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PMID |
Sentence |
1 |
11017071
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This putative diabetes-susceptibility gene encodes a ubiquitously expressed member of the calpain-like cysteine protease family, calpain-10 (CAPN10).
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2 |
11018080
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A calpain-10 gene polymorphism is associated with reduced muscle mRNA levels and insulin resistance.
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3 |
11018080
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A decreased rate of insulin-mediated glucose turnover, or insulin resistance, is one mechanism by which the polymorphism in CAPN10 may increase susceptibility to type 2 diabetes mellitus in older persons.
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4 |
11018080
|
A calpain-10 gene polymorphism is associated with reduced muscle mRNA levels and insulin resistance.
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5 |
11018080
|
A decreased rate of insulin-mediated glucose turnover, or insulin resistance, is one mechanism by which the polymorphism in CAPN10 may increase susceptibility to type 2 diabetes mellitus in older persons.
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6 |
11197848
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Attempts are being made to differentiate non-beta cells(including ES cells) into insulin-producing cells in vitro or in vivo. 2) Very recently, an intron variation in calpain 10 gene was found to be associated with type 2 diabetes, which confirmed the importance of SNPs in common diseases.
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7 |
11307309
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This form of diabetes can result from mutations in at least seven different genes: hepatocyte nuclear factor(HNF)-4 alpha/MODY1, glucokinase/MODY2, HNF-1 alpha/MODY3, insulin promoter factor(IPF-1)/MODY4, HNF-1 beta/MODY5, NeuroD1/MODY6 and Islet(Isl)-1/MODY7.
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8 |
11307309
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Mutations in HNF-1 alpha/MODY3 are the most common cause of MODY in Japanese identified to date accounting for about 15% of cases of MODY.
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9 |
11307309
|
Mutations in the HNF-4 alpha/MODY1, glucokinase/MODY2, HNF-1 beta/MODY5 and Isl-1/MODY7 genes have also been found in Japanese; however, they are rare causes of MODY.
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10 |
11307309
|
Patients who have mutations in the HNF-1 beta/MODY5 gene have non-diabetic kidney dysfunction including renal cysts.
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11 |
11307309
|
Genetic approach for type 2 diabetes had done by using non-parameteric linkage analysis such as sibpair analysis which worked well and NIDDM1 and NIDDM2 have been identified to date.
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12 |
11307309
|
The responsible gene for NIDDM1 was recently identified to be Calpain 10, and SNP43 in this gene could explain all of the evidence for linkage in Mexican American type 2 diabetes.
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13 |
11350192
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The DNA polymorphism SNP-43 in the calpain-10 gene is associated with insulin resistance and reduced skeletal muscle transcript in Pima Indians.
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14 |
11473094
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Absence of association of type 2 diabetes with CAPN10 and PC-1 polymorphisms in Oji-Cree.
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15 |
11481585
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Variation in CAPN10, the gene encoding the ubiquitously expressed cysteine protease calpain-10, has been associated with type 2 diabetes in Mexican Americans and in two northern-European populations, from Finland and Germany.
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16 |
11516996
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Overactivation of calpain 1 and calpain 2 (and their small subunit) has long been tied to acute neurological disorders (e.g. stroke and traumatic brain injury) and recently to Alzheimer's disease.
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17 |
11516996
|
Calpain 10 was recently identified as a susceptibility gene for type 2 diabetes, whereas calpain 9 appears to be a gastric cancer suppressor.
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18 |
11522666
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Studies of the genetic basis of type 2 diabetes suggest that variation in the calpain-10 gene affects susceptibility to this common disorder, raising the possibility that calpain-sensitive pathways may play a role in regulating insulin secretion and/or action.
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19 |
11522666
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Here, we report that short-term (4-h) exposure to the cell-permeable calpain inhibitors calpain inhibitor II and E-64-d increases the insulin secretory response to glucose in mouse pancreatic islets.
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20 |
11522666
|
In muscle strips and adipocytes, exposure to both calpain inhibitor II and E-64-d reduced insulin-mediated glucose transport.
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21 |
11522685
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Functional significance of the UCSNP-43 polymorphism in the CAPN10 gene for proinsulin processing and insulin secretion in nondiabetic Germans.
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22 |
11683767
|
Many common variants in functional and positional candidate genes, including ADRB3, PPARG, ENPP1, and CAPN10, have also been studied for their possible role as determinants of type 2 diabetes, with varying levels of agreement between studies.
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23 |
11756349
|
Studies in nondiabetic Pima Indians showed that one of the at-risk DNA polymorphisms, single-nucleotide polymorphism (SNP)-43, in CAPN10 was associated with insulin resistance, and individuals with the G/G-genotype had significantly higher fasting plasma glucose and 2-h insulin concentrations after a 75-g oral glucose tolerance test (OGTT).
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24 |
11756349
|
We have examined the effect of variation in CAPN10 on plasma glucose and insulin levels in a group of 285 nondiabetic British subjects after a 75-g OGTT.
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25 |
11756349
|
We conclude that genetic variation in the CAPN10 gene influences blood glucose levels in nondiabetic British subjects and that this is due, at least in part, to the effects of calpain-10 on the early insulin secretory response.
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26 |
11756349
|
Studies in nondiabetic Pima Indians showed that one of the at-risk DNA polymorphisms, single-nucleotide polymorphism (SNP)-43, in CAPN10 was associated with insulin resistance, and individuals with the G/G-genotype had significantly higher fasting plasma glucose and 2-h insulin concentrations after a 75-g oral glucose tolerance test (OGTT).
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27 |
11756349
|
We have examined the effect of variation in CAPN10 on plasma glucose and insulin levels in a group of 285 nondiabetic British subjects after a 75-g OGTT.
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28 |
11756349
|
We conclude that genetic variation in the CAPN10 gene influences blood glucose levels in nondiabetic British subjects and that this is due, at least in part, to the effects of calpain-10 on the early insulin secretory response.
|
29 |
11756349
|
Studies in nondiabetic Pima Indians showed that one of the at-risk DNA polymorphisms, single-nucleotide polymorphism (SNP)-43, in CAPN10 was associated with insulin resistance, and individuals with the G/G-genotype had significantly higher fasting plasma glucose and 2-h insulin concentrations after a 75-g oral glucose tolerance test (OGTT).
|
30 |
11756349
|
We have examined the effect of variation in CAPN10 on plasma glucose and insulin levels in a group of 285 nondiabetic British subjects after a 75-g OGTT.
|
31 |
11756349
|
We conclude that genetic variation in the CAPN10 gene influences blood glucose levels in nondiabetic British subjects and that this is due, at least in part, to the effects of calpain-10 on the early insulin secretory response.
