SLC12A3 Antibody [G5P18]

Catalog No.: F4003

Application: Reactivity: Human, Mouse, Rat

Lane 1: Mouse kidney

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IHC1:100

Application
WB, IHC

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Mouse, Rat

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

Predicted MW Observed MW
113 kDa 150 kDa,36 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

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

Clone
G5P18

Synonym(s)
NCC; TSC; SLC12A3; Solute carrier family 12 member 3; Na-Cl cotransporter; Na-Cl symporter; Thiazide-sensitive sodium-chloride cotransporter

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.

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.

References
[1] Moes AD, et al. Pflugers Arch. 2014 Jan;466(1):107-18. [2] Grillone T, et al. World J Nephrol. 2016 Nov 6;5(6):551-555.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%