Gotowa bibliografia na temat „Calpain 2”
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Artykuły w czasopismach na temat "Calpain 2"
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 źródłaWang, Yubin, Yan Liu, Xiaoning Bi i Michel Baudry. "Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death". Cells 9, nr 12 (16.12.2020): 2698. http://dx.doi.org/10.3390/cells9122698.
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 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 źródłaMuniappan, Latha, Michihiro Okuyama, Aida Javidan, Devi Thiagarajan, Weihua Jiang, Jessica J. Moorleghen, Lihua Yang i in. "Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice". Arteriosclerosis, Thrombosis, and Vascular Biology 41, nr 5 (5.05.2021): 1694–709. http://dx.doi.org/10.1161/atvbaha.120.315546.
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 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 źródłaTheopold, U., M. Pintér, S. Daffre, Y. Tryselius, P. Friedrich, D. R. Nässel i D. Hultmark. "CalpA, a Drosophila calpain homolog specifically expressed in a small set of nerve, midgut, and blood cells." Molecular and Cellular Biology 15, nr 2 (luty 1995): 824–34. http://dx.doi.org/10.1128/mcb.15.2.824.
Pełny tekst źródłaRozprawy doktorskie na temat "Calpain 2"
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
Breiden, Maike [Verfasser], Michael [Akademischer Betreuer] Ehrmann i Markus [Akademischer Betreuer] Kaiser. "Charakterisierung der Interaktion von HTRA1 und Calpain 2 / Maike Breiden. Gutachter: Markus Kaiser. Betreuer: Michael Ehrmann". Duisburg, 2014. http://d-nb.info/1058323385/34.
Pełny tekst źródłaHowells, Anwen. "The impact of innate immune cells on immunopathology in dengue". Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:0a251372-4d0e-416d-ad3c-8e07e6729e1b.
Pełny tekst źródłaLiu, Tongzheng. "Regulation of Inflammtory Activation in Endothelial Cells by PIN1". The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1242756227.
Pełny tekst źródłaStroop, 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 źródłaSanchez, Brualla Irene. "The potassium-chloride cotransporter KCC2 : a new therapeutic target for spasticity and neuropathic pain". Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0677.
Pełny tekst źródłaSpasticity and neuropathic pain are two symptoms that arise frequently after a spinal cord injury. Spasticity is defined as an increase of the muscle tone contributing to cramps, whereas neuropathic pain consists of painful responses caused by a damaged nervous system. Both symptoms arise, in part, due to a loss of inhibition in the sublesional neural networks, linked to a downregulation of the expression of potassium-chloride cotransporter type 2 (KCC2). For inhibition to be efficient, the action of this protein, which extrudes chloride ions from neurons, is needed.The objective of this thesis is, therefore, to identify drugs capable of activating KCC2 to recover inhibition with the objective of treating spasticity and neuropathic pain.First, our results have proven that the activation of serotonin receptors 5-HT2A with TCB-2 restores KCC2 expression in the dorsal horn after a spinal cord or peripheral nerve injury. However, TCB-2 reduces neuropathic pain after a spinal cord injury exclusively.In the next stage of the work, we have identified prochlorperazine as an enhancer of KCC2 activity. Prochlorperazine is efficient against spasticity, although it only showed a modest reduction of mechanical hyperalgesia in animals with a spinal cord injury.Lastly, we have proven that KCC2 downregulation and motoneuron hyperexcitability after a spinal cord injury depend on the overactivation of calpains.This thesis validates KCC2 as a druggable target to treat spasticity and neuropathic pain after spinal cord injury
Muir, Matthew Stewart. "Proteomics of the ovine cataract". Diss., Lincoln University, 2008. http://hdl.handle.net/10182/792.
Pełny tekst źródłaRuppert, Anne-Marie. "Rôle des calpaïnes extracellulaires dans la progression des adénocarcinomes lépidiques". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066317/document.
