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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Calpain 10

calpain-10, CAPN10, calcium-activated neutral protease, NIDDM1
Calpains represent a ubiquitous, well-conserved family of calcium-dependent cysteine proteases. The calpain proteins are heterodimers consisting of an invariant small subunit and variable large subunits. The large catalytic subunit has four domains: domain I, the N-terminal regulatory domain that is processed upon calpain activation; domain II, the protease domain; domain III, a linker domain of unknown function; and domain IV, the calmodulin-like calcium-binding domain. This gene encodes a large subunit. It is an atypical calpain in that it lacks the calmodulin-like calcium-binding domain and instead has a divergent C-terminal domain. It is similar in organization to calpains 5 and 6. This gene is associated with type 2 or non-insulin-dependent diabetes mellitus (NIDDM), and is located within the NIDDM1 region. Multiple alternative transcript variants have been described for this gene. [provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: Calpain, Insulin, HAD, CAN, ACID
Papers on calpain-10
Detection of CAPN10 copy number variation in Thai patients with type 2 diabetes by denaturing high performance liquid chromatography and real-time quantitative polymerase chain reaction.
Yenchitsomanus et al., Bangkok, Thailand. In J Diabetes Investig, Nov 2015
A genetic case-control association study in 216 Thai diabetic patients and 192 non-diabetic controls found that, after excluding genotyping errors, genotype distribution of calpain 10 (CAPN10) SNP44 (rs2975760) deviated from HWE.
Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia-reperfusion.
Yoshida et al., Tokyo, Japan. In Int J Cardiol, Nov 2015
We aimed to characterize mitochondrial calpains in the rat heart and to investigate the roles of calpains in mPTP opening after ischemia-reperfusion. METHODS AND RESULTS: Western blotting analysis showed the expression of μ-calpain, m-calpain and calpain 10 in mitochondria isolated from male Sprague-Dawley rats, but casein zymography detected only m-calpain activity.
Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition.
Banik et al., Charleston, United States. In Brain Res, Nov 2015
In our previous studies, activation of calpain, a calcium-activated neutral protease has been found to cause detrimental alterations in spinal motor neurons following ethanol (EtOH) exposure in vitro.
Gene-gene and gene-environment interactions in the etiology of type 2 diabetes mellitus in the population of Hyderabad, India.
Reddy et al., Hyderābād, India. In Meta Gene, Sep 2015
Significant gene-gene and gene-environment interactions were also observed with reference to TCF7L2, CAPN10 and CDKAL1 genes, highlighting their importance in the pathophysiology of T2DM.
Genetic association studies of obesity in Africa: a systematic review.
Kengne et al., Cape Town, South Africa. In Obes Rev, Mar 2015
Polymorphisms in genes such as ACE, ADIPOQ, ADRB2, AGRP, AR, CAPN10, CD36, C7orf31, DRD4, FTO, MC3R, MC4R, SGIP1 and LEP were found to be associated with various measures of obesity.
Association between Genetic Variants and Diabetes Mellitus in Iranian Populations: A Systematic Review of Observational Studies.
Amoli et al., Tehrān, Iran. In J Diabetes Res, 2014
We found significant association between CTLA-4, IL-18, VDR, TAP2, IL-12, and CD4 genes and T1DM, HNFα and MODY, haptoglobin, paraoxonase, leptin, TCF7L2, calreticulin, ERα, PPAR-γ2, CXCL5, calpain-10, IRS-1 and 2, GSTM1, KCNJ11, eNOS, VDR, INSR, ACE, apoA-I, apo E, adiponectin, PTPN1, CETP, AT1R, resistin, MMP-3, BChE K, AT2R, SUMO4, IL-10, VEGF, MTHFR, and GSTM1 with T2DM or its complications.
Apoptosis of beta cells in diabetes mellitus.
Rani et al., Hyderābād, India. In Dna Cell Biol, 2014
The genetic alterations in apoptosis signaling machinery and the pathogenesis of diabetes include Fas, FasL, Akt, caspases, calpain-10, and phosphatase and tensin homolog (Pten).
The calpain system and diabetes.
Cho et al., Seoul, South Korea. In Pathophysiology, 2014
Positional cloning experiments revealed that there is a NIDDM susceptibility to calpain 10 (CAPN10).
