Anti-NCC (Thiazide Sensitive NaCl Cotransporter) (Thr53) Antibody

from PhosphoSolutions Datasheet Trial Size Trial Size Pooled Serum Pooled Serum
43 Citations

Our Anti-NCC (Thiazide sensitve NaCl cotransporter) (Thr53) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions is produced in-house. It detects human, mouse, and rat NCC (Thiazide sensitve NaCl cotransporter) and is antigen affinity purified from pooled serum. It is great for use in WB, IHC.

Primary Antibody
Mouse
Guinea Pig, Hamster
IHC, WB
Rabbit
Antigen Affinity Purified from Pooled Serum
SLC12A3
160 kDa

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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).
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 left and the absence of staining in the KO on the right. (Image courtesy of Lauren Miller, Ellison Lab, OHSU.)
Two Western blots show the abundance of pNCCT53 (cat. p1311-53, 1:200) and tNCC in male Kcnj10fl/fl mice and in Ks-Kir4.1–KO mice treated with vehicle (control) and FK506 (0.75 mg/kg BW). Image from publication CC-BY-4.0. PMID: 36821372
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).
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).
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 left and the absence of staining in the KO on the right. (Image courtesy of Lauren Miller, Ellison Lab, OHSU.)
Two Western blots show the abundance of pNCCT53 (cat. p1311-53, 1:200) and tNCC in male Kcnj10fl/fl mice and in Ks-Kir4.1–KO mice treated with vehicle (control) and FK506 (0.75 mg/kg BW). Image from publication CC-BY-4.0. PMID: 36821372