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32 |
11836299
|
Common intronic variants seem to alter CAPN10 mRNA levels and were associated with insulin resistance but not diabetes in Pima Indians.
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33 |
11836299
|
We found some evidence for linkage of T2DM to chromosome 2q approximately 20 cM proximal to the NIDDM1/CAPN10 locus.
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34 |
11836299
|
To test the hypothesis that CAPN10 is a diabetes susceptibility locus in Caucasian families at high risk for T2DM, we examined the influence of the three previously implicated CAPN10 variants on both diabetes risk and measures of insulin sensitivity and glucose homeostasis.
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35 |
11836299
|
However, CAPN10 influences insulin sensitivity and glucose homeostasis in nondiabetic members of kindreds at high risk for T2DM.
|
36 |
11836299
|
Common intronic variants seem to alter CAPN10 mRNA levels and were associated with insulin resistance but not diabetes in Pima Indians.
|
37 |
11836299
|
We found some evidence for linkage of T2DM to chromosome 2q approximately 20 cM proximal to the NIDDM1/CAPN10 locus.
|
38 |
11836299
|
To test the hypothesis that CAPN10 is a diabetes susceptibility locus in Caucasian families at high risk for T2DM, we examined the influence of the three previously implicated CAPN10 variants on both diabetes risk and measures of insulin sensitivity and glucose homeostasis.
|
39 |
11836299
|
However, CAPN10 influences insulin sensitivity and glucose homeostasis in nondiabetic members of kindreds at high risk for T2DM.
|
40 |
11836299
|
Common intronic variants seem to alter CAPN10 mRNA levels and were associated with insulin resistance but not diabetes in Pima Indians.
|
41 |
11836299
|
We found some evidence for linkage of T2DM to chromosome 2q approximately 20 cM proximal to the NIDDM1/CAPN10 locus.
|
42 |
11836299
|
To test the hypothesis that CAPN10 is a diabetes susceptibility locus in Caucasian families at high risk for T2DM, we examined the influence of the three previously implicated CAPN10 variants on both diabetes risk and measures of insulin sensitivity and glucose homeostasis.
|
43 |
11836299
|
However, CAPN10 influences insulin sensitivity and glucose homeostasis in nondiabetic members of kindreds at high risk for T2DM.
|
44 |
11836299
|
Common intronic variants seem to alter CAPN10 mRNA levels and were associated with insulin resistance but not diabetes in Pima Indians.
|
45 |
11836299
|
We found some evidence for linkage of T2DM to chromosome 2q approximately 20 cM proximal to the NIDDM1/CAPN10 locus.
|
46 |
11836299
|
To test the hypothesis that CAPN10 is a diabetes susceptibility locus in Caucasian families at high risk for T2DM, we examined the influence of the three previously implicated CAPN10 variants on both diabetes risk and measures of insulin sensitivity and glucose homeostasis.
|
47 |
11836299
|
However, CAPN10 influences insulin sensitivity and glucose homeostasis in nondiabetic members of kindreds at high risk for T2DM.
|
48 |
11891618
|
Recently, a positional cloning study proposed that haplotypes at the calpain-10 locus (CAPN10) are associated with increased risk of type 2 diabetes, or non-insulin-dependent diabetes mellitus, in Mexican Americans, Finns, and Germans.
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49 |
11932299
|
Recent evidence suggests that variation in the gene encoding the cysteine protease calpain-10 influences susceptibility to type 2 diabetes.
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50 |
12021163
|
However, only NIDDM1 has been mapped to a single gene, and that gene (calpain 10) appears to have a major role only in selected populations.
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51 |
12083814
|
No evidence for involvement of the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus in early onset obesity.
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52 |
12083814
|
In light of evidence of linkage of obesity to chromosome 2q31-q37, we hypothesized that the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus (NIDDM) is involved in early onset obesity.
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53 |
12083814
|
No evidence for involvement of the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus in early onset obesity.
|
54 |
12083814
|
In light of evidence of linkage of obesity to chromosome 2q31-q37, we hypothesized that the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus (NIDDM) is involved in early onset obesity.
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55 |
12107250
|
Polymorphism in the calpain-10 gene is linked to type 2 diabetes, insulin resistance, and decreased thermogenesis.
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56 |
12133483
|
[The UCSNP44 variation of calpain 10 gene on NIDDM1 locus and its impact on plasma glucose levels in type 2 diabetic patients].
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57 |
12145185
|
Variants in the calpain-10 gene predispose to insulin resistance and elevated free fatty acid levels.
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58 |
12145185
|
Because FFA and insulin resistance are known to predict type 2 diabetes, the finding that variation in the CAPN10 gene influences FFA levels and insulin resistance may provide an explanation for how the CAPN10 gene increases susceptibility to type 2 diabetes.
|
59 |
12145185
|
Variants in the calpain-10 gene predispose to insulin resistance and elevated free fatty acid levels.
|
60 |
12145185
|
Because FFA and insulin resistance are known to predict type 2 diabetes, the finding that variation in the CAPN10 gene influences FFA levels and insulin resistance may provide an explanation for how the CAPN10 gene increases susceptibility to type 2 diabetes.
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61 |
12201821
|
The peroxisome proliferator-activated receptor gamma (PPARgamma) and calpain-10 (CAPN10) genes have recently been identified as T2DM susceptibility genes, and the lessons learnt from these studies are helping to shape future strategies to search for additional susceptibility genes in T2DM and insulin resistance.
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62 |
12324979
|
The Japanese have a higher prevalence of polymorphisms for at least three genes that code for proteins thought to play key roles in lipid and glucose metabolism: the beta 3-adrenergic receptor, the peroxisome proliferator-activated receptor gamma, and calpain-10.
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63 |
12453914
|
Variants within the calpain-10 gene on chromosome 2q37 (NIDDM1) and relationships to type 2 diabetes, insulin resistance, and impaired acute insulin secretion among Scandinavian Caucasians.
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64 |
12453914
|
In conclusion, the frequency of the 112/121 at-risk haplotype of CAPN10 is low among Scandinavians and we were unable to demonstrate significant associations between the CAPN10 variants and type 2 diabetes, insulin resistance, or impaired insulin secretion.
|
65 |
12453914
|
Variants within the calpain-10 gene on chromosome 2q37 (NIDDM1) and relationships to type 2 diabetes, insulin resistance, and impaired acute insulin secretion among Scandinavian Caucasians.
|
66 |
12453914
|
In conclusion, the frequency of the 112/121 at-risk haplotype of CAPN10 is low among Scandinavians and we were unable to demonstrate significant associations between the CAPN10 variants and type 2 diabetes, insulin resistance, or impaired insulin secretion.
|
67 |
12457873
|
Casein zymography, immunoblot analysis for alpha-spectrin, calpain 2, and calpain 10 were performed to detect activation of calpain in lens samples.
