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Artykuły w czasopismach na temat „Calpain 1”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 19 lutego 2022

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1

Upla, Paula, Varpu Marjomäki, Liisa Nissinen, Camilla Nylund, Matti Waris, Timo Hyypiä, and Jyrki Heino. "Calpain 1 and 2 Are Required for RNA Replication of Echovirus 1." Journal of Virology 82, no. 3 (November 21, 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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Weber, Jonasz J., Eva Haas, Yacine Maringer, Stefan Hauser, Nicolas L. P. Casadei, Athar H. Chishti, Olaf Riess, and Jeannette Hübener-Schmid. "Calpain-1 ablation partially rescues disease-associated hallmarks in models of Machado-Joseph disease." Human Molecular Genetics 29, no. 6 (January 21, 2020): 892–906. http://dx.doi.org/10.1093/hmg/ddaa010.

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Abstract Proteolytic fragmentation of polyglutamine-expanded ataxin-3 is a concomitant and modifier of the molecular pathogenesis of Machado–Joseph disease (MJD), the most common autosomal dominant cerebellar ataxia. Calpains, a group of calcium-dependent cysteine proteases, are important mediators of ataxin-3 cleavage and implicated in multiple neurodegenerative conditions. Pharmacologic and genetic approaches lowering calpain activity showed beneficial effects on molecular and behavioural disease characteristics in MJD model organisms. However, specifically targeting one of the calpain isofo
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3

Ben-Aharon, Irit, Paula R. Brown, Nir Etkovitz, Edward M. Eddy, and Ruth Shalgi. "The expression of calpain 1 and calpain 2 in spermatogenic cells and spermatozoa of the mouse." Reproduction 129, no. 4 (April 2005): 435–42. http://dx.doi.org/10.1530/rep.1.00255.

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There is some evidence suggesting that Ca2+is involved in processes that occur during the development and function of spermatozoa. Calcium-dependent proteins, such as calmodulin, are expressed during mammalian spermatogenesis further suggesting that Ca2+takes part in its regulation. However, the precise roles of Ca2+in spermatogenesis remain to be elucidated. Calpains are a family of Ca2+-dependent cysteine proteases whose members are expressed ubiquitously or in a tissue-specific manner. Calpain has been demonstrated to mediate specific Ca2+-dependent processes including cell fusion, mitosis
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4

Baudry, Michel. "Calpain-1 and Calpain-2 in the Brain: Dr. Jekill and Mr Hyde?" Current Neuropharmacology 17, no. 9 (August 22, 2019): 823–29. http://dx.doi.org/10.2174/1570159x17666190228112451.

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While the calpain system has now been discovered for over 50 years, there is still a paucity of information regarding the organization and functions of the signaling pathways regulated by these proteases, although calpains play critical roles in many cell functions. Moreover, calpain overactivation has been shown to be involved in numerous diseases. Among the 15 calpain isoforms identified, calpain-1 (aka µ-calpain) and calpain-2 (aka m-calpain) are ubiquitously distributed in most tissues and organs, including the brain. We have recently proposed that calpain-1 and calpain- 2 play op
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5

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 (січень 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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6

McCartney, Christian-Scott E., Qilu Ye, Robert L. Campbell, and Peter L. Davies. "Insertion sequence 1 from calpain-3 is functional in calpain-2 as an internal propeptide." Journal of Biological Chemistry 293, no. 46 (September 25, 2018): 17716–30. http://dx.doi.org/10.1074/jbc.ra118.004803.

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Calpains are intracellular, calcium-activated cysteine proteases. Calpain-3 is abundant in skeletal muscle, where its mutation-induced loss of function causes limb-girdle muscular dystrophy type 2A. Unlike the small subunit–containing calpain-1 and -2, the calpain-3 isoform homodimerizes through pairing of its C-terminal penta-EF-hand domain. It also has two unique insertion sequences (ISs) not found in the other calpains: IS1 within calpain-3's protease core and IS2 just prior to the penta-EF-hand domain. Production of either native or recombinant full-length calpain-3 to characterize the fun
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7

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 (March 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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8

Piper, Ann-Katrin, Reece A. Sophocleous, Samuel E. Ross, Frances J. Evesson, Omar Saleh, Adam Bournazos, Joe Yasa, et al. "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, no. 6 (June 1, 2020): C1226—C1237. http://dx.doi.org/10.1152/ajpcell.00408.2019.

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The ubiquitous calpains, calpain-1 and -2, play important roles in Ca2+-dependent membrane repair. Mechanically active tissues like skeletal muscle are particularly reliant on mechanisms to repair and remodel membrane injury, such as those caused by eccentric damage. We demonstrate that calpain-1 and -2 are master effectors of Ca2+-dependent repair of mechanical plasma membrane scrape injuries, although they are dispensable for repair/removal of small wounds caused by pore-forming agents. Using CRISPR gene-edited human embryonic kidney 293 (HEK293) cell lines, we established that loss of both
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9

Pánico, Pablo, Marcia Hiriart, Patricia Ostrosky-Wegman, and Ana María Salazar. "TUG is a calpain-10 substrate involved in the translocation of GLUT4 in adipocytes." Journal of Molecular Endocrinology 65, no. 3 (October 2020): 45–57. http://dx.doi.org/10.1530/jme-19-0253.