Pełny tekst źródłaCalpain 1 is pro inflammatory calcium-activated cysteine proteases, which can be partly externalized. Extracellular calpains limit inflammatory processes and promote tissue repair, through cell proliferation and migration. Toll like receptor (TLR) 2 has been identified as a target of extracellular calpains in lymphocytes. The aim was to investigate the role of extracellular calpain 1 in tumor progression of lepidic pulmonary adenocarcinoma (LPA). Extracellular calpain 1, soluble fragment of TLR2 and cytokines were analyzed by ELISA in bronchoalveolar lavage fluid (BALF) supernatants from patients with LPA (n=68). Source of calpain was analyzed by immunohistochemistry. TLR2 as target of extracellular calpain was studied by flow cytometry on polymorphonuclear neutrophils (PMN) and human lung cancer cell lines. Extracellular Calpain 1, secreted by tumor cells, was associated to tumor progression, neutrophilic inflammation, with a poor prognostic factor on survival (p=0,003). TLR2 was expressed on PMN or tumor cells and decreased after calpain treatment. The soluble fragment of TLR2 was correlated to the extracellular calpain 1 concentration in the BALF supernatants (r=0.624; p<0.001). High soluble fragment of TLR2 was associated with tumor progression and a pro-inflammatory environment. Extracellular Calpain 1 secreted by tumor cell, promotes inflammatory microenvironment and tumor progression through TLR2 in LPA
Hanna, Rachel. "REGULATION OF CALPAIN 2 BY CALPASTATIN". Thesis, 2010. http://hdl.handle.net/1974/5639.
Pełny tekst źródłaThesis (Ph.D, Biochemistry) -- Queen's University, 2010-04-29 15:27:16.208
Lal, Sangeet Kumar. "Calpain 2 proteolysis regulates glioblastoma cell invasion". Thesis, 2010. http://hdl.handle.net/1957/19988.
Pełny tekst źródłaGraduation date: 2011
Access restricted to the OSU Community at author's request from Jan. 31, 2011 - Jan. 31, 2012
Części książek na temat "Calpain 2"
Carragher, Neil O. "Calpain". W Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_782-2.
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 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 źródłaPénisson-Besnier, I., I. Richard, F. Dubas, J. S. Beckmann i M. Fardeau. "Exercise Intolerance in Calpain Deficiency and in α-Sarcoglycanopathy". W Exercise Intolerance and Muscle Contracture, 63–66. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0855-0_6.
Pełny tekst źródłaSorimachi, Hiroyuki, Shoji Hata i Yasuko Ono. "Calpain-2/m-Calpain". W Handbook of Proteolytic Enzymes, 2007–11. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-382219-2.00454-3.
Pełny tekst źródła"Calpain-2". W Class 3 Hydrolases, 61–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-85705-1_7.
Pełny tekst źródłaRandriamboavonjy, Voahanginirina, i Ingrid Fleming. "The Role of Calpain in Diabetes-Associated Platelet Hyperactivation". W Cardiovascular Pharmacology - Heart and Circulation, 235–57. Elsevier, 2010. http://dx.doi.org/10.1016/s1054-3589(10)59008-2.
Pełny tekst źródłaStreszczenia konferencji na temat "Calpain 2"
Singh, Vinay K., Jacqueline C. Kelly, R. John MacLeod i Zongchao Jia. "Abstract 4226: Curcumin induced CaSR stimulates calpain autolysis in colon cancer". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4226.
Pełny tekst źródłaSupinski, Gerald S., Alexander Alimov, Lin Wang, Xiao-Hong Song i Leigh Ann P. Callahan. "NSmase 2 Is Required For Infection Induced Skeletal Muscle Calpain Activation". W 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.a2716.
Pełny tekst źródłaColman, 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 źródłaPuri, R. N., F. Zhou, H. Bradford, E. J. Gustafson, R. F. Colman i R. W. Colman. "HIGH MOLECULAR WEIGHT KININOGEN SPECIFICALLY BLOCKS THROMBIN-INDUCED AGGREGATION BY INHIBITING PLATELET CALPAIN". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643860.
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 źródłaLandowski, Terry H., Aluvia M. Escalante, Ryan McGrath, Matthew R. Karolak, Meredith Henderson, Georgia O. Perrian i Ron Lynch. "Abstract 2643: Inhibition of calpain disrupts the autophagic response initiated by bortezomib resulting in increased death of myeloma cells". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2643.
Pełny tekst źródłaWallace, Robert W., E. Ann Tallant i Lynn M. Brumley. "POSSIBLE ROLE FOR THE CA2+-DEPENDENT PROTEASE (CALPAIN I) AS AN IRREVERSIBLE ACTIVATOR OF CA2+/CALMODULIN-MEDIATED REACTIONS IN THE HUMAN PLATELET". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644528.
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 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.
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