoma, we have shown that inhibition of extracellular calpain by only extracellular calpastatin overexpression preserves TLR2 and thus limit the progression of the tumor.Calpains intra- and extracellular are major mediators of inflammatory response and modulate the "inflammaging" and the anti-tumor immune response
Mendes, Atlante Silva. "Verapamil diminui a expressão proteica de calpaína-1 e metaloproteinase de matriz-2 na hipertrofia cardíaca induzida por hipertensão renovascular". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-08112018-150232/.
Pełny tekst źródłaIntroduction: The chronic hemodynamic overload-induced cardiac hypertrophy (CH) is characterized by thickening of the left ventricle walls and hypertrophy of the cardiomyocytes and interstitial tissue. Increased activity of calpain-1 and matrix metalloproteinase(MMP)-2 was observed in different models of arterial hypertension models and contributes to the pathophysiologic changes shown in CH. On the other hand, MMP-2 activity is also positively modulated by activation of calpain-1 in different animal models of cardiovascular diseases. The objectives here are to analyze whether calpain-1 contributes to increase the activity of MMP-2 in the heart and whether this mechanism results in chronic cardiac changes in the renovascular hypertension. Methods: Two kidney-one clip (2K1C) hypertensive male Wistar rats (180-200g) and their respective controls (Sham) were orally treated with verapamil (VRP), a L-type calcium channels blocker (LCCB, 8mg/kg/bid), or vehicle during 8 weeks. The LCCB reduces the intracellular concentration of calcium, thus decreasing the activation of calpain-1, and then may modulate the activity of MMP-2. Systolic blood pressure (SBP) was monitored in the rats during 10 weeks of hypertension. Left ventricle (LV) was analyzed by histology and echocardiography to evaluate ventricle thickening. Calpain- 1 and MMP-2 activities were analyzed by zymography and their expression by immunofluorescence and western blot. Hearts were submitted to functional evaluation by Langendorff. All the protocols were approved by the Ethical Committee in Animal Research of Ribeirao Preto Medical School (43/2017). Results: After 10 weeks, the systolic blood pressure had sustained increase and treatment with VRP was not able to decrease it in any time of hypertension. The body weight did not present significant changes between the groups. Hypertensive group had significant increase in the ventricle/body weight ratio (VW/BW) when compared to sham and treatment with VRP decreased it. Analysis of ventricle thickening showed that VRP is able to revert CHinduced pressure overload. The 2K-1C rats showed a significant increase in the activity and expression of calpain-1 in the heart and VRP reverted it. It was also observed increased activity of MMP-2 forms in the hypertensive rats and VRP decreased the 64kDa MMP-2 activity. The 2K-1C group had cardiac dysfunction when compared to controls groups, and VRP did not alter it. The ejection fraction was not changed in 2K- 1C rats. Conclusion: VRP decreased expression and activity of calpain-1 and MMP-2 in the hearts of 2K-1C rats and then contributed to ameliorate hypertension-induced cardiac hypertrophy
Marion, Allison. "La calpaïne - 6 : une nouvelle cible thérapeutique dans les ostéosarcomes". Paris 7, 2011. http://www.theses.fr/2011PA077134.
Pełny tekst źródłaOsteosarcomas are chemoresistant tumours that frequently relapse and metastasize. The aim of this study is to identify new mechanisms involved in the regulation of cellular response to cytotoxic agents. We previously showed that syndecan-2 controls apoptosis and cell response to cytotoxic agent in ostosarcomas. To identify new factors involved in osteosarcoma cell survival, we examined genes modified upon syndecan-2 overexpression using a microarray analysis. We found that calpain-6 is one of the genes significantly down-regulated by syndecan-2. We have demonstrated that syndecan-2 modulates Endothelin-1 dependent signalling to reduce calpain-6 expression including PI3K, ERK1/2 and NF-KB signaling pathways. We have also showed that calpain-6 is abnormally expressed in osteosarcoma compared to osteoblastic cell Unes and in tumours. Moreover, we have established an inverse relationship between calpain-6 expression and response to chemotherapy. We have observed a strong calpain-6 expression in recurrent tumours and in resistant cells to doxorubicin. We have showed that calpain-6 inhibition with shRNA increases apoptosis induced by chemotherapy. We identified calpain-6 as a protective factor in osteosarcoma cells. We also showed that RANKL and hypoxia cooperate to induce calpain-6 expression in osteosarcoma cells but also in cancer cells that could metastasize to the bone like breast and prostate cancer cells. Our results led us to identify calpain-6 as a new factor implicated in résistance to chemotherapy in bone cancer cells. Calpain-6 appears to be modulated by the microenvironment. It could be a new therapeutic target to improve response to chemotherapeutic agents
Peltier, Julie. "Implication du TGF-BETA1 et des calpaïnes dans la glomérulopathie induite par les anticorps anti-membrane basale glomérulaire". Paris 7, 2006. http://www.theses.fr/2006PA077129.