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68 |
12457873
|
The WBN/Kob model may be useful for elucidating the roles of calpain 2 and calpain 10 in human cataractogenesis.
|
69 |
12457873
|
Casein zymography, immunoblot analysis for alpha-spectrin, calpain 2, and calpain 10 were performed to detect activation of calpain in lens samples.
|
70 |
12457873
|
The WBN/Kob model may be useful for elucidating the roles of calpain 2 and calpain 10 in human cataractogenesis.
|
71 |
12759879
|
Genetic variation in the gene for a cytosolic cysteine protease, calpain-10, increases the susceptibility to type 2 diabetes apparently by altering levels of gene expression.
|
72 |
12759879
|
Exposure of islets to inhibitors of other proteases, ie, cathepsin B and proteasome, did not affect insulin secretion.
|
73 |
12974673
|
Calpain facilitates GLUT4 vesicle translocation during insulin-stimulated glucose uptake in adipocytes.
|
74 |
12974673
|
Furthermore, inhibition of calpain activity prevented the translocation of insulin-responsive glucose transporter 4 (GLUT4) vesicles to the plasma membrane, as demonstrated by fluorescent microscopy of whole cells and isolated plasma membranes; it did not, however, alter the total GLUT4 protein content.
|
75 |
12974673
|
While inhibition of calpain did not affect the insulin-mediated proximal steps of the phosphoinositide 3-kinase pathway, it did prevent the insulin-stimulated cortical actin reorganization required for GLUT4 translocation.
|
76 |
12974673
|
Specific inhibition of calpain 10 by antisense expression reduced insulin-stimulated GLUT4 translocation and actin reorganization.
|
77 |
12974673
|
Based on these findings, we propose a role for calpain in the actin reorganization required for insulin-stimulated GLUT4 translocation to the plasma membrane in 3T3-L1 adipocytes.
|
78 |
14500039
|
Association of the SNP-19 genotype 22 in the calpain-10 gene with elevated body mass index and hemoglobin A1c levels in Japanese.
|
79 |
14722160
|
Progress in gene identification for more common, multifactorial forms of type 2 diabetes has been slower, but there is now compelling evidence that common variants in the PPARG, KCNJ11 and CAPN10 genes influence T2D-susceptibility, and positional cloning efforts within replicated regions of linkage promise to deliver additional components of inherited susceptibility.
|
80 |
14749260
|
Since then, studies on calpain 10 have been started in correlation with diabetes and insulin-mediated signaling.
|
81 |
14749260
|
Further, special features of the structure of calpain 10 that differ from those of typical micro - or m-calpain used in most studies are summarized together with discussion of the physiological function of calpain with respect to type 2 diabetes.
|
82 |
14749260
|
Since then, studies on calpain 10 have been started in correlation with diabetes and insulin-mediated signaling.
|
83 |
14749260
|
Further, special features of the structure of calpain 10 that differ from those of typical micro - or m-calpain used in most studies are summarized together with discussion of the physiological function of calpain with respect to type 2 diabetes.
|
84 |
14749261
|
There are association studies on genetic variation at CAPN10 in different human populations over a range of phenotypes related to type 2 diabetes, physiological studies on the biological functions of calpain proteases, and evolutionary studies on CAPN10 and the NIDDM1 region.
|
85 |
15044459
|
RyR2 and calpain-10 delineate a novel apoptosis pathway in pancreatic islets.
|
86 |
15044459
|
Thus RyR2 activity seems to play an essential role in beta-cell survival in vitro by suppressing a death pathway mediated by calpain-10, a type 2 diabetes susceptibility gene with previously unknown function.
|
87 |
15044459
|
RyR2 and calpain-10 delineate a novel apoptosis pathway in pancreatic islets.
|
88 |
15044459
|
Thus RyR2 activity seems to play an essential role in beta-cell survival in vitro by suppressing a death pathway mediated by calpain-10, a type 2 diabetes susceptibility gene with previously unknown function.
|
89 |
15336956
|
In two cases, however, the alteration of a member of the calpain family has been clearly identified as being responsible for a human disease: the loss of function of calpain 3 causes limb girdle muscular dystrophy type 2A, and mutations in the gene coding for calpain 10 have been shown to correlate with non-insulin-dependent diabetes.
|
90 |
15362498
|
A number of calpains have been identified in the lens, including calpain 2, calpain 10 and two isozymes of calpain 3: Lp82 and Lp85.
|
91 |
15362498
|
The use of animal hereditary cataract models have suggested that calpain 2 and/or Lp82 may be the major calpains involved in murine cataractogenesis with contributions from calpain 10 and Lp85.
|
92 |
15362498
|
A number of calpains have been identified in the lens, including calpain 2, calpain 10 and two isozymes of calpain 3: Lp82 and Lp85.
|
93 |
15362498
|
The use of animal hereditary cataract models have suggested that calpain 2 and/or Lp82 may be the major calpains involved in murine cataractogenesis with contributions from calpain 10 and Lp85.
|
94 |
15362499
|
Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10.
|
95 |
15362499
|
The presence of both calpain 10 and its mRNA have been demonstrated in tissues from several mammalian species whilst calpain 10 appears to be associated with pathways involved in glucose metabolism, insulin secretion and insulin action.
|
96 |
15362499
|
Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10.
|
97 |
15362499
|
The presence of both calpain 10 and its mRNA have been demonstrated in tissues from several mammalian species whilst calpain 10 appears to be associated with pathways involved in glucose metabolism, insulin secretion and insulin action.