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The calpain-10 (CAPN10) protease is implicated in the translocation of the glucose transporter 4 (GLUT4), which is retained in the Golgi matrix via the Tether containing a UBX domain for GLUT4 (TUG) protein. Insulin stimulation induces the proteolytic processing of TUG, which leads to the translocation of GLUT4 to the cell membrane. We tested whether TUG is a CAPN10 substrate. Proteolysis of TUG by calpains was assessed using a cell-free system containing calpain-1 and TUG. In situ proteolysis of TUG by calpains was demonstrated in 3T3-L1 adipocytes in the presence of insulin or calpain inhibi
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10

Ou, B. R., and N. E. Forsberg. "Determination of skeletal muscle calpain and calpastatin activities during maturation." American Journal of Physiology-Endocrinology and Metabolism 261, no. 6 (December 1, 1991): E677—E683. http://dx.doi.org/10.1152/ajpendo.1991.261.6.e677.

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Our objectives were to characterize events underlying changes in skeletal muscle calpain and calpastatin activities, using maturation as a model. Muscle samples were taken from rabbits of four ages (newborn and 1, 2, and 5 mo old). Concentrations of RNA and protein and activities of calpains I and II and calpastatin were determined. Steady-state concentrations of mRNAs encoding calpain I, calpain II, calpastatin, alpha- and beta-tubulin, and beta-actin were determined using Northern blot analysis. Calpain and calpastatin activities declined markedly between birth and 1 mo of age and remained u
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11

Wang, Yubin, Yan Liu, Xiaoning Bi, and Michel Baudry. "Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death." Cells 9, no. 12 (December 16, 2020): 2698. http://dx.doi.org/10.3390/cells9122698.

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Calpains are a family of soluble calcium-dependent proteases that are involved in multiple regulatory pathways. Our laboratory has focused on the understanding of the functions of two ubiquitous calpain isoforms, calpain-1 and calpain-2, in the brain. Results obtained over the last 30 years led to the remarkable conclusion that these two calpain isoforms exhibit opposite functions in the brain. Calpain-1 activation is required for certain forms of synaptic plasticity and corresponding types of learning and memory, while calpain-2 activation limits the extent of plasticity and learning. Calpain
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12

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 (February 1, 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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Kuchay, Shafi M., William P. Fay, and Athar H. Chishti. "Double Knockouts Reveal That Protein Tyrosine Phosphatase 1B Is a Physiological Substrate of Calpain-1 in Platelets." Blood 108, no. 11 (November 16, 2006): 396. http://dx.doi.org/10.1182/blood.v108.11.396.396.

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Abstract Calpains are ubiquitous calcium-regulated cysteine proteases that have been implicated in cytoskeletal organization, cell proliferation, apoptosis, cell motility, and hemostasis. Previously we used gene-targeting to evaluate the physiological function of mouse calpain-1, and established that its inactivation results in reduced platelet aggregation and clot retraction, potentially by causing dephosphorylation of platelet proteins. Here, we present data showing that calpain-1 null platelets accumulate protein tyrosine phosphatase 1B (PTP1B) that correlates with enhanced tyrosine phospha
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Moshal, Karni S., Mahavir Singh, Utpal Sen, Dorothea Susanne E. Rosenberger, Brooke Henderson, Neetu Tyagi, Hong Zhang, and Suresh C. Tyagi. "Homocysteine-mediated activation and mitochondrial translocation of calpain regulates MMP-9 in MVEC." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (December 2006): H2825—H2835. http://dx.doi.org/10.1152/ajpheart.00377.2006.

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Hyperhomocysteinemia (HHcy) is associated with atherosclerosis, stroke, and dementia. Hcy causes extracellular matrix remodeling by the activation of matrix metalloproteinase-9 (MMP-9), in part, by inducing redox signaling and modulating the intracellular calcium dynamics. Calpains are the calcium-dependent cysteine proteases that are implicated in mitochondrial damage via oxidative burst. Mitochondrial abnormalities have been identified in HHcy. The mechanism of Hcy-induced extracellular matrix remodeling by MMP-9 activation via mitochondrial pathway is largely unknown. We report a novel role
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Vermaelen, Marianne, Pascal Sirvent, Fabrice Raynaud, Catherine Astier, Jacques Mercier, Alain Lacampagne, and Olivier Cazorla. "Differential localization of autolyzed calpains 1 and 2 in slow and fast skeletal muscles in the early phase of atrophy." American Journal of Physiology-Cell Physiology 292, no. 5 (May 2007): C1723—C1731. http://dx.doi.org/10.1152/ajpcell.00398.2006.

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Calpains have been proposed to be involved in the cytoskeletal remodeling and wasting of skeletal muscle. However, limited data are available about the specific involvement of each calpain in the early stages of muscle atrophy. The aims of this study were to determine whether calpains 1 and 2 are autolyzed after a short period of muscle disuse, and, if so, where in the myofibers the autolyzed products are localized. In the rat soleus muscle, 5 days of immobilization increased autolyzed calpain 1 in the particulate and not the soluble fraction. Conversely, autolyzed calpain 2 was not found in t
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Liu, Xiuli, Juanita J. Rainey, Jay F. Harriman, and Rick G. Schnellmann. "Calpains mediate acute renal cell death: role of autolysis and translocation." American Journal of Physiology-Renal Physiology 281, no. 4 (October 1, 2001): F728—F738. http://dx.doi.org/10.1152/ajprenal.2001.281.4.f728.

