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WNK家族基因在小鼠肾脏表达的特性分析 被引量：2

Expression of WNK genes in the mouse kidney
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摘要 目的检测WNK1和WNK4基因在小鼠肾脏组织中的表达位点。方法RT-PCR方法扩增WNK1和WNK4基因片段作为探针,在小鼠多组织膜上进行Northern印迹杂交。将上述片段克隆入pGEM-T载体,测序证实后,体外转录RNA探针并在小鼠肾脏石蜡组织切片上进行原位杂交。结果WNK1基因广泛表达在小鼠各组织中,在肾脏有9.5kb强杂交信号。WNK4基因主要表达在肾脏组织中,有4.4kb杂交信号。原位杂交显示WNK1基因仅表达在肾脏远曲小管中,而WNK4除表达在肾脏远曲小管外,还表达在髓质集合管上。结论WNK1和WNK4基因均在肾脏中有表达,WNK4基因在肾脏中表达比WNK1基因更广泛。 Objective To investigate the expression of WNK1 and WNK4 genes in the mouse kidney. Methods The probes corresponding to the genes were amplified by RT PCR from mouse kidney, and then Northern blotting was performed on mouse multiple tissues membrane. The fragments were cloned into pGEM T vector,the correct plasmids were linearized and transcripted into RNA probes in vitro. In situ hybridization was performed on the mouse kidney sections. Results WNK1 gene was widely expressed in mouse tissues. There was a 9 5 kb strong signal in kidney. WNK4 gene was mainly expressed in kidney and had a 4 4 kb signal. In situ hybridization showed WNK1 gene was mostly expressed in the distal convoluted tubule whereas WNK4 gene was expressed in the medullary collecting ducts besides the distal convoluted tubules. Conclusion Both WNK1 and WNK4 genes were expressed in kidney. WNK4 was expressed more widely than WNK1 in mouse kidney.
作者 吕晶玉 Jean Marie GASC Xavier Jeunemaitre 赵彦艳
机构地区 中国医科大学医学遗传学教研室 INSERM U
出处 《中华肾脏病杂志》 CAS CSCD 北大核心 2004年第2期90-93,共4页 Chinese Journal of Nephrology
关键词 WNK家族基因 小鼠 肾脏表达 肾脏组织 RT-PCR 原位杂交 WNK1 gene WNK4 gene Northern blot In situ hybridization Psendohypoal dosteronism type Ⅱ
分类号 R692 [医药卫生—泌尿科学] R-332 [医药卫生]
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参考文献11

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二级参考文献9

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共引文献38

同被引文献19

  • 1Wilson FH, Disse-Nicodeme S, Choate KA, et al. Human hypertension caused by mutations in WNK Kinases. Science, 2001,293,1107-1112.
  • 2Kahle KT, MacGregor GG, Wilson FH, et al. Paracellular Cl-permeability is regulated by WNK4 kinase: Insight into normal physiology and hypertension. Proc Natl Acad Sci, 2004,101:14877-14882.
  • 3Cope G, Golbang A, O'shaugh nessy KM. WNK4 Kinases and the control of blood pressure. Pharmacology & Therapeutics, 2005, 106: 221-223.
  • 4Yu A. S. L, Enck AH, lencer WI, et al. Claudin 8 expression in madindarby canine kidney cells augments the paracellular barrier to cation permeation. J Bio Chem, 2003,278(19) :17350-17359.
  • 5Daniel L, Anita LD, Martin GL, et al. Evidence for a gene influencing blood pressare on chromosomel7. Hypertension, 2000,36:477-483.
  • 6Yamauchi K, Rai T, Kobayashi K, et al. Disease-causing mutant WNK4 increases paracelluler chloride permeability and phosphorylates claudins. Proc Natl Acad Sci, 2004,101 ( 13 ) :4690-4694.
  • 7Wilson FH, Kahle KT, Sabath E, et al. Molecular Pothogenesis of inherited hypertension with hyperkalemia : The NaC1 cotransporter is inhibited by wild-type but not mutant WNK4. Proc Natl Acad Sci, 2003,100 ( 2 ) :680-684.
  • 8Kahle KT, Wilson FH, leng Q, et al. WNK4 regulates the balance between renal NaC1 reabsorption and K^+ secretion. Nature genetics, 2003,35 (4) :372-376.
  • 9Xu B, English JM, Wilsbacher JL, et al. WNK1, a novel mammalian serine/threonine protein kinase lacking the catalytic lysinein subdomain Ⅱ. J BiolChem, 2000, 275:16795-16801.
  • 10Wilson FH, Disse-Nicodeme S, Choate KA, et al. Human hypertension caused by mutations in WNK kinases. Science, 2001, 293: 1107-1112.

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中华肾脏病杂志
2004年 第2期

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