Phospho NCC Thr53 - Top-Cited Antibodies Series

Anti-Phospho Thr53 Anti-NCC (Thiazide Sensitve NaCl Cotransporter) (cat. p1311-53)

Our NCC thr53 antibody is KO validated and works great in IHC.

Immunostaining of PFA perfused frozen kidney sections from WT and NCC KO mice showing specific labeling of the NCC protein phosphorylated at Thr53 (cat. p1311-53, red, 1:100,000) on the top and the absence of staining in the KO on the left. (Image courtesy of Lauren Miller, Ellison Lab, OHSU.)

As the major NaCl transport protein in the distal convoluted tubule (DCT), NCC plays an important role in maintaining blood pressure.

​​NCC can be regulated by changes in expression, trafficking and phosphorylation (Lou et al., 2016). Phosphorylation of NCC at Thr-53, Thr-58, and Ser-71 is an essential mediator of NCC function (Rosenbaek et al., 2014). Phosphorylation of NCC at threonine 53 (Thr53) is mediated by serum- and glucocorticoid-inducible kinase 1 (SGK1). NCC is constitutively cycled to the plasma membrane, and upon stimulation, it can be phosphorylated to both increase NCC activity and decrease NCC endocytosis, together increasing NaCl transport in the DCT (Feng et al., 2015).

Western blot of our NCC antibody shows specific labeling of NCC thr53 on a phosphatase treated mouse kidney blot.

Western blot of mouse kidney lysate showing specific immunolabeling of the ~160 kDa NCC protein phosphorylated at Thr53 in the first lane (-). Phosphospecificity is shown in the second lane (+) where immunolabeling is completely eliminated by blot treatment with lambda phosphatase (λ-Ptase, 1200 units for 30 min).

Many researchers have published with our NCC thr53 antibody in the last year and a half!

NCC thr53 Publications, 2021-2022
PMID Species Application Dilution Publication
35274831 Mouse WB 1:1000 Hu, C., et al. 2022. Profiling renal sodium transporters in mice with nephron Ift88 disruption: Association with sex, cysts, and blood pressure. Physiological Reports, 10(5), e15206.
34029145 Mouse WB 1:3000 Xiao, Y., et al. 2021. Deletion of renal Nedd4-2 abolishes the effect of high K+ intake (HK) on Kir4. 1/Kir5. 1 and NCC activity in the distal convoluted tubule. American Journal of Physiology-Renal Physiology, 321(1), F1-F11.
33900854 Mouse WB 1:3000 Duan, X.P., et al. 2021. Deletion of Kir5. 1 abolishes the effect of high-Na+-intake on Kir4. 1 and Na-Cl-cotransporter. American Journal of Physiology-Renal Physiology, 320(6), F1045-F1058.
35466690 Rat WB 1:1000 Staruschenko, A., et al. 2022. SGLT2 inhibition effect on salt-induced hypertension, RAAS, and sodium transport in Dahl SS Rats. American Journal of Physiology-Renal Physiology, Epub ahead of print
34904226 Rat WB not listed Isaeva, E., et al. 2021. Crosstalk between epithelial sodium channels (ENaC) and basolateral potassium channels (Kir4.1/Kir5.1) in the cortical collecting duct. British Journal of Pharmacology
  1. Lou Y, Zhang F, Luo Y, Wang L, Huang S, Jin F. Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis. (2016) Int J Mol Sci. 10;17(8):1307
  2. Rosenbaek LL, Kortenoeven ML, Aroankins TS, Fenton RA. (2014) J Biol Chem. 289(19):13347-13361.
  3. Feng X, Zhang Y, Shao N, Wang Y, Zhuang Z, Wu P, Lee MJ, Liu Y, Wang X, Zhuang J, Delpire E, Gu D, Cai H. (2015) Am J Physiol Renal Physiol. 308(10):F1119-27 
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