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The goals of this study were to determine 1) the expression of calpain isoforms in rabbit renal proximal tubules (RPT); 2) calpain autolysis and translocation, and calpastatin levels during RPT injury; and 3) the effect of a calpain inhibitor (PD-150606) on calpain levels, mitochondrial function, and ion transport during RPT injury. RT-PCR, immunoblot analysis, and FITC-casein zymography demonstrated the presence of only μ- and m-calpains in rabbit RPT. The mitochondrial inhibitor antimycin A decreased RPT μ- and m-calpain and calpastatin levels in conjunction with cell death and increased pla
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17

Elagib, Kamaleldin E., Lorrie L. Delehanty, Ivailo Mihaylov, and Adam Goldfarb. "Calpain Regulation of Megakaryopoiesis through a Positive Regulatory Loop Involving P-TEFb, GATA-1, and RUNX1." Blood 114, no. 22 (November 20, 2009): 566. http://dx.doi.org/10.1182/blood.v114.22.566.566.

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Abstract Abstract 566 GATA-1 and RUNX1 cooperate in programming megakaryocytic development through the critical intermediation of the active P-TEFb kinase complex (Cdk9/cyclin T1). RUNX1 on its own traps P-TEFb in inactive chromatin loops and causes RNA pol II (RNAP II) stalling. GATA-1 by contrast remodels chromatin loops and promotes RNAP II elongation. Thus, P-TEFb most likely integrates and resolves conflicting signals from RUNX1 and GATA-1 to coordinate orderly activation of megakaryocytic target genes during development. P-TEFb activity is tightly regulated by a large network of interact
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Larsen, Anna K., René Lametsch, John S. Elce, Jørgen K. Larsen, Bo Thomsen, Martin R. Larsen, Moira A. Lawson, Peter A. Greer, and Per Ertbjerg. "Genetic disruption of calpain correlates with loss of membrane blebbing and differential expression of RhoGDI-1, cofilin and tropomyosin." Biochemical Journal 411, no. 3 (April 14, 2008): 657–66. http://dx.doi.org/10.1042/bj20070522.

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Dynamic regulation of the actin cytoskeleton is important for cell motility, spreading and the formation of membrane surface extensions such as lamellipodia, ruffles and blebs. The ubiquitous calpains contribute to integrin-mediated cytoskeletal remodelling during cell migration and spreading, by cleavage of focal adhesion components and signalling molecules. In the present study, the live-cell morphology of calpain-knockout and wild-type cells was examined by time-lapse fluorescence microscopy, and a role of calpain in mediating the formation of sporadic membrane blebs was established. Membra
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Muniappan, Latha, Michihiro Okuyama, Aida Javidan, Devi Thiagarajan, Weihua Jiang, Jessica J. Moorleghen, Lihua Yang, et al. "Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 5 (May 5, 2021): 1694–709. http://dx.doi.org/10.1161/atvbaha.120.315546.

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Objective: Cytoskeletal structural proteins maintain cell structural integrity by bridging extracellular matrix with contractile filaments. During abdominal aortic aneurysm (AAA) development, (1) aortic medial degeneration is associated with loss of smooth muscle cell integrity and (2) fibrogenic mesenchymal cells mediate extracellular matrix remodeling. Calpains cleave cytoskeletal proteins that maintain cell structural integrity. Pharmacological inhibition of calpains exert beneficial effects on Ang II (angiotensin II)–induced AAAs in LDLR −/− (low-density receptor deficient) mice. Here, we
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Wieschhaus, Adam, Anwar Khan, Asma Zaidi, Henry Rogalin, Toshihiko Hanada, Fei Liu, Lucia De Franceschi, Carlo Brugnara, Alicia Rivera, and Athar H. Chishti. "Calpain-1 knockout reveals broad effects on erythrocyte deformability and physiology." Biochemical Journal 448, no. 1 (October 18, 2012): 141–52. http://dx.doi.org/10.1042/bj20121008.

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Pharmacological inhibitors of cysteine proteases have provided useful insights into the regulation of calpain activity in erythrocytes. However, the precise biological function of calpain activity in erythrocytes remains poorly understood. Erythrocytes express calpain-1, an isoform regulated by calpastatin, the endogenous inhibitor of calpains. In the present study, we investigated the function of calpain-1 in mature erythrocytes using our calpain-1-null [KO (knockout)] mouse model. The calpain-1 gene deletion results in improved erythrocyte deformability without any measurable effect on eryth
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Gafni, Juliette, Evan Hermel, Jessica E. Young, Cheryl L. Wellington, Michael R. Hayden, and Lisa M. Ellerby. "Inhibition of Calpain Cleavage of Huntingtin Reduces Toxicity." Journal of Biological Chemistry 279, no. 19 (February 23, 2004): 20211–20. http://dx.doi.org/10.1074/jbc.m401267200.

