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排序方式: 共有267条查询结果,搜索用时 31 毫秒
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Naresh C. Bal Ashoke Sharon Subash C. Gupta Nivedita Jena Sana Shaikh Sandor Gyorke Muthu Periasamy 《The Journal of biological chemistry》2010,285(22):17188-17196
Calsequestrin undergoes dynamic polymerization with increasing calcium concentration by front-to-front dimerization and back-to-back packing, forming wire-shaped structures. A recent finding that point mutation R33Q leads to lethal catecholaminergic polymorphic ventricular tachycardia (CPVT) implies a crucial role for the N terminus. In this study, we demonstrate that this mutation resides in a highly conserved alternately charged residue cluster (DGKDR; cluster 1) in the N-terminal end of calsequestrin. We further show that this cluster configures itself as a ring system and that the dipolar arrangement within the cluster brings about a critical conformational flip of Lys31-Asp32 essential for dimer stabilization by formation of a H-bond network. We additionally show that Ca2+-induced calsequestrin aggregation is nonlinear and reversible and can regain the native conformation by Ca2+ chelation with EGTA. This study suggests that cluster 1 works as a molecular switch and governs the bidirectional transition between the CASQ2 monomer and dimer. We further demonstrate that mutations disrupting the alternating charge pattern of the cluster, including R33Q, impair Ca2+-CASQ2 interaction, leading to altered polymerization-depolymerization dynamics. This study provides new mechanistic insight into the functional effects of the R33Q mutation and its potential role in CPVT. 相似文献
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The C‐terminal calcium‐sensitive disordered motifs regulate isoform‐specific polymerization characteristics of calsequestrin 下载免费PDF全文
Naresh C. Bal Nivedita Jena Harapriya Chakravarty Amit Kumar Mei Chi Tuniki Balaraju Sharad V. Rawale Jayashree S. Rawale Ashoke Sharon Muthu Periasamy 《Biopolymers》2015,103(1):15-22
Calsequestrin (CASQ) exists as two distinct isoforms CASQ1 and CASQ2 in all vertebrates. Although the isoforms exhibit unique functional characteristic, the structural basis for the same is yet to be fully defined. Interestingly, the C‐terminal region of the two isoforms exhibit significant differences both in length and amino acid composition; forming Dn‐motif and DEXn‐motif in CASQ1 and CASQ2, respectively. Here, we investigated if the unique C‐terminal motifs possess Ca2+‐sensitivity and affect protein function. Sequence analysis shows that both the Dn‐ and DEXn‐motifs are intrinsically disordered regions (IDRs) of the protein, a feature that is conserved from fish to man. Using purified synthetic peptides, we show that these motifs undergo distinctive Ca2+‐mediated folding suggesting that these disordered motifs are Ca2+‐sensitivity. We generated chimeric proteins by swapping the C‐terminal portions between CASQ1 and CASQ2. Our studies show that the C‐terminal portions do not play significant role in protein folding. An interesting finding of the current study is that the switching of the C‐terminal portion completely reverses the polymerization kinetics. Collectively, these data suggest that these Ca2+‐sensitivity IDRs located at the back‐to‐back dimer interface influence isoform‐specific Ca2+‐dependent polymerization properties of CASQ. © 2014 Wiley Periodicals, Inc. Biopolymers 103: 15–22, 2015. 相似文献
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Durgesh K. Dwivedi Gopabandhu Jena Vinod Kumar 《Journal of biochemical and molecular toxicology》2020,34(6)
The present study was designed to investigate the hepatoprotective potential of dimethyl fumarate (DMF) against thioacetamide (TAA)‐induced liver damage. Wistar rats were treated with DMF (12.5, 25, and 50 mg/kg/day, orally) and TAA (200 mg/kg intraperitoneally, every third day) for 6 consecutive weeks. TAA exposure significantly reduced body weight, increased liver weight and index, and intervention with DMF did not ameliorate these parameters. DMF treatment significantly restored TAA‐induced increase in the levels of aspartate aminotransferase, alanine aminotransferase, γ‐glutamyl transferase, total bilirubin, uric acid, malondialdehyde, reduced glutathione, and histopathological findings such as inflammatory cell infiltration, deposition of collagen, necrosis, and bridging fibrosis. DMF treatment significantly ameliorated TAA‐induced hepatic stellate cell activation, increase in inflammatory cascade markers (NACHT, LRR, and PYD domains‐containing protein 3; NLRP3, apoptosis‐associated speck like protein containing a caspase recruitment domain; ASC, caspase‐1, nuclear factor‐kappa B; NF‐κB, interleukin‐6), fibrogenic makers (α‐smooth muscle actin; ɑ‐SMA, transforming growth factor; TGF‐β1, fibronectin, collagen 1) and antioxidant markers (nuclear factor (erythroid‐derived 2)‐like factor 2; Nrf2, superoxide dismutase‐1; SOD‐1, catalase). The present findings concluded that DMF protects against TAA‐induced hepatic damage mediated through the downregulation of inflammatory cascades and upregulation of antioxidant status. 相似文献
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Rebecca T. Kimball Edward L. Braun F. Keith Barker Rauri C.K. Bowie Michael J. Braun Jena L. Chojnowski Shannon J. Hackett Kin-Lan Han John Harshman Victoria Heimer-Torres Wallace Holznagel Christopher J. Huddleston Ben D. Marks Kathleen J. Miglia William S. Moore Sushma Reddy Frederick H. Sheldon Jordan V. Smith Christopher C. Witt Tamaki Yuri 《Molecular phylogenetics and evolution》2009,50(3):654-660
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Chowdhury Labrechai Mog Maurya Rajesh Kumar Singh Rajeev Kumar Mishra Shubhi Chauhan Nishita Jena J. K. Mohindra Vindhya 《Molecular biology reports》2021,48(11):7333-7342