Pełny tekst źródłaInflammatory process in qlomerulonephritis is regulated by many mediators. Of them, transforming qrowth factor-beta1 (TGF-β1) may act as an anti-inflammatory agent. In contrary, calpain, a calcium-activated neutral cysteine protease, participates in the development of inflammation. We first demonstrate that TGF-β1 increase glucocorticoid receptor (GR) synthesis by macrophages after activation of Smad 2/3 and AP-1. And increase the ability of GR to deactivate macrophages. Second, we show that in glomerulonephritis, calpain activity is increased in the kidney cortex, and that in parallel. Active calpains appear in the urines. These calpains oriqinate mainly from abnormal transglomerular passage of plasma proteins and from tubular secretion. Active calpains in the renal cortex promote glomerular injury through activation of NF-KB. While urinary calpains are responsible for the shedding of nephrin from the surface of podocytes. Thereby worsening proteinura
Stroop, Davis M. "The Epidemiology of Early Type 2 Diabetes Mellitus in Black and White Females: Genetic and Environmental Factors". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1377870493.
Pełny tekst źródłaMuir, Matthew Stewart. "Proteomics of the ovine cataract". Diss., Lincoln University, 2008. http://hdl.handle.net/10182/792.
Pełny tekst źródłaKriegel, Christian. "Untersuchungen zur kapazitationsassoziierten Signaltransduktion in humanen Spermatozoen und Evaluation des MACS-Verfahrens zur Ejakulataufbereitung". Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-114339.
Pełny tekst źródłaMoubarak, Rana. "Caractérisation de la voie de mort cellulaire programmée induite par le dommage à l'ADN : rôles de PARP-1, calpaine, Bax et AIF". Paris 6, 2007. http://www.theses.fr/2007PA066045.
Pełny tekst źródłaFromberg, Iris [Verfasser]. "Immunhistochemische Untersuchungen zur Expression von Calpain 1, Calpain 2 und Calpastatin in Endometrium- und Ovarialkarzinom / vorgelegt von Iris Fromberg". 2009. http://d-nb.info/1006602755/34.
Pełny tekst źródłaKsiążki na temat "Calpain 1"
Messer, Jeannette S., red. Calpain. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1.
Pełny tekst źródłaCzęści książek na temat "Calpain 1"
van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis i in. "Calpain". W Encyclopedia of Signaling Molecules, 225–28. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_23.
Pełny tekst źródłaCarragher, Neil O. "Assaying Calpain Activity". W Adhesion Protein Protocols, 109–19. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-353-0_9.
Pełny tekst źródłaBiswas, Ashim Kumar, i Samarth Tandon. "Casein Zymography for Analysis of Calpain-1 and Calpain-2 Activity". W Methods in Molecular Biology, 31–38. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_3.
Pełny tekst źródłaNguyen, Anh T. H., Matthew Campbell, Paul F. Kenna, Anna-Sophia Kiang, Lawrence Tam, Marian M. Humphries i Peter Humphries. "Calpain and Photoreceptor Apoptosis". W Retinal Degenerative Diseases, 547–52. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_69.
Pełny tekst źródłaBiswas, Ashim Kumar, i Samarth Tandon. "Single-Step Purification of Calpain-1, Calpain-2, and Calpastatin Using Anion-Exchange Chromatography". W Methods in Molecular Biology, 3–11. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_1.