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Huntington's disease (HD) is a neurodegenerative disorder caused by a polyglutamine (polyQ) tract expansion near the N terminus of huntingtin (Htt). Proteolytic processing of mutant Htt and abnormal calcium signaling may play a critical role in disease progression and pathogenesis. Recent work indicates that calpains may participate in the increased and/or altered patterns of Htt proteolysis leading to the selective toxicity observed in HD striatum. Here, we identify two calpain cleavage sites in Htt and show that mutation of these sites renders the polyQ expanded Htt less susceptible to prote
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Kuchay, Shafi M., Nayoung Kim, Elizabeth A. Grunz, William P. Fay, and Athar H. Chishti. "Double Knockouts Reveal that Protein Tyrosine Phosphatase 1B Is a Physiological Target of Calpain-1 in Platelets." Molecular and Cellular Biology 27, no. 17 (June 18, 2007): 6038–52. http://dx.doi.org/10.1128/mcb.00522-07.

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ABSTRACT Calpains are ubiquitous calcium-regulated cysteine proteases that have been implicated in cytoskeletal organization, cell proliferation, apoptosis, cell motility, and hemostasis. Gene targeting was used to evaluate the physiological function of mouse calpain-1 and establish that its inactivation results in reduced platelet aggregation and clot retraction potentially by causing dephosphorylation of platelet proteins. Here, we report that calpain-1 null (Capn1 −/−) platelets accumulate protein tyrosine phosphatase 1B (PTP1B), which correlates with enhanced tyrosine phosphatase activity
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Zhao, Ming, Yang Yang, Xueyuan Bi, Xiaojiang Yu, Hanghuan Jia, Huanle Fang та Weijin Zang. "Acetylcholine Attenuated TNF-α-Induced Apoptosis in H9c2 Cells: Role of Calpain and the p38-MAPK Pathway". Cellular Physiology and Biochemistry 36, № 5 (2015): 1877–89. http://dx.doi.org/10.1159/000430157.

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Background: Previous studies have shown that inflammation is associated with excessive activation of calpains. Acetylcholine (ACh) has been reported to inhibit pro-inflammatory cytokine release and protect against cardiomyocyte injury. However, there is no direct evidence regarding whether ACh can regulate calpains to exert cardioprotection. To this end, we investigated the effect of ACh on tumour necrosis factor alpha (TNF-α)-induced cardiomyocyte injury and further explored the underlying mechanism. Methods: Flow cytometry and transmission electron microscopy were performed to evaluate apopt
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McClung, J. M., A. R. Judge, E. E. Talbert, and S. K. Powers. "Calpain-1 is required for hydrogen peroxide-induced myotube atrophy." American Journal of Physiology-Cell Physiology 296, no. 2 (February 2009): C363—C371. http://dx.doi.org/10.1152/ajpcell.00497.2008.

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Recent reports suggest numerous roles for cysteine proteases in the progression of skeletal muscle atrophy due to disuse or disease. Nonetheless, a specific requirement for these proteases in the progression of skeletal muscle atrophy has not been demonstrated. Therefore, this investigation determined whether calpains or caspase-3 is required for oxidant-induced C2C12 myotube atrophy. We demonstrate that exposure to hydrogen peroxide (25 μM H2O2) induces myotube oxidative damage and atrophy, with no evidence of cell death. Twenty-four hours of exposure to H2O2 significantly reduced both myotub
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Douillard, Aymeric, Olivier Galbes, Bernadette Rossano, Barbara Vernus, Anne Bonnieu, Robin Candau, and Guillaume Py. "Time course in calpain activity and autolysis in slow and fast skeletal muscle during clenbuterol treatment." Canadian Journal of Physiology and Pharmacology 89, no. 2 (February 2011): 117–25. http://dx.doi.org/10.1139/y10-114.

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Calpains are Ca2+ cysteine proteases that have been proposed to be involved in the cytoskeletal remodeling and wasting of skeletal muscle. Cumulative evidence also suggests that β2-agonists can lead to skeletal muscle hypertrophy through a mechanism probably related to calcium-dependent proteolytic enzyme. The aim of our study was to monitor calpain activity as a function of clenbuterol treatment in both slow and fast phenotype rat muscles. For this purpose, for 21 days we followed the time course of the calpain activity and of the ubiquitous calpain 1 and 2 autolysis, as well as muscle remode
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GOLL, DARREL E., VALERY F. THOMPSON, HONGQI LI, WEI WEI, and JINYANG CONG. "The Calpain System." Physiological Reviews 83, no. 3 (July 2003): 731–801. http://dx.doi.org/10.1152/physrev.00029.2002.

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Goll, Darrel E., Valery F. Thompson, Hongqi Li, Wei Wei, and Jinyang Cong. The Calpain System. Physiol Rev 83: 731–801, 2003; 10.1152/physrev.00029.2002.—The calpain system originally comprised three molecules: two Ca2+-dependent proteases, μ-calpain and m-calpain, and a third polypeptide, calpastatin, whose only known function is to inhibit the two calpains. Both μ- and m-calpain are heterodimers containing an identical 28-kDa subunit and an 80-kDa subunit that shares 55–65% sequence homology between the two proteases. The crystallographic structure of m-calpain reveals six “domains” in the 8
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Alvarez-Arce, Alejandro, Irene Lee-Rivera, Edith López, Arturo Hernández-Cruz, and Ana María López-Colomé. "Thrombin-Induced Calpain Activation Promotes Protease-Activated Receptor 1 Internalization." International Journal of Cell Biology 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/1908310.