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98 |
15471947
|
Functional data have been hitherto elusive, but we report here a corresponding increase between CAPN10 expression level and regulated insulin secretion.
|
99 |
15471947
|
Pancreatic beta-cell secretory granule exocytosis is mediated by the soluble N-ethylmaleimide-sensitive fusion protein attachment receptor protein complex of synaptosomal-associated protein of 25 kDa (SNAP-25), syntaxin 1, and vesicle-associated membrane protein 2.
|
100 |
15471947
|
Furthermore, SNAP-25 undergoes a Ca2+-dependent partial proteolysis during exocytosis, with calpain protease inhibitor similarly suppressing both insulin secretion and SNAP-25 proteolysis.
|
101 |
15489534
|
We describe applications of the method to simulated data and to data from a Mendelian locus (CFTR, responsible for cystic fibrosis) and from a proposed complex trait locus (calpain-10, implicated in type 2 diabetes).
|
102 |
15641690
|
Relationship between calpain-10 gene polymorphism and insulin resistance phenotypes in Chinese.
|
103 |
15641690
|
For all subjects, the height, weight, waist-to-hip ratio (W/H) and blood pressure, as well as following parameters were measured: (1) 75-g oral glucose tolerance test with insulin, C-peptide, HbA1c and blood lipid profiles; (2) Genomic DNA extracted from peripheral blood lymphocytes was genotyped for UCSNP-43 (calpain-10-g. 4852 G/A) and UCSNP-44 (calpain-10-g. 4841 T/C) by sequencing a polymerase chain reaction (PCR)-amplified fragment.
|
104 |
15641690
|
It was demonstrated that the Calpain-10 gene polymorphism UCSNP-44 was associated with insulin sensitivity and Fins and P2hIns in newly diagnosed T2DM, although Calpain-10 doesn't appear as a major diabetes susceptible gene in this population.
|
105 |
15641690
|
Relationship between calpain-10 gene polymorphism and insulin resistance phenotypes in Chinese.
|
106 |
15641690
|
For all subjects, the height, weight, waist-to-hip ratio (W/H) and blood pressure, as well as following parameters were measured: (1) 75-g oral glucose tolerance test with insulin, C-peptide, HbA1c and blood lipid profiles; (2) Genomic DNA extracted from peripheral blood lymphocytes was genotyped for UCSNP-43 (calpain-10-g. 4852 G/A) and UCSNP-44 (calpain-10-g. 4841 T/C) by sequencing a polymerase chain reaction (PCR)-amplified fragment.
|
107 |
15641690
|
It was demonstrated that the Calpain-10 gene polymorphism UCSNP-44 was associated with insulin sensitivity and Fins and P2hIns in newly diagnosed T2DM, although Calpain-10 doesn't appear as a major diabetes susceptible gene in this population.
|
108 |
15641690
|
Relationship between calpain-10 gene polymorphism and insulin resistance phenotypes in Chinese.
|
109 |
15641690
|
For all subjects, the height, weight, waist-to-hip ratio (W/H) and blood pressure, as well as following parameters were measured: (1) 75-g oral glucose tolerance test with insulin, C-peptide, HbA1c and blood lipid profiles; (2) Genomic DNA extracted from peripheral blood lymphocytes was genotyped for UCSNP-43 (calpain-10-g. 4852 G/A) and UCSNP-44 (calpain-10-g. 4841 T/C) by sequencing a polymerase chain reaction (PCR)-amplified fragment.
|
110 |
15641690
|
It was demonstrated that the Calpain-10 gene polymorphism UCSNP-44 was associated with insulin sensitivity and Fins and P2hIns in newly diagnosed T2DM, although Calpain-10 doesn't appear as a major diabetes susceptible gene in this population.
|
111 |
15696418
|
Population genetics of CAPN10 and GPR35: implications for the evolution of type 2 diabetes variants.
|
112 |
15696418
|
To this end, we surveyed sequence variation in CAPN10 and in an adjacent gene, G-protein-coupled receptor 35 (GPR35), in four population samples from different ethnic groups.
|
113 |
15696418
|
These data revealed two distinct deviations from the standard neutral model in CAPN10, whereas GPR35 variation was largely consistent with neutrality.
|
114 |
15696418
|
Population genetics of CAPN10 and GPR35: implications for the evolution of type 2 diabetes variants.
|
115 |
15696418
|
To this end, we surveyed sequence variation in CAPN10 and in an adjacent gene, G-protein-coupled receptor 35 (GPR35), in four population samples from different ethnic groups.
|
116 |
15696418
|
These data revealed two distinct deviations from the standard neutral model in CAPN10, whereas GPR35 variation was largely consistent with neutrality.
|
117 |
15696418
|
Population genetics of CAPN10 and GPR35: implications for the evolution of type 2 diabetes variants.
|
118 |
15696418
|
To this end, we surveyed sequence variation in CAPN10 and in an adjacent gene, G-protein-coupled receptor 35 (GPR35), in four population samples from different ethnic groups.
|
119 |
15696418
|
These data revealed two distinct deviations from the standard neutral model in CAPN10, whereas GPR35 variation was largely consistent with neutrality.
|
120 |
15737467
|
Because of recent studies showing linkage of type 2 diabetes with the calpain 10 gene, we investigated the ability of calpains to regulate GLUT4 expression in 3T3-L1 adipocytes.
|
121 |
15737467
|
Treatment of 3T3-L1 adipocytes with the calpain inhibitor ALLN significantly decreased the mRNA and protein expression of GLUT4.
|
122 |
15737467
|
GLUT4 expression was not affected by treatment with the more selective calpain inhibitors PD150606, calpeptin, or a calpastatin peptide.
|
123 |
15793266
|
CAPN10 was also associated with both insulin sensitivity and insulin secretion.
|
124 |
15823385
|
Several mechanisms have been proposed, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction for insulin resistance, and glucotoxicity, lipotoxicity, and amyloid formation for beta-cell dysfunction.
|
125 |
15823385
|
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.
|
126 |
15862281
|
These studies confirm calpain 10 expression in cultured human muscle cells and support a role for calpains in insulin-stimulated glucose uptake in human skeletal muscle cells that may be relevant to the pathogenesis of the peripheral insulin resistance in type 2 diabetes.
|
127 |
15912330
|
To date, only a few susceptibility genes have been identified (such as PPARG, KCNJ11, CAPN10).
|
128 |
16028216
|
Many investigators, but not all, have subsequently found associations between CAPN10 polymorphism and type 2 diabetes (T2D) as well as insulin action, insulin secretion, aspects of adipocyte biology and microvascular function.
|
129 |
16028216
|
Both genetic and functional data indicates that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with the adipocyte.
|
130 |
16028216
|
In this regard, emerging evidence would suggest that calpain-10 facilitates GLUT4 translocation and acts in reorganization of the cytoskeleton.
|
131 |
16028216
|
In conclusion, the discovery of calpain-10 by a genetic approach has identified it as a molecule of importance to insulin signaling and secretion that may have relevance to the future development of novel therapeutic targets for the treatment of T2D.