Pełny tekst źródłaWang, Kevin K. W. "Calpain Zymography: General Methodology and Protocol". W Zymography, 279–85. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7111-4_26.
Pełny tekst źródładel Carmen Lafita-Navarro, Maria, i Maralice Conacci-Sorrell. "Identification of Calpain-Activated Protein Functions". W Methods in Molecular Biology, 149–60. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_12.
Pełny tekst źródłaSamanta, Krishna, Pulak Kar, Tapati Chakraborti i Sajal Chakraborti. "An Overview of Endoplasmic Reticulum Calpain System". W Proteases in Health and Disease, 3–19. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9233-7_1.
Pełny tekst źródładuVerle, David A., i Hiroshi Mamitsuka. "CalCleaveMKL: a Tool for Calpain Cleavage Prediction". W Methods in Molecular Biology, 121–47. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_11.
Pełny tekst źródłaKitagawa, Seiichi. "Experimental Manipulation of Calpain Activity In Vitro". W Methods in Molecular Biology, 209–18. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_16.
Pełny tekst źródłaStreszczenia konferencji na temat "Calpain 1"
Colman, Robert W., Harlan Bradford i Anjanayaki Annamalai. "FACTOR V IS ACTIVATED AND CLEAVED BY PLATELET CALPAIN: COMPARISON WITH THROMBIN PROTEOLYSIS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643884.
Pełny tekst źródłaverhallen, P. F. J., E. M. Bevers, P. Comfurius, W. M. A. Linkskens i R. F. A. Zwaal. "CALPAIN-MEDIATED CYTOSKELETAL DEGRADATION CORRELATES WITH STIMULATION OF PLATELET PROCOAGULANT ACTIVITY". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642821.
Pełny tekst źródłaOh, Eunhye, Daeil Sung, Youngkwan Cho, Ji Young Kim, Nahyun Lee, Yoon-Jae Kim, Tae-Min Cho i Jae Hong Seo. "Abstract 5463: Disulfiram suppresses metastasis via induction of anoikis and calpain activation in triple-negative breast cancer". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5463.
Pełny tekst źródłaOkita, J. R., M. M. Frojmovic, S. Kristopeit, T. Wong i T. J. Kunicki. "MONTREAL PLATELET SYNDROME: DECREASED ACTIVITY OF PLATELET CALPAINS ASSOCIATED WITH AGGREGATION ABNORMALITIES". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642822.
Pełny tekst źródłaChoo, Y., T. Sakai, R. Ikebe, A. Jeffers, S. Idell, T. A. Tucker i M. Ikebe. "Calponin 1 Promotes Myofibroblast Differentiation of Human Pleural Mesothelial Cells During Mesothelial Mesenchymal Transition". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4420.
Pełny tekst źródłaBerndt, M. "STRUCTURE AND FUNCTION OF THE GLYCOPROTEIN Ib-IX COMPLEX". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643729.
Pełny tekst źródłaDriscoll, Tristan P., Su-Jin Heo i Robert L. Mauck. "Dynamic Tensile Loading and Altered Cell Contractility Modulate Nuclear Deformation and Cytoskeletal Connectivity". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80550.
Pełny tekst źródłaLavenne-Pardonge, E., C. Col-De Beys, R. Dion, R. Ponlot i M. Moriau. "EFFECT OF ANTIAGGREGANT ON OCCLUSION OF SAPHENOUS GRAFT CORONARY BYPASS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644823.
Pełny tekst źródłaIshiguro, H., S. Higashiyama, C. Namikawa, I. Ohkubo i M. Sasaki. "MAPPING OF FUNCTIONAL DOMAINS OF HUMAN HIGH MOLECULAR WEIGHT (HMW) AND LOW MOLECULAR WEIGHT (LMW) KININOGENS BY USING MURINE MONOCLONAL ANTIBODIES (MAbs)". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642849.
Pełny tekst źródłaMcCarrick, Michael T., i Robert K. Rosencrance. "World’s First LM5000 to LM6000 Cogeneration Plant Repowering". W ASME Turbo Expo 2000: Power for Land, Sea, and Air. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/2000-gt-0190.
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