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The serine protease thrombin activates Protease-Activated Receptors (PARs), a family of G-protein-coupled receptors (GPCRs) activated by the proteolytic cleavage of their extracellular N-terminal domain. Four members of this family have been identified: PAR1–4. The activation of Protease-Activated Receptor 1(PAR1), the prototype of this receptor family, leads to an increase in intracellular Ca+2concentration ([Ca+2]i) mediated byGq11αcoupling and phospholipase C (PLC) activation. We have previously shown that the stimulation of PAR1 by thrombin promotes intracellular signaling leading to RPE c
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NATH, Rathna, Kadee J. RASER, Daniel STAFFORD, Iradj HAJIMOHAMMADREZA, Avigail POSNER, Hamish ALLEN, Robert V. TALANIAN, Po-wai YUEN, Richard B. GILBERTSEN та Kevin K. W. WANG. "Non-erythroid α-spectrin breakdown by calpain and interleukin 1 β-converting-enzyme-like protease(s) in apoptotic cells: contributory roles of both protease families in neuronal apoptosis". Biochemical Journal 319, № 3 (1 листопада 1996): 683–90. http://dx.doi.org/10.1042/bj3190683.

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The cytoskeletal protein non-erythroid α-spectrin is well documented as an endogenous calpain substrate, especially under pathophysiological conditions. In cell necrosis (e.g. maitotoxin-treated neuroblastoma SH-SY5Y cells), α-spectrin breakdown products (SBDPs) of 150 kDa and 145 kDa were produced by cellular calpains. In contrast, in neuronal cells undergoing apoptosis (cerebellar granule neurons subjected to low potassium and SH-SY5Y cells treated with staurosporine), an additional SBDP of 120 kDa was also observed. The formation of the 120 kDa SBDP was insensitive to calpain inhibitors but
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Arnandis, Teresa, Ivan Ferrer-Vicens, Luis Torres, Concha García, Elena R. Garcia-Trevijano, Rosa Zaragoza, and Juan R. Viña. "Differential functions of calpain 1 during epithelial cell death and adipocyte differentiation in mammary gland involution." Biochemical Journal 459, no. 2 (March 28, 2014): 355–68. http://dx.doi.org/10.1042/bj20130847.

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The results of the present study unveil novel and important nuclear functions of calpains in tissue remodelling. Although inducing nuclear permeability during programmed cell death, histone H3 is identified as a new target of calpain-1 upon adipocyte differentiation.
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Macqueen, Daniel J., and Alexander H. Wilcox. "Characterization of the definitive classical calpain family of vertebrates using phylogenetic, evolutionary and expression analyses." Open Biology 4, no. 4 (April 2014): 130219. http://dx.doi.org/10.1098/rsob.130219.

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The calpains are a superfamily of proteases with extensive relevance to human health and welfare. Vast research attention is given to the vertebrate ‘classical’ subfamily, making it surprising that the evolutionary origins, distribution and relationships of these genes is poorly characterized. Consequently, there exists uncertainty about the conservation of gene family structure, function and expression that has been principally defined from work with mammals. Here, more than 200 vertebrate classical calpains were incorporated in phylogenetic analyses spanning an unprecedented range of taxa, i
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31

Laajala, Mira, Minna M. Hankaniemi, Juha A. E. Määttä, Vesa P. Hytönen, Olli H. Laitinen, and Varpu Marjomäki. "Host Cell Calpains Can Cleave Structural Proteins from the Enterovirus Polyprotein." Viruses 11, no. 12 (November 28, 2019): 1106. http://dx.doi.org/10.3390/v11121106.

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Enteroviruses are small RNA viruses that cause diseases with various symptoms ranging from mild to severe. Enterovirus proteins are translated as a single polyprotein, which is cleaved by viral proteases to release capsid and nonstructural proteins. Here, we show that also cellular calpains have a potential role in the processing of the enteroviral polyprotein. Using purified calpains 1 and 2 in an in vitro assay, we show that addition of calpains leads to an increase in the release of VP1 and VP3 capsid proteins from P1 of enterovirus B species, detected by western blotting. This was prevente
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32

Suzuki, K., K. Shimizu, T. Hamamoto, Y. Nakagawa, T. Murachi, and T. Yamamuro. "Characterization of proteoglycan degradation by calpain." Biochemical Journal 285, no. 3 (August 1, 1992): 857–62. http://dx.doi.org/10.1042/bj2850857.

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Degradation of cartilage proteoglycans was investigated under neutral conditions (pH 7.5) by using pig kidney calpain II (EC 3.4.22.17; Ca(2+)-dependent cysteine proteinase). Aggregate and monomer degradation reached a maximum in 5 min at 30 degrees C when the substrate/enzyme ratio was less than 1000:1. The mode of degradation was limited proteolysis of the core protein; the size of the products was larger than that of papain-digested products and comparable with that of trypsin-digested products. The hyaluronic acid-binding region was lost from the major glycosaminoglycan-bearing region afte
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Rintanen, Nina, Mikko Karjalainen, Jonna Alanko, Lassi Paavolainen, Anita Mäki, Liisa Nissinen, Moona Lehkonen та ін. "Calpains promote α2β1 integrin turnover in nonrecycling integrin pathway". Molecular Biology of the Cell 23, № 3 (лютий 2012): 448–63. http://dx.doi.org/10.1091/mbc.e11-06-0548.