|
132 |
16028216
|
Many investigators, but not all, have subsequently found associations between CAPN10 polymorphism and type 2 diabetes (T2D) as well as insulin action, insulin secretion, aspects of adipocyte biology and microvascular function.
|
133 |
16028216
|
Both genetic and functional data indicates that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with the adipocyte.
|
134 |
16028216
|
In this regard, emerging evidence would suggest that calpain-10 facilitates GLUT4 translocation and acts in reorganization of the cytoskeleton.
|
135 |
16028216
|
In conclusion, the discovery of calpain-10 by a genetic approach has identified it as a molecule of importance to insulin signaling and secretion that may have relevance to the future development of novel therapeutic targets for the treatment of T2D.
|
136 |
16028216
|
Many investigators, but not all, have subsequently found associations between CAPN10 polymorphism and type 2 diabetes (T2D) as well as insulin action, insulin secretion, aspects of adipocyte biology and microvascular function.
|
137 |
16028216
|
Both genetic and functional data indicates that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with the adipocyte.
|
138 |
16028216
|
In this regard, emerging evidence would suggest that calpain-10 facilitates GLUT4 translocation and acts in reorganization of the cytoskeleton.
|
139 |
16028216
|
In conclusion, the discovery of calpain-10 by a genetic approach has identified it as a molecule of importance to insulin signaling and secretion that may have relevance to the future development of novel therapeutic targets for the treatment of T2D.
|
140 |
16028216
|
Many investigators, but not all, have subsequently found associations between CAPN10 polymorphism and type 2 diabetes (T2D) as well as insulin action, insulin secretion, aspects of adipocyte biology and microvascular function.
|
141 |
16028216
|
Both genetic and functional data indicates that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with the adipocyte.
|
142 |
16028216
|
In this regard, emerging evidence would suggest that calpain-10 facilitates GLUT4 translocation and acts in reorganization of the cytoskeleton.
|
143 |
16028216
|
In conclusion, the discovery of calpain-10 by a genetic approach has identified it as a molecule of importance to insulin signaling and secretion that may have relevance to the future development of novel therapeutic targets for the treatment of T2D.
|
144 |
16186407
|
Our aim was to study the impact of genetic (heritability and polymorphisms) and nongenetic (insulin, free fatty acids, and age) factors on CAPN10 mRNA expression in skeletal muscle using two different study designs.
|
145 |
16186407
|
We found hereditary effects on both basal and insulin-exposed CAPN10 mRNA expression.
|
146 |
16186407
|
Insulin had no significant effect on CAPN10 mRNA levels, neither in the twins nor in the basal state of the Intralipid study.
|
147 |
16186407
|
However, after a 24-h infusion of Intralipid, we noted a significant increase in CAPN10 mRNA in response to insulin in subjects with NGT but not in subjects with IGT.
|
148 |
16186407
|
Our aim was to study the impact of genetic (heritability and polymorphisms) and nongenetic (insulin, free fatty acids, and age) factors on CAPN10 mRNA expression in skeletal muscle using two different study designs.
|
149 |
16186407
|
We found hereditary effects on both basal and insulin-exposed CAPN10 mRNA expression.
|
150 |
16186407
|
Insulin had no significant effect on CAPN10 mRNA levels, neither in the twins nor in the basal state of the Intralipid study.
|
151 |
16186407
|
However, after a 24-h infusion of Intralipid, we noted a significant increase in CAPN10 mRNA in response to insulin in subjects with NGT but not in subjects with IGT.
|
152 |
16186407
|
Our aim was to study the impact of genetic (heritability and polymorphisms) and nongenetic (insulin, free fatty acids, and age) factors on CAPN10 mRNA expression in skeletal muscle using two different study designs.
|
153 |
16186407
|
We found hereditary effects on both basal and insulin-exposed CAPN10 mRNA expression.
|
154 |
16186407
|
Insulin had no significant effect on CAPN10 mRNA levels, neither in the twins nor in the basal state of the Intralipid study.
|
155 |
16186407
|
However, after a 24-h infusion of Intralipid, we noted a significant increase in CAPN10 mRNA in response to insulin in subjects with NGT but not in subjects with IGT.
|
156 |
16186407
|
Our aim was to study the impact of genetic (heritability and polymorphisms) and nongenetic (insulin, free fatty acids, and age) factors on CAPN10 mRNA expression in skeletal muscle using two different study designs.
|
157 |
16186407
|
We found hereditary effects on both basal and insulin-exposed CAPN10 mRNA expression.
|
158 |
16186407
|
Insulin had no significant effect on CAPN10 mRNA levels, neither in the twins nor in the basal state of the Intralipid study.
|
159 |
16186407
|
However, after a 24-h infusion of Intralipid, we noted a significant increase in CAPN10 mRNA in response to insulin in subjects with NGT but not in subjects with IGT.
|
160 |
16857402
|
The first type 2 diabetes (T2D) gene to be identified in a genome wide scan followed by positional cloning was CAPN10 encoding the cysteine protease calpain-10.
|
161 |
16873988
|
Calpain-10 (NIDDM1) as a Susceptibility Gene for Common Type 2 Diabetes.
|
162 |
17003256
|
However, AtT20 cells did exhibit an extremely low abundance of both m-calpain and the 54 kDa isoform of calpain-10 relative to their expression in INS-1 and GH3 cells.
|
163 |
17142981
|
In a prior study, we reported on a significant decrease in calpain10 gene expression in white blood cells (WBC) as well as the major insulin-target tissues including liver and adipose tissue, before the onset of diabetes in Otsuka Long-Evans Tokushima Fatty (OLETF) rats.
|
164 |
17151322
|
Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10.
|
165 |
17151322
|
Here we review recent studies, which in addition to the latter enzyme, have linked calpain 5, calpain 3, and its splice variants, calpain 2 and calpain 1 to T2DM-related metabolic pathways along with T2DM-associated phenotypes, such as obesity and impaired insulin secretion, and T2DM-related complications, such as epithelial dysfunction and diabetic cataract.
|
166 |
17331067
|
Some genes that have become accepted as contributors to diabetes risk include: calpain 10, peroxisome proliferator-activated receptor-gamma, ATP-sensitive inwardly rectifying potassium channel subunit Kir6.2, hepatocyte nuclear factor 4alpha and hepatic transcription factor 1.
|
167 |
17331067
|
In particular, we highlight recent reports of associations between Type 2 diabetes and the transcription factor 7-like 2 gene, associations with micro-opioid receptor and supressor of cytokine signaling 2 genes, and expression and functional analyses of adipokines vaspin and retinol binding protein 4.
