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Chou Long Huang
Researcher at Roy J. and Lucille A. Carver College of Medicine
Publications - 117
Citations - 7145
Chou Long Huang is an academic researcher from Roy J. and Lucille A. Carver College of Medicine. The author has contributed to research in topics: WNK1 & ROMK. The author has an hindex of 46, co-authored 111 publications receiving 6252 citations. Previous affiliations of Chou Long Huang include University of Texas at Dallas & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
Direct activation of inward rectifier potassium channels by PIP2 and its stabilization by Gβγ
TL;DR: It is reported that several cloned inward rectifier K+ channels directly bind PIP2, and that this binding correlates with channel activity and coexpression of Gβγ with GIRK channels slows the inhibition of K+ currents by PIP1 antibodies.
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Removal of sialic acid involving Klotho causes cell-surface retention of TRPV5 channel via binding to galectin-1
Seung Kuy Cha,Bernardo Ortega,Hiroshi Kurosu,Kevin P. Rosenblatt,Makoto Kuro-o,Chou Long Huang +5 more
TL;DR: Klotho participates in specific removal of α2,6-linked sialic acids and regulates cell surface retention of TRPV5 through this activity, which represents a novel mechanism for regulation of the activity of cell-surface glycoproteins and likely contributes to maintenance of calcium balance by Klotho.
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Mechanism of Hypokalemia in Magnesium Deficiency
Chou Long Huang,Elizabeth Kuo +1 more
TL;DR: Books suggesting that magnesium deficiency exacerbates potassium wasting by increasing distal potassium secretion are reviewed, suggesting that an increase in distal sodium delivery or elevated aldosterone levels may be required for exacerbating potassium wasting in magnesium deficiency.
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Cardioprotection by Klotho through downregulation of TRPC6 channels in the mouse heart
Jian Xie,Seung Kuy Cha,Seung Kuy Cha,Sung Wan An,Makoto Kuro-o,Lutz Birnbaumer,Chou Long Huang +6 more
TL;DR: It is demonstrated that deletion of Trpc6 prevents stress-induced exaggerated cardiac remodeling in Klotho-deficient mice and KlothO overexpression ameliorates cardiac pathologies in these mice and improves their long-term survival.
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Soluble Klotho Protects against Uremic Cardiomyopathy Independently of Fibroblast Growth Factor 23 and Phosphate
TL;DR: The results suggest that the decreased level of circulating soluble Klotho in CKD is an important cause of uremic cardiomyopathy independent of FGF23 and phosphate, opening new avenues for treatment of this disease.