Extracellular-regulated-kinase 5-mediated renal protection against ischemia-reperfusion injury.

Extracellular-regulated-kinase 5-mediated renal protection against ischemia-reperfusion injury.
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DOI:
10.1016/j.bbrc.2012.01.043
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发表时间:
2012-02-24
影响因子:
3.1
通讯作者:
Yang, Jay
Yang, Jay
中科院分区:
生物学4区
文献类型:
--
作者:
Kawakami, Tomoko;Park, Sang Won;Kaku, Ryuji;Yang, Jay

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ERK5 是丝裂原激活蛋白激酶的成员,在肾脏中表达的表观分子质量 (~80 kDa) 比其他器官 (~120 kDa) 更小。封闭肽实验证实,蛋白质印迹上检测到的约 80 kDa 是抗 ERK5 抗体检测到的特异性条带。已知 ERK5 变体 ERK5a、b、c 和 T 的表达证实没有已知的剪接变体编码肾脏特异性~80 kDa 蛋白。然而,使用针对潜在剪接位点的引物进行的 RT-PCR 并未揭示肾脏中的新转录本。肾脏特异性 ERK5 免疫反应蛋白的较小分子量表明,这种细胞保护分子在肾脏中可能无法完全发挥作用。慢病毒介导的小鼠肾脏体内全长 ERK5 过表达提供了针对肾 IR 损伤的保护作用。肾脏特异性~80 kDa ERK5 的身份仍然未知,但更好地了解肾脏中 ERK5 的表达和翻译后加工可能会揭示一种新的肾脏保护策略。
ERK5, a member of the mitogen activated protein kinase, expressed in the kidneys was smaller (~80 kDa) in apparent molecular mass compared to other organs (~120 kDa). A blocking peptide experiment confirmed that the ~80 kDa detected on Western blots was a specific band detected by the anti-ERK5 antibody. Expression of the known ERK5 variants ERK5a, b, c, and T confirmed that none of the known splice variants encoded for the renal-specific ~80 kDa protein. However, RT-PCR with primers targeting the potential splice sites did not reveal a novel transcript in the kidney. The smaller molecular mass of the kidney-specific ERK5-immunoreactive protein suggested that this cyto-protective molecule may not be fully functional in the kidneys. Lentivirus-mediated in vivo overexpression of full length ERK5 in the mouse kidneys provided protection against renal IR injury. The identity of the renal-specific ~80 kDa ERK5 remains unknown but a better understanding of the ERK5 expression and post-translational processing in the kidneys may reveal a novel strategy for renal protection.
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