|
168 |
17560157
|
Coordinated control of both insulin secretion and insulin action through calpain-10-mediated regulation of exocytosis?
|
169 |
17560157
|
Both genetic and functional data has since indicated that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with adipocytes and skeletal muscle.
|
170 |
17560157
|
Evidence presented in this issue by Brown, Yeaman, and Walker utilizes siRNA technology to specifically knock down calpain-10 expression, and suggests that calpain-10 facilitates GLUT4 translocation through effects on the distal secretory pathway.
|
171 |
17560157
|
In addition, calpain-10 has also been implicated in reorganization of the actin cytoskeleton that accompanies both GLUT4 vesicle translocation and insulin secretion.
|
172 |
17560157
|
Coordinated control of both insulin secretion and insulin action through calpain-10-mediated regulation of exocytosis?
|
173 |
17560157
|
Both genetic and functional data has since indicated that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with adipocytes and skeletal muscle.
|
174 |
17560157
|
Evidence presented in this issue by Brown, Yeaman, and Walker utilizes siRNA technology to specifically knock down calpain-10 expression, and suggests that calpain-10 facilitates GLUT4 translocation through effects on the distal secretory pathway.
|
175 |
17560157
|
In addition, calpain-10 has also been implicated in reorganization of the actin cytoskeleton that accompanies both GLUT4 vesicle translocation and insulin secretion.
|
176 |
17560157
|
Coordinated control of both insulin secretion and insulin action through calpain-10-mediated regulation of exocytosis?
|
177 |
17560157
|
Both genetic and functional data has since indicated that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with adipocytes and skeletal muscle.
|
178 |
17560157
|
Evidence presented in this issue by Brown, Yeaman, and Walker utilizes siRNA technology to specifically knock down calpain-10 expression, and suggests that calpain-10 facilitates GLUT4 translocation through effects on the distal secretory pathway.
|
179 |
17560157
|
In addition, calpain-10 has also been implicated in reorganization of the actin cytoskeleton that accompanies both GLUT4 vesicle translocation and insulin secretion.
|
180 |
17560157
|
Coordinated control of both insulin secretion and insulin action through calpain-10-mediated regulation of exocytosis?
|
181 |
17560157
|
Both genetic and functional data has since indicated that calpain-10 has an important role in insulin resistance and intermediate phenotypes, including those associated with adipocytes and skeletal muscle.
|
182 |
17560157
|
Evidence presented in this issue by Brown, Yeaman, and Walker utilizes siRNA technology to specifically knock down calpain-10 expression, and suggests that calpain-10 facilitates GLUT4 translocation through effects on the distal secretory pathway.
|
183 |
17560157
|
In addition, calpain-10 has also been implicated in reorganization of the actin cytoskeleton that accompanies both GLUT4 vesicle translocation and insulin secretion.
|
184 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
185 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
186 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
187 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
188 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
189 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
190 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
191 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
192 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
193 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
194 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
195 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
196 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
197 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
198 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
199 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
200 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
201 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
202 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
203 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
204 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
205 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
206 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
207 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
208 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
209 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
210 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
211 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
212 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
213 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
214 |
17572128
|
Targeted suppression of calpain-10 expression impairs insulin-stimulated glucose uptake in cultured primary human skeletal muscle cells.
|
215 |
17572128
|
As skeletal muscle is the principal site of the peripheral insulin resistance for glucose disposal in type 2 diabetes, we investigated whether targeted suppression of calpain-10 expression directly affects insulin action in cultured human skeletal muscle cells.
|
216 |
17572128
|
Suppression of CAPN10 mRNA expression (75% decrease compared to untransfected myotubes) was associated with a significant decrease (p=0.04) in insulin-stimulated glucose uptake (1.03+/-0.06 [mean+/-SEM]-fold increase over basal) compared to the untransfected myotubes (1.43+/-0.16-fold increase).
|
217 |
17572128
|
In contrast, decreased suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-stimulated phosphorylation of protein kinase B, a key component of the insulin-signalling pathway.
|
218 |
17572128
|
This study confirms that calpain-10 plays a role in insulin-stimulated glucose uptake in human skeletal muscle cells.
|
219 |
17572128
|
Suppression of calpain-10 expression did not affect insulin-stimulated glycogen synthesis nor insulin-signalling via PKB, suggesting that calpain-10 may exert a direct regulatory effect upon the glucose uptake mechanism.
|
220 |
17855447
|
Calpain-10 (CAPN10) protein may play a role in glucose metabolisms, pancreatic beta-cell insulin secretion and thermogenesis.
|
221 |
18089694
|
Calpain-10 gene and protein expression in human skeletal muscle: effect of acute lipid-induced insulin resistance and type 2 diabetes.
|
222 |
18698425
|
The CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
223 |
18698425
|
We have found that CAPN10 gene in our population is mainly associated with two indicators of the presence of insulin resistance: glucose levels two hours after a 75-g oral glucose tolerance test (OGTT) and HOMA values, although cholesterol levels and blood pressure values are also influenced by CAPN10 variants.
|
224 |
18698425
|
Our results suggest that CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
225 |
18698425
|
The CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
226 |
18698425
|
We have found that CAPN10 gene in our population is mainly associated with two indicators of the presence of insulin resistance: glucose levels two hours after a 75-g oral glucose tolerance test (OGTT) and HOMA values, although cholesterol levels and blood pressure values are also influenced by CAPN10 variants.
|
227 |
18698425
|
Our results suggest that CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
228 |
18698425
|
The CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
229 |
18698425
|
We have found that CAPN10 gene in our population is mainly associated with two indicators of the presence of insulin resistance: glucose levels two hours after a 75-g oral glucose tolerance test (OGTT) and HOMA values, although cholesterol levels and blood pressure values are also influenced by CAPN10 variants.
|
230 |
18698425
|
Our results suggest that CAPN10 gene is associated with insulin resistance phenotypes in the Spanish population.
|
231 |
18802475
|
After 2-month exercise (treadmill running), the body weight (BW) and expression of calpain 10, mu-calpain, and m-calpain in skeletal muscles were determined by RT-PCR, using beta-actin as internal standard.
|
232 |
19297292
|
Calpaïn 10 (CAPN10) is the first diabetes gene to be identified through a genome scan followed by positional cloning, encoding the cysteine protease, the calpaïn 10 encodes for a ubiquitously expressed protease implicated in the two fundamental pathophysiological aspects of T2DM insulinoresistance and insulinosecretion.