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Collagen receptor integrins recycle between the plasma membrane and endosomes and facilitate formation and turnover of focal adhesions. In contrast, clustering of α2β1 integrin with antibodies or the human pathogen echovirus 1 (EV1) causes redistribution of α2 integrin to perinuclear multivesicular bodies, α2-MVBs. We show here that the internalized clustered α2 integrin remains in α2-MVBs and is not recycled back to the plasma membrane. Instead, receptor clustering and internalization lead to an accelerated down-regulation of α2β1 integrin compared to the slow turnover of unclustered α2 integ
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Meier, Markus, Harald H. Klein, Jan Kramer, Maren Drenckhan, and Morten Schütt. "Calpain inhibition impairs glycogen syntheses in HepG2 hepatoma cells without altering insulin signaling." Journal of Endocrinology 193, no. 1 (April 2007): 45–51. http://dx.doi.org/10.1677/joe.1.07087.

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Calpains are a family of non-lysosomal cytoplasmatic cysteine proteases. Since calpain 10 (CAPN10), a member of the calpain family of proteases, has been found to represent a putative diabetes susceptibility gene, it was argued that calpains may be involved in the development of type 2 diabetes. The functional role of calpains in insulin signaling and/or insulin action is, however, not clear. We investigated the effects of the calpains 1 and 2 inhibitor PD151746 on insulin signaling and insulin action in human hepatoma G2 cells (HepG2). HepG2 cells were incubated without (−PD) or with (+PD) 5.
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35

Bartus, Raymond T. "The Calpain Hypothesis of Neurodegeneration: Evidence for a Common Cytotoxic Pathway." Neuroscientist 3, no. 5 (September 1997): 314–27. http://dx.doi.org/10.1177/107385849700300513.

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Calpain's general function and pathogenic role in the CNS are reviewed. Collectively, the literature indicates that calpain proteolysis plays a common and important role in a variety of acute neurodegenerative conditions, including focal ischemia (stroke), global ischemia, traumatic brain injury, and spinal cord injury. This evidence indicates that 1) calpain is activated in an abnormally sustained fashion during cellular events commonly associated with neurodegeneration (e.g., excessive interstitial glutamate and cytosolic calcium); 2) many of calpain's preferred substrates are degraded as im
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Goll, Darrel E., Valery F. Thompson, Richard G. Taylor, and Ahmed Ouali. "The calpain system and skeletal muscle growth." Canadian Journal of Animal Science 78, no. 4 (December 1, 1998): 503–12. http://dx.doi.org/10.4141/a98-081.

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The first protein of a group of proteins now identified as belonging to the calpain system was purified in 1976. The calpain system presently is known to be constituted of three well-characterized proteins; several lesser studied proteins that have been isolated from invertebrates; and 10 mRNAs, two each in Drosophila and C. elegans and six in vertebrates, that encode proteins, which, based on sequence homology, belong to the calpain family. The three well-characterized proteins in the calpain family include two Ca2+-dependent proteolytic enzymes, µ-calpain and m-calpain, and a protein, calpas
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Saatman, Kathryn E., Babak Abai, Ashley Grosvenor, Christian K. Vorwerk, Douglas H. Smith, and David F. Meaney. "Traumatic Axonal Injury Results in Biphasic Calpain Activation and Retrograde Transport Impairment in Mice." Journal of Cerebral Blood Flow & Metabolism 23, no. 1 (January 2003): 34–42. http://dx.doi.org/10.1097/01.wcb.0000035040.10031.b0.

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Traumatic axonal injury (TAI) is one of the most important pathologies associated with closed head injury, and contributes to ensuing morbidity. The authors evaluated the potential role of calpains in TAI using a new model of optic nerve stretch injury in mice. Male C57BL/6 mice were anesthetized, surgically prepared, and subjected to a 2.0-mm optic nerve stretch injury (n = 34) or sham injury (n = 18). At various intervals up to 2 weeks after injury, optic nerves were examined for neurofilament proteins and calpain-mediated spectrin breakdown products using immunohistochemistry. In addition,
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38

Nwankwo, Jennifer O., Sha Huang, Jongyoon Han, and Athar H. Chishti. "Genetic Deletion of Calpain-1 Improves Reticulocyte Deformability in a Mouse Model of Severe Sickle Cell Disease." Blood 124, no. 21 (December 6, 2014): 2698. http://dx.doi.org/10.1182/blood.v124.21.2698.2698.

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Abstract Introduction: Sickle cell disease (SCD) is caused by the substitution of a valine residue for glutamic acid in the β-globin chain of hemoglobin. The resulting sickle hemoglobin rapidly polymerizes upon deoxygenation, forming sickle RBCs (sRBCs) with reduced deformability. Less deformable sRBCs have an impaired ability to navigate the microvasculature, thereby potentiating vaso-occlusive crises, the hallmark of SCD. Deoxygenation-mediated sickling also induces influx of calcium leading to calpain-1 mediated RBC dehydration via the Gardos channel. Calpains are calcium-activated cysteine
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Watson, P. H., S. T. Mortimer, K. K. W. Wang, D. E. Croall, and D. A. Hanley. "Calcium-activated proteases in the bovine parathyroid gland: potential role in degradation of parathyroid hormone to peptide fragments." Journal of Molecular Endocrinology 15, no. 1 (August 1995): 61–71. http://dx.doi.org/10.1677/jme.0.0150061.

