The disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct

نویسندگان

  • Xiao-Tong Su
  • Chengbiao Zhang
  • Lijun Wang
  • Ruimin Gu
  • Dao-Hong Lin
  • Wen-Hui Wang
چکیده

The disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting 1 duct. 2 Xiao-Tong Su, Chengbiao Zhang, Lijun Wang, Ruimin Gu Dao-Hong Lin and Wen-Hui 3 Wang 4 Department of Pharmacology, New York Medical College, Valhalla, NY 10595 and 5 Department of Physiology, Harbin Medical University, Harbin, China 15086. 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Corresponding Address 24 Dr. Wen-Hui Wang 25 Department of Pharmacology 26 New York Medical College 27 15 Dana Road 28 Valhalla, NY 10595 29 (tel) 914 594 4139 30 (Fax) 914 347 4956 31 E-mail: [email protected] 32 33

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منابع مشابه

Disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct.

Kcnj10 encodes the inwardly rectifying K(+) channel 4.1 (Kir4.1) and is expressed in the basolateral membrane of late thick ascending limb, distal convoluted tubule (DCT), connecting tubule (CNT), and cortical collecting duct (CCD). In the present study, we perform experiments in postneonatal day 9 Kcnj10(-/-) or wild-type mice to examine the role of Kir.4.1 in contributing to the basolateral K...

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The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney.

Kir4.1 is an inwardly rectifying potassium (K(+)) channel and is expressed in the brain, inner ear, and kidney. In the kidney, Kir4.1 is expressed in the basolateral membrane of the late thick ascending limb (TAL), the distal convoluted tubule (DCT), and the connecting tubule (CNT)/cortical collecting duct (CCD). It plays a role in K(+) recycling across the basolateral membrane in corresponding...

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Insulin and IGF - 1 activate Kir 4 . 1 / 5 . 1 channels in cortical 1 collecting duct principal cells to control basolateral membrane

25 26 Potassium Kir4.1/5.1 channels are abundantly expressed at the basolateral membrane of 27 principal cells in the cortical collecting duct (CCD) where they are thought to modulate 28 transport rates by controlling trans-epithelial voltage. Insulin and insulin-like growth factor-1 29 (IGF-1) stimulate apically localized ENaC to augment sodium reabsorption in the CCD. 30 However, little is kn...

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Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.

Potassium Kir4.1/5.1 channels are abundantly expressed at the basolateral membrane of principal cells in the cortical collecting duct (CCD), where they are thought to modulate transport rates by controlling transepithelial voltage. Insulin and insulin-like growth factor-1 (IGF-1) stimulate apically localized epithelial sodium channels (ENaC) to augment sodium reabsorption in the CCD. However, l...

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KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb.

The aim of the present study is to examine the role of Kcnj10 (Kir.4.1) in contributing to the basolateral K conductance in the cortical thick ascending limb (cTAL) using Kcnj10(+/+) wild-type (WT) and Kcnj10(-/-) knockout (KO) mice. The patch-clamp experiments detected a 40- and an 80-pS K channel in the basolateral membrane of the cTAL. Moreover, the probability of finding the 40-pS K was sig...

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تاریخ انتشار 2016