|
233 |
19418728
|
[Effect of the Gly972Arg, SNP43 and Prol2Ala polymorphisms of the genes IRS1, CAPN10 and PPARG2 on secondary failure to sulphonylurea and metformin in patients with type 2 diabetes in Yucatán, México].
|
234 |
19418728
|
A possible explanation may be due to polymorphisms in the genes IRS1, CAPN10, PPARG2, which are involved in pancreatic beta cell dysfunction and a poor response to the action of insulin.
|
235 |
19418728
|
The association of the polymorphisms Gly972Arg, SNP43, and Pro12Ala, of the genes IRS1, CAPN10, PPARG2, with the risk of failure to sulphonylurea and metformin therapies was determinated in patients with DT2 in Yucatán, México.
|
236 |
19418728
|
[Effect of the Gly972Arg, SNP43 and Prol2Ala polymorphisms of the genes IRS1, CAPN10 and PPARG2 on secondary failure to sulphonylurea and metformin in patients with type 2 diabetes in Yucatán, México].
|
237 |
19418728
|
A possible explanation may be due to polymorphisms in the genes IRS1, CAPN10, PPARG2, which are involved in pancreatic beta cell dysfunction and a poor response to the action of insulin.
|
238 |
19418728
|
The association of the polymorphisms Gly972Arg, SNP43, and Pro12Ala, of the genes IRS1, CAPN10, PPARG2, with the risk of failure to sulphonylurea and metformin therapies was determinated in patients with DT2 in Yucatán, México.
|
239 |
19418728
|
[Effect of the Gly972Arg, SNP43 and Prol2Ala polymorphisms of the genes IRS1, CAPN10 and PPARG2 on secondary failure to sulphonylurea and metformin in patients with type 2 diabetes in Yucatán, México].
|
240 |
19418728
|
A possible explanation may be due to polymorphisms in the genes IRS1, CAPN10, PPARG2, which are involved in pancreatic beta cell dysfunction and a poor response to the action of insulin.
|
241 |
19418728
|
The association of the polymorphisms Gly972Arg, SNP43, and Pro12Ala, of the genes IRS1, CAPN10, PPARG2, with the risk of failure to sulphonylurea and metformin therapies was determinated in patients with DT2 in Yucatán, México.
|
242 |
20142250
|
We evaluated associations in the Atherosclerosis Risk in Communities study between PrCa and nine T2D single nucleotide polymorphisms from genome-wide association studies of T2D (in CDKAL1, CDKN2A/B, FTO, HHEX, IGF2BP2, KCNJ11, PPARG, SLC30A8, and TCF7L2) and four T2D single nucleotide polymorphisms from pre-genome-wide association studies (in ADRB2, CAPN10, SLC2A2, and UCP2).
|
243 |
20142250
|
PrCa was positively associated with the CAPN10 rs3792267 G allele [hazard ratio (HR) 1.20; 95% confidence interval (CI), 1.00-1.44] and inversely associated with the SLC2A2 rs5400 Thr110 allele (HR, 0.85; 95% CI, 0.72, 1.00), the UCP2 rs660339 Val55 allele (HR, 0.84; 95% CI, 0.73, 0.97) and the IGF2BP2 rs4402960 T allele (HR, 0.79; 95% CI, 0.61-1.02; blacks only).
|
244 |
20142250
|
We evaluated associations in the Atherosclerosis Risk in Communities study between PrCa and nine T2D single nucleotide polymorphisms from genome-wide association studies of T2D (in CDKAL1, CDKN2A/B, FTO, HHEX, IGF2BP2, KCNJ11, PPARG, SLC30A8, and TCF7L2) and four T2D single nucleotide polymorphisms from pre-genome-wide association studies (in ADRB2, CAPN10, SLC2A2, and UCP2).
|
245 |
20142250
|
PrCa was positively associated with the CAPN10 rs3792267 G allele [hazard ratio (HR) 1.20; 95% confidence interval (CI), 1.00-1.44] and inversely associated with the SLC2A2 rs5400 Thr110 allele (HR, 0.85; 95% CI, 0.72, 1.00), the UCP2 rs660339 Val55 allele (HR, 0.84; 95% CI, 0.73, 0.97) and the IGF2BP2 rs4402960 T allele (HR, 0.79; 95% CI, 0.61-1.02; blacks only).
|
246 |
20406624
|
Association of CAPN10 gene with insulin sensitivity, glucose tolerance and renal function in essential hypertensive patients.
|
247 |
21389182
|
Calpain-10 interacts with plasma saturated fatty acid concentrations to influence insulin resistance in individuals with the metabolic syndrome.
|
248 |
22012129
|
High glucose increased mitochondrial calpain 10 substrates (NDUFB8 and ATP synthase β), decreased basal and uncoupled respiration, and initiated cell apoptosis as indicated by cleaved caspase 3 and nuclear condensation.
|
249 |
22012129
|
In agreement with our in vitro data, the kidneys of streptozotocin-induced diabetic rats had elevated calpain 10 substrates and cleaved caspase 3.
|
250 |
22012129
|
Finally, specific siRNA-induced knockdown of calpain 10 in the proximal tubules of control rats resulted in decreased renal function as evidenced by increased serum creatinine, and increased caspase 3 cleavage compared with rats receiving scrambled siRNA.
|
251 |
22012129
|
High glucose increased mitochondrial calpain 10 substrates (NDUFB8 and ATP synthase β), decreased basal and uncoupled respiration, and initiated cell apoptosis as indicated by cleaved caspase 3 and nuclear condensation.
|
252 |
22012129
|
In agreement with our in vitro data, the kidneys of streptozotocin-induced diabetic rats had elevated calpain 10 substrates and cleaved caspase 3.
|
253 |
22012129
|
Finally, specific siRNA-induced knockdown of calpain 10 in the proximal tubules of control rats resulted in decreased renal function as evidenced by increased serum creatinine, and increased caspase 3 cleavage compared with rats receiving scrambled siRNA.
|
254 |
22012129
|
High glucose increased mitochondrial calpain 10 substrates (NDUFB8 and ATP synthase β), decreased basal and uncoupled respiration, and initiated cell apoptosis as indicated by cleaved caspase 3 and nuclear condensation.
|
255 |
22012129
|
In agreement with our in vitro data, the kidneys of streptozotocin-induced diabetic rats had elevated calpain 10 substrates and cleaved caspase 3.
|
256 |
22012129
|
Finally, specific siRNA-induced knockdown of calpain 10 in the proximal tubules of control rats resulted in decreased renal function as evidenced by increased serum creatinine, and increased caspase 3 cleavage compared with rats receiving scrambled siRNA.