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ABSTRACT Our studies suggest that protein kinase C is involved in low calcium (Ca2+)-stimulated secretion of parathyroid hormone (PTH) but not directly in high Ca2+-stimulated intracellular degradation of PTH to secreted carboxyl-terminal fragments (C-PTH), an important component of Ca2+-regulated PTH secretion. The present study was undertaken to determine the presence of calciumactivated proteases, 84 kDa (micro)-calpain and 80 kDa (milli)-calpain, in the bovine parathyroid, and whether they could degrade PTH to C-terminal fragments. Immunocytochemistry of bovine parathyroid tissue using ant
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40

Liu, Ming Cheng, Veronica Akle, Wenrong Zheng, Jitendra R. Dave, Frank C. Tortella, Ronald L. Hayes, and Kevin K. W. Wang. "Comparing calpain- and caspase-3-mediated degradation patterns in traumatic brain injury by differential proteome analysis." Biochemical Journal 394, no. 3 (February 24, 2006): 715–25. http://dx.doi.org/10.1042/bj20050905.

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A major theme of TBI (traumatic brain injury) pathology is the over-activation of multiple proteases. We have previously shown that calpain-1 and -2, and caspase-3 simultaneously produced αII-spectrin BDPs (breakdown products) following TBI. In the present study, we attempted to identify a comprehensive set of protease substrates (degradome) for calpains and caspase-3. We further hypothesized that the TBI differential proteome is likely to overlap significantly with the calpain- and caspase-3-degradomes. Using a novel HTPI (high throughput immunoblotting) approach and 1000 monoclonal antibodie
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41

Yeh, J.-Y., B.-R. Ou, and N. E. Forsberg. "Effects of dexamethasone on muscle protein homeostasis and on calpain and calpastatin activities and gene expression in rabbits." Journal of Endocrinology 141, no. 2 (May 1994): 209–17. http://dx.doi.org/10.1677/joe.0.1410209.

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Abstract The objectives were to investigate the mechanisms by which glucocorticoids control proteolysis in muscle cells and the relationship between the calpain:calpastatin system and proteolysis in muscle. Female rabbits were treated with 1 mg dexamethasone (Dex)/kg body weight per day for 0, 1, 2 or 4 days after which animals were killed and muscle samples taken for analyses. Dex reduced urinary Nτ-methylhistidine (NMH) 48% (day 4 versus day 1 of Dex treatment) and muscle NMH concentrations by 49% (day 1) to 40% (day 2) respectively, suggesting that protein degradation was reduced. To invest
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42

Lehti, Maarit, Riikka Kivelä, Paavo Komi, Jyrki Komulainen, Heikki Kainulainen, and Heikki Kyröläinen. "Effects of fatiguing jumping exercise on mRNA expression of titin-complex proteins and calpains." Journal of Applied Physiology 106, no. 4 (April 2009): 1419–24. http://dx.doi.org/10.1152/japplphysiol.90660.2008.

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Eccentric exercise induced by electrostimulation increases mRNA expression of titin-complex proteins in rodent skeletal muscle. In this study, mRNA expression of titin, muscle LIM protein (MLP), cardiac ankyrin repeat protein (CARP), ankyrin repeat domain protein 2 (Ankrd2), diabetes-related ankyrin repeat protein (DARP), and calcium-activated proteinases, calpains, were investigated in human skeletal muscle after fatiguing jumping exercise. Fatiguing jumping exercise did not change mRNA expression of titin, DARP, calpain 1, or calpain 3. MLP, Ankrd2 and calpain 2 mRNA levels were increased 2
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Verheijden, Kim A. T., Ramon Sonneveld, Marinka Bakker-van Bebber, Jack F. M. Wetzels, Johan van der Vlag, and Tom Nijenhuis. "The Calcium-Dependent Protease Calpain-1 Links TRPC6 Activity to Podocyte Injury." Journal of the American Society of Nephrology 29, no. 8 (June 28, 2018): 2099–109. http://dx.doi.org/10.1681/asn.2016111248.

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BackgroundThe hallmark of podocytopathies, such as FSGS, is podocyte injury resulting in proteinuria. Transient receptor potential channel C6 (TRPC6) is a calcium-conducting ion channel expressed at the slit diaphragm. TRPC6 gain-of-function mutations and glomerular TRPC6 overexpression are associated with proteinuria. However, the pathways linking TRPC6 to podocyte injury, which is characterized by loss of the slit diaphragm protein nephrin, activation of several intracellular pathways (including calcineurin-NFAT signaling), and cytoskeletal rearrangement, remain elusive.MethodsWe tested whet
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RAVULAPALLI, Ravikiran, Beatriz GARCIA DIAZ, Robert L. CAMPBELL, and Peter L. DAVIES. "Homodimerization of calpain 3 penta-EF-hand domain." Biochemical Journal 388, no. 2 (May 24, 2005): 585–91. http://dx.doi.org/10.1042/bj20041821.

