Datasheet

生物学的記述

Specificity	SLC12A3 Antibody [G5P18] detects endogenous levels of total SLC12A3 protein.
Background	SLC12A3, encoding the thiazide-sensitive Na-Cl cotransporter (NCC) within the SLC12 cation-chloride cotransporter family, mediates electroneutral apical sodium and chloride reabsorption exclusively in the distal convoluted tubule to fine-tune renal salt excretion and maintain extracellular volume. NCC operates through an alternating access mechanism where conserved transmembrane helices coordinate Na+ and Cl- binding in outward-open conformation, undergoing WNK kinase-dependent phosphorylation at the C-terminal regulatory domain that relieves autoinhibition and recruits 14-3-3 scaffolds to stabilize plasma membrane residency; SPAK/OSR1 kinases activated by upstream WNK1/4 sensing low intracellular Cl- phosphorylate NCC at critical serines/threonines, doubling transport velocity while trafficking motifs govern basolateral recycling via endosomal sorting. This pathway integrates dietary salt variation with hormonal fine-tuning, where angiotensin II sustains NCC via AT1R-PLCβ-PKC cascade, while aldosterone indirectly amplifies through serum/glucocorticoid kinase activation of NCC phosphorylation cascades. NCC handles 5-10% of filtered sodium load as the final rheostat preventing natriuresis under hypovolemia, positioning it as the primary thiazide target for hypertension management and essential readout for researchers modeling tubulopathy in kidney organoids or quantifying phosphoregulation via tubule-specific phosphoantibodies. Inactivating mutations disrupt folding/trafficking, causing Gitelman syndrome with profound salt wasting, hypokalemic alkalosis, hypomagnesemia, and secondary hyperaldosteronism that paradoxically lowers blood pressure through volume contraction.

Specificity

SLC12A3 Antibody [G5P18] detects endogenous levels of total SLC12A3 protein.

Background

SLC12A3, encoding the thiazide-sensitive Na-Cl cotransporter (NCC) within the SLC12 cation-chloride cotransporter family, mediates electroneutral apical sodium and chloride reabsorption exclusively in the distal convoluted tubule to fine-tune renal salt excretion and maintain extracellular volume. NCC operates through an alternating access mechanism where conserved transmembrane helices coordinate Na+ and Cl- binding in outward-open conformation, undergoing WNK kinase-dependent phosphorylation at the C-terminal regulatory domain that relieves autoinhibition and recruits 14-3-3 scaffolds to stabilize plasma membrane residency; SPAK/OSR1 kinases activated by upstream WNK1/4 sensing low intracellular Cl- phosphorylate NCC at critical serines/threonines, doubling transport velocity while trafficking motifs govern basolateral recycling via endosomal sorting. This pathway integrates dietary salt variation with hormonal fine-tuning, where angiotensin II sustains NCC via AT1R-PLCβ-PKC cascade, while aldosterone indirectly amplifies through serum/glucocorticoid kinase activation of NCC phosphorylation cascades. NCC handles 5-10% of filtered sodium load as the final rheostat preventing natriuresis under hypovolemia, positioning it as the primary thiazide target for hypertension management and essential readout for researchers modeling tubulopathy in kidney organoids or quantifying phosphoregulation via tubule-specific phosphoantibodies. Inactivating mutations disrupt folding/trafficking, causing Gitelman syndrome with profound salt wasting, hypokalemic alkalosis, hypomagnesemia, and secondary hyperaldosteronism that paradoxically lowers blood pressure through volume contraction.

使用情報

Application

WB, IHC

Dilution

WB	IHC
1:1000	1:100

Reactivity

Human, Mouse, Rat

Source

Rabbit Monoclonal Antibody

MW

113 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/24310820/
https://pubmed.ncbi.nlm.nih.gov/27872838/

Application Data

WB

Validated by Selleck

Lane 1: Mouse kidney