|
257 |
22391941
|
We searched for relevant published papers and used STATA v.11.0 to perform a meta-analysis on six single-nucleotide polymorphisms in five genes-ADIPOQ-rs2241766 (SNP45) and -rs1501299 (SNP276), ADRB3-rs4994 (Trp64Arg), CAPN10-rs3792267 (SNP43), ENPP1-rs1044498 (K121Q), and PPARGC1A-rs8192678 (Gly482Ser)-in the Chinese Han population under an additive genetic model.
|
258 |
22391941
|
The pooled odds ratios (95% confidence intervals and P-values) were 0.71 (0.60-0.83; P < 0.001) for ADIPOQ-rs2241766, 0.79 (0.64-0.97; P = 0.027) for ADIPOQ-rs1501299, 1.27 (1.07-1.51; P = 0.006) for ADRB3-rs4994, 0.79 (0.57-1.10; P = 0.163) for CAPN10-rs3792267, 1.41 (1.13-1.76; P = 0.003) for ENPP1-rs1044498, and 1.54 (1.34-1.81; P < 0.001) for PPARGC1A-rs8192678.
|
259 |
22391941
|
There was high heterogeneity for ADIPOQ-rs2241766, ADIPOQ-rs1501299, and CAPN10-rs3792267 (I² = 74.9, 69.4, and 75.8%, respectively), but not for ADRB3-rs4994, ENPP1-rs1044498, and PPARGC1A-rs8192678 (I² = 0.0, 43.4, and 23.3%, respectively).
|
260 |
22391941
|
We searched for relevant published papers and used STATA v.11.0 to perform a meta-analysis on six single-nucleotide polymorphisms in five genes-ADIPOQ-rs2241766 (SNP45) and -rs1501299 (SNP276), ADRB3-rs4994 (Trp64Arg), CAPN10-rs3792267 (SNP43), ENPP1-rs1044498 (K121Q), and PPARGC1A-rs8192678 (Gly482Ser)-in the Chinese Han population under an additive genetic model.
|
261 |
22391941
|
The pooled odds ratios (95% confidence intervals and P-values) were 0.71 (0.60-0.83; P < 0.001) for ADIPOQ-rs2241766, 0.79 (0.64-0.97; P = 0.027) for ADIPOQ-rs1501299, 1.27 (1.07-1.51; P = 0.006) for ADRB3-rs4994, 0.79 (0.57-1.10; P = 0.163) for CAPN10-rs3792267, 1.41 (1.13-1.76; P = 0.003) for ENPP1-rs1044498, and 1.54 (1.34-1.81; P < 0.001) for PPARGC1A-rs8192678.
|
262 |
22391941
|
There was high heterogeneity for ADIPOQ-rs2241766, ADIPOQ-rs1501299, and CAPN10-rs3792267 (I² = 74.9, 69.4, and 75.8%, respectively), but not for ADRB3-rs4994, ENPP1-rs1044498, and PPARGC1A-rs8192678 (I² = 0.0, 43.4, and 23.3%, respectively).
|
263 |
22391941
|
We searched for relevant published papers and used STATA v.11.0 to perform a meta-analysis on six single-nucleotide polymorphisms in five genes-ADIPOQ-rs2241766 (SNP45) and -rs1501299 (SNP276), ADRB3-rs4994 (Trp64Arg), CAPN10-rs3792267 (SNP43), ENPP1-rs1044498 (K121Q), and PPARGC1A-rs8192678 (Gly482Ser)-in the Chinese Han population under an additive genetic model.
|
264 |
22391941
|
The pooled odds ratios (95% confidence intervals and P-values) were 0.71 (0.60-0.83; P < 0.001) for ADIPOQ-rs2241766, 0.79 (0.64-0.97; P = 0.027) for ADIPOQ-rs1501299, 1.27 (1.07-1.51; P = 0.006) for ADRB3-rs4994, 0.79 (0.57-1.10; P = 0.163) for CAPN10-rs3792267, 1.41 (1.13-1.76; P = 0.003) for ENPP1-rs1044498, and 1.54 (1.34-1.81; P < 0.001) for PPARGC1A-rs8192678.
|
265 |
22391941
|
There was high heterogeneity for ADIPOQ-rs2241766, ADIPOQ-rs1501299, and CAPN10-rs3792267 (I² = 74.9, 69.4, and 75.8%, respectively), but not for ADRB3-rs4994, ENPP1-rs1044498, and PPARGC1A-rs8192678 (I² = 0.0, 43.4, and 23.3%, respectively).
|
266 |
22612451
|
Calpain 10 is a ubiquitously expressed mitochondrial and cytosolic Ca(2+)-regulated cysteine protease in which overexpression or knockdown leads to mitochondrial dysfunction and cell death.
|
267 |
22612451
|
Therefore, we created a homology model using the calpain 10 amino acid sequence and calpain 1 3-D structure and docked CYGAK in the active site.
|
268 |
22612451
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RPTC treated with 10 μM CYGAK-OC for 24 h induced accumulation of ATP synthase β and NDUFB8, two calpain 10 substrates.
|
269 |
22612451
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Calpain 10 is a ubiquitously expressed mitochondrial and cytosolic Ca(2+)-regulated cysteine protease in which overexpression or knockdown leads to mitochondrial dysfunction and cell death.
|
270 |
22612451
|
Therefore, we created a homology model using the calpain 10 amino acid sequence and calpain 1 3-D structure and docked CYGAK in the active site.
|
271 |
22612451
|
RPTC treated with 10 μM CYGAK-OC for 24 h induced accumulation of ATP synthase β and NDUFB8, two calpain 10 substrates.
|
272 |
22612451
|
Calpain 10 is a ubiquitously expressed mitochondrial and cytosolic Ca(2+)-regulated cysteine protease in which overexpression or knockdown leads to mitochondrial dysfunction and cell death.
|
273 |
22612451
|
Therefore, we created a homology model using the calpain 10 amino acid sequence and calpain 1 3-D structure and docked CYGAK in the active site.
|
274 |
22612451
|
RPTC treated with 10 μM CYGAK-OC for 24 h induced accumulation of ATP synthase β and NDUFB8, two calpain 10 substrates.
|
275 |
23349674
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Single nucleotide polymorphisms (SNPs) in the calpain-10 gene (CAPN-10), which encodes a protein involved in the secretion and action of insulin, and chronic exposure to inorganic arsenic (iAs) through drinking water have been independently associated with an increase in the risk for T2DM.
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