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Calpains 1 and 2 are heterodimeric proteases in which large (relative molecular mass Mr 80000) and small (Mr 28000) subunits are linked through their respective PEF (penta-EF-hand) domains. The skeletal muscle-specific calpain 3 is believed not to form a heterodimer with the small subunit but might homodimerize through its PEF domain. Size-exclusion chromatography and analytical ultracentrifugation of the recombinant PEF domain of calpain 3 show that it forms a stable homodimer that does not dissociate on dilution. Molecular modelling suggests that there would be no barriers to the dimerizatio
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Parnaud, Géraldine, Eva Hammar, Dominique G. Rouiller та Domenico Bosco. "Inhibition of calpain blocks pancreatic β-cell spreading and insulin secretion". American Journal of Physiology-Endocrinology and Metabolism 289, № 2 (серпень 2005): E313—E321. http://dx.doi.org/10.1152/ajpendo.00006.2005.

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In addition to promoting insulin secretion, an increase in cytosolic Ca2+ triggered by glucose has been shown to be crucial for spreading of β-cells attached on extracellular matrix (804G matrix). Calpains are Ca2+-dependent cysteine proteases involved in an extended spectrum of cellular responses, including cytoskeletal rearrangements and vesicular trafficking. The present work aimed to assess whether calpain is also implicated in the process of Ca2+-induced insulin secretion and spreading of rat pancreatic β-cells. The results indicate calpain dependency of β-cell spreading on 804G matrix. I
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Berkholz, Janine, Andreas Zakrzewicz, and Barbara Munz. "skNAC depletion stimulates myoblast migration and perturbs sarcomerogenesis by enhancing calpain 1 and 3 activity." Biochemical Journal 453, no. 2 (June 28, 2013): 303–10. http://dx.doi.org/10.1042/bj20130195.

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skNAC (skeletal and heart muscle specific variant of nascent polypeptide-associated complex α) is a skeletal and heart muscle-specific protein known to be involved in the regulation of sarcomerogenesis. The respective mechanism, however, is largely unknown. In the present paper, we demonstrate that skNAC regulates calpain activity. Specifically, we show that inhibition of skNAC gene expression leads to enhanced, and overexpression of the skNAC gene to repressed, activity of calpain 1 and, to a lesser extent, calpain 3 in myoblasts. In skNAC siRNA-treated cells, enhanced calpain activity is ass
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Briz, Victor, and Michel Baudry. "Calpains: Master Regulators of Synaptic Plasticity." Neuroscientist 23, no. 3 (May 17, 2016): 221–31. http://dx.doi.org/10.1177/1073858416649178.

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Although calpain was proposed to participate in synaptic plasticity and learning and memory more than 30 years ago, the mechanisms underlying its activation and the roles of different substrates have remained elusive. Recent findings have provided evidence that the two major calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in synaptic plasticity. In particular, while calpain-1 activation is the initial trigger for certain forms of synaptic plasticity, that is, long-term potentiation, calpain-2 activation restricts the extent of plasticity. Moreover, while calpain
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Yoshikawa, Yoshiro, Hiroji Hagihara, Yoshimi Ohga, Chikako Nakajima-Takenaka, Ken-ya Murata, Shigeki Taniguchi, and Miyako Takaki. "Calpain inhibitor-1 protects the rat heart from ischemia-reperfusion injury: analysis by mechanical work and energetics." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (April 2005): H1690—H1698. http://dx.doi.org/10.1152/ajpheart.00666.2004.

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We hypothesized that calpain inhibitor-1 protected left ventricular (LV) function from ischemia-reperfusion injury by inhibiting the proteolysis of α-fodrin. To test this hypothesis, we investigated the effect of calpain inhibitor-1 on LV mechanical work and energetics in the cross-circulated rat hearts that underwent 15-min global ischemia and 60-min reperfusion ( n = 9). After ischemia-reperfusion with calpain inhibitor-1, mean end-systolic pressure at midrange LV volume and systolic pressure-volume area (PVA) at midrange LV volume (total mechanical energy per beat) were hardly changed, alth
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Fareed, Moin U., Amy R. Evenson, Wei Wei, Michael Menconi, Vitaliy Poylin, Victoria Petkova, Bernadette Pignol, and Per-Olof Hasselgren. "Treatment of rats with calpain inhibitors prevents sepsis-induced muscle proteolysis independent of atrogin-1/MAFbx and MuRF1 expression." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (June 2006): R1589—R1597. http://dx.doi.org/10.1152/ajpregu.00668.2005.

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Muscle wasting in sepsis is a significant clinical problem because it results in muscle weakness and fatigue that may delay ambulation and increase the risk for thromboembolic and pulmonary complications. Treatments aimed at preventing or reducing muscle wasting in sepsis, therefore, may have important clinical implications. Recent studies suggest that sepsis-induced muscle proteolysis may be initiated by calpain-dependent release of myofilaments from the sarcomere, followed by ubiquitination and degradation of the myofilaments by the 26S proteasome. In the present experiments, treatment of ra
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SAVART, M., V. PALLET, P. LETRAD, C. BOSSUET, and A. DUCASTAING. "Calpain 1-protein kinase C complex: effect of calpain inhibitors after dissociation." Biochimie 73, no. 11 (November 1991): 1409–16. http://dx.doi.org/10.1016/0300-9084(91)90172-w.

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