Role of calpain-10 in the development of diabetes mellitus and its complications.
Ostrosky-Wegman et al., Mexico. In Arch Med Res, 2014
Calpain-10 has been implicated in the development of type 2 diabetes, and polymorphisms in the CAPN10 gene have been associated with an increased risk of developing this disease.
Identification of copy number variation of CAPN10 in Thais with type 2 diabetes by multiplex PCR and denaturing high performance liquid chromatography (DHPLC).
Yenchitsomanus et al., Bangkok, Thailand. In Gene, 2012
analysis of copy number variation of CAPN10 in Thais with type 2 diabetes by multiplex PCR and denaturing high performance liquid chromatography
Loss of calpain 10 causes mitochondrial dysfunction during chronic hyperglycemia.
Schnellmann et al., Charleston, United States. In Arch Biochem Biophys, 2012
diabetes-induced renal mitochondrial dysfunction and renal injury may directly result from the loss of renal calpain 10
Four polymorphisms of the CAPN 10 gene and their relationship to polycystic ovary syndrome susceptibility: a meta-analysis.
Chen et al., Guangzhou, China. In Clin Endocrinol (oxf), 2012
Studies indicate UCSNP-63 of CAPN 10 gene was significantly associated with polycystic ovary syndrome (PCOS).
Association of CAPN10 SNPs and haplotypes with polycystic ovary syndrome among South Indian Women.
Reddy et al., Hyderābād, India. In Plos One, 2011
CAPN10 SNPs and haplotypes are associated with polycystic ovary syndrome among South Indian Women
Calpain-10 interacts with plasma saturated fatty acid concentrations to influence insulin resistance in individuals with the metabolic syndrome.
Lopez-Miranda et al., Córdoba, Spain. In Am J Clin Nutr, 2011
genetic association studies in a European cohort: CAPN10 SNP (rs2953171) may influence insulin sensitivity by interacting with plasma fatty acid composition in subjects with metabolic syndrome
A novel method for testing association of multiple genetic markers with a multinomial trait.
Guo et al., Houston, United States. In Proc Am Stat Assoc, 2010
Applying the method to study 32 genes in our Mexican-American samples for association with prediabetes through either impaired glucose tolerance (IGT) or impaired fasting glucose (IFG), we found 3 genes (SORCS1, AMPD1, PPAR) associated with both IGT and IFG, while 5 genes (AMPD2, PRKAA2, C5, TCF7L2, ITR) with the IGT mechanism only and 6 genes (CAPN10, IL4,NOS3, CD14, GCG, SORT1) with the IFG mechanism only.
Type 2 diabetes: principles of pathogenesis and therapy.
van Haeften et al., Leipzig, Germany. In Lancet, 2005
Moreover, the disease has a strong genetic component, but only a handful of genes have been identified so far: genes for calpain 10, potassium inward-rectifier 6.2, peroxisome proliferator-activated receptor gamma, insulin receptor substrate-1, and others.
Genetic variation in the gene encoding calpain-10 is associated with type 2 diabetes mellitus.
Bell et al., Chicago, United States. In Nat Genet, 2000
This putative diabetes-susceptibility gene encodes a ubiquitously expressed member of the calpain-like cysteine protease family, calpain-10 (CAPN10).
Loci on chromosomes 2 (NIDDM1) and 15 interact to increase susceptibility to diabetes in Mexican Americans.
Kong et al., Chicago, United States. In Nat Genet, 1999
Using this method, we show that the interaction of genes on chromosomes 2 (NIDDM1) and 15 (near CYP19) makes a contribution to susceptibility to type 2 diabetes in Mexican Americans from Starr County, Texas.
A genome-wide search for human non-insulin-dependent (type 2) diabetes genes reveals a major susceptibility locus on chromosome 2.
Bell et al., Houston, United States. In Nat Genet, 1996
We propose that this locus be designated NIDDM1.
Mutations in the proteolytic enzyme calpain 3 cause limb-girdle muscular dystrophy type 2A.
Roudaut et al., France. In Cell, 1995
The gene encoding the muscle-specific calcium-activated neutral protease 3 (CANP3) large subunit is located in this region.
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