NDLI: Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms

Content Provider	PubMed Central
Author	Lazrak, Ahmed Liu, Zhen Huang, Chou-long
Copyright Year	2006
Abstract	WNK kinases are serine-threonine kinases with an atypical placement of the catalytic lysine. Intronic deletions with increased expression of a ubiquitous long WNK1 transcript cause pseudohypoaldosteronism type 2 (PHA II), characterized by hypertension and hyperkalemia. Here, we report that long WNK1 inhibited ROMK1 by stimulating its endocytosis. Inhibition of ROMK by long WNK1 was synergistic with, but not dependent on, WNK4. A smaller transcript of WNK1 lacking the N-terminal 1-437 amino acids is expressed highly in the kidney. Whether expression of the KS-WNK1 (kidney-specific, KS) is altered in PHA II is not known. We found that KS-WNK1 did not inhibit ROMK1 but reversed the inhibition of ROMK1 caused by long WNK1. Consistent with the lack of inhibition by KS-WNK1, we found that amino acids 1-491 of the long WNK1 were sufficient for inhibiting ROMK. Dietary K+ restriction decreases ROMK abundance in the renal cortical-collecting ducts by stimulating endocytosis, an adaptative response important for conservation of K+ during K+ deficiency. We found that K+ restriction in rats increased whole-kidney transcript of long WNK1 while decreasing that of KS-WNK1. Thus, KS-WNK1 is a physiological antagonist of long WNK1. Hyperkalemia in PHA II patients with PHA II mutations may be caused, at least partially, by increased expression of long WNK1 with or without decreased expression of KS-WNK1.
Related Links	http://dx.doi.org/10.1073/pnas.0510609103
Ending Page	1620
Page Count	6
Starting Page	1615
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	5
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-01-31
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Regulation of ROMK Channel and K+ Homeostasis by Kidney-specific WNK1 Kinase*

Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms

Regulation of ROMK Channel and K+ Homeostasis by Kidney-specific WNK1 Kinase

The kidney-specific WNK1 isoform is induced by aldosterone and stimulates epithelial sodium channel-mediated Na+ transport

Antagonistic regulation of myogenesis by two deubiquitinating enzymes, UBP45 and UBP69

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension

Regulation of distal nephron K+ channels (ROMK) mRNA expression by aldosterone in rat kidney

Differential curvature sensing and generating activities of dynamin isoforms provide opportunities for tissue-specific regulation

Activation of PI3-Kinase Stimulates Endocytosis of ROMK via Akt1/SGK1-Dependent Phosphorylation of WNK1

Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms

Similar Documents

Regulation of ROMK Channel and K+ Homeostasis by Kidney-specific WNK1 Kinase*

Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms

Regulation of ROMK Channel and K+ Homeostasis by Kidney-specific WNK1 Kinase

The kidney-specific WNK1 isoform is induced by aldosterone and stimulates epithelial sodium channel-mediated Na+ transport

Antagonistic regulation of myogenesis by two deubiquitinating enzymes, UBP45 and UBP69

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension

Regulation of distal nephron K+ channels (ROMK) mRNA expression by aldosterone in rat kidney

Differential curvature sensing and generating activities of dynamin isoforms provide opportunities for tissue-specific regulation

Activation of PI3-Kinase Stimulates Endocytosis of ROMK via Akt1/SGK1-Dependent Phosphorylation of WNK1

Antagonistic regulation of ROMK by long and kidney-specific WNK1 isoforms