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PanK4 inhibits pancreatic p-cell apoptosis by decreasing the transcriptional level of pro-caspase-9

PanK4 inhibits pancreatic p-cell apoptosis by decreasing the transcriptional level of pro-caspase-9
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摘要 Dear Editor: Coenzyme A (CoA) is a primary and predominant acyl group carrier involved in a wide variety of important biochemical processes. The CoA biosynthetic pathway is composed of five enzymatic steps, of which Pantothenate kinase (PanK) is a key regulatory enzyme. The multiple isoforms of PanK are encoded by four different genes [1,2]. In our previous studies of SNP markers by genotyping the case-controlled DNAs, we found that one SNP within the hPANK4 gene on chromosome 1 was associated with type 2 diabetes [3-5]. We subsequently showed that rat PanK4 (rPanK4) was up-regulated when rats were challenged by high concentration of glucose [6]. M2-type pyruvate kinase (Pkm2) was found, both in vitro and in vivo, to be associated with rPanK4 [7]. These data suggest that PanK4 may have a role in diabetes pathogenesis. The development of type 2 diabetes is due partly to the loss of the pancreatic β-cell mass, therefore the secreted amount of insulin is insufficient to maintain the glucose homoestasis [8]. In the present study, we evaluated the effect ofrPanK4 on β-cell apoptosis. We aimed to determine the potential ofrPanK4 gene in β-cell apoptosis induced by the cytotoxic agent streptozotocin (STZ).
出处 《Cell Research》 SCIE CAS CSCD 2007年第11期966-968,共3页 细胞研究(英文版)
基金 We are indebted to Dr Jin Ming Gao for critical reading of this manuscript. This work was supported by the National Basic Research Program of China (2004CB518602 and 2006CB503909), the National Natural Science Foundation of China (30471930) and the Beijing Natural Science Foundation (5072042).
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