Anti-NCC (Thiazide Sensitive NaCl Cotransporter) (Thr53) Antibody
SKU: p1311-53

Volume: 100 µL
Price:
$415

Bulk Order Anti-NCC (Thiazide Sensitive NaCl Cotransporter) (Thr53) Antibody

Product Specific References for Applications and Species

Immunohistochemistry: Human
PMID Dilution Publication
21963515 not listed Hoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
Immunohistochemistry: Mouse
PMID Dilution Publication
30517856 1:100 Saritas, T., et al. 2018. Optical Clearing in the Kidney Reveals Potassium-Mediated Tubule Remodeling. Cell reports, 25(10), pp.2668-2675.
29412704 1:10,000 Terker, A.S., et al. 2018. With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo. American Journal of Physiology-Renal Physiology, 315(4), pp.F781-F790.
29263298 1:10,000 Ferdaus, M.Z., et al. 2017. Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects. JCI insight, 2(24).
24799612 not listed Terker, A.S., et al. 2014. Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension. Hypertension, 64(1), pp.178-184.
22651238 not listed Komers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21963515 not listed Hoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
21907141 1:500 McCormick, J.A., et al. 2011. A SPAK isoform switch modulates renal salt transport and blood pressure. Cell metabolism, 14(3), pp.352-364.
21896937 not listed McCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.
Immunohistochemistry: Rat
PMID Dilution Publication
22651238 not listed Komers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21896937 not listed McCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.
Western Blot: Human
PMID Dilution Publication
29547703 1:2000 Tutakhel, O.A., et al. 2018. Dominant functional role of the novel phosphorylation site S811 in the human renal NaCl cotransporter. The FASEB Journal, pp.fj-201701047R.
21963515 not listed Hoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
Western Blot: Mouse
PMID Dilution Publication
370169341:2000Gao, Z.X., et al. 2023. Kir4.1 Deletion Prevents Salt-Sensitive Hypertension in Early Streptozotocin-Induced Diabetic Mice via Na + -Cl - Cotransporter in the Distal Convoluted Tubule. Journal of Hypertension, 958-970.
368213721:200Zhang, D.D., et al. 2023. Calcineurin-inhibitors Stimulate Kir4.1/Kir5.1 of Distal-Convoluted-Tubule to Increase Na-Cl Cotransporter (NCC). JCI Insight, e165987.
35274831 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 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 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.
33818128 1:3000 Zhang, D.D., et al. 2021. Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4. 1, ENaC and NCC, and causes hypokalemia during HS. American Journal of Physiology-Renal Physiology.
32924546 1:2000 Tahaei, E., et al. 2020. Distal convoluted tubule sexual dimorphism revealed by advanced 3D imaging. American Journal of Physiology-Renal Physiology, 319(5), pp.F754-F764.
32715760 1:1000 Wang, L.J., et al. 2020. PGF2α stimulates 10-pS Cl channel and thiazide-sensitive Na-Cl cotransporter (NCC) in distal convoluted tubule. American Journal of Physiology-Renal Physiology.
32633545 not listed Gilani, A., et al. 2020. Proximal tubule-targeted overexpression of the Cyp4a12-20-HETE synthase promotes salt-sensitive hypertension in male mice. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 319(1), pp.R87-R95.
32295826 not listed Wu, P., et al. 2020. Renal Tubule Nedd4-2 Deficiency Stimulates Kir4. 1/Kir5. 1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule. Journal of the American Society of Nephrology, Apr 15; ASN.2019090923.
31941842 1:1000 Jobbagy, S., et al. 2020. Nrf2 activation protects against lithium-induced nephrogenic diabetes insipidus. JCI Insight, 5(1).
31239388 not listed Wu, P., et al. 2019. . Deletion of Kir5. 1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake. Journal of the American Society of Nephrology, Aug;30(8):1425-1438.
30728179 not listed Khamaysi, A., et al. 2019. Systemic Succinate Homeostasis and Local Succinate Signaling Affect Blood Pressure and Modify Risks for Calcium Oxalate Lithogenesis. Journal of the American Society of Nephrology, pp.ASN-2018030277.
30571558 1:1000 Duan, X.P., et al. 2019. Norepinephrine-Induced Stimulation of Kir4. 1/Kir5. 1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule. Hypertension,73:112-120.
30355950 not listed Xu, J., et al. 2018. Slc4a8 in the Kidney: Expression, Subcellular Localization and Role in Salt Reabsorption. Cellular Physiology and Biochemistry, 50(4), pp.1361-1375.
30301860 1:2000 Cornelius, R.J., et al. 2018. Renal COP9 signalosome deficiency alters CUL3-KLHL3-WNK signaling pathway. Journal of the American Society of Nephrology, 29(11), pp.2627-2640.
30252533 1:1000 Cherezova, A., et al. 2018. Urinary concentrating defect in mice lacking Epac1 or Epac2. The FASEB Journal, pp.fj-201800435R.
29412704 1:2000 Terker, A.S., et al. 2018. With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo. American Journal of Physiology-Renal Physiology, 315(4), pp.F781-F790.
29310825 1:6000 Wang, M.X., et al. 2018. Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4. 1 potassium channel. Kidney international, 93(4), pp.893-902.
29263298 1:2000 Ferdaus, M.Z., et al. 2017. Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects. JCI insight, 2(24).
28052988 1:1000 Cuevas, C.A., et al. 2017. Potassium sensing by renal distal tubules requires Kir4. 1. Journal of the American Society of Nephrology, 28(6), pp.1814-1825.
27068441 1:2000 Ferdaus, M.Z., et al. 2016. SPAK and OSR1 play essential roles in potassium homeostasis through actions on the distal convoluted tubule. The Journal of physiology, 594(17), pp.4945-4966.
26712527 not listed Terker, A.S., et al. 2016. Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport. J Am Soc Nephrol. (8):2436-45
26432904 1:6000 Lazelle, R.A., et al. 2016. Renal deletion of 12 kDa FK506-binding protein attenuates tacrolimus-induced hypertension. Journal of the American Society of Nephrology, 27(5), pp.1456-1464.
26422504 not listed Terker, A.S., et al. 2015. Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis. Kidney international, 89(1), pp.127-134.
25565204 not listed Terker, A.S., et al. 2015. Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. Cell Metab. (1):39-50.
25250572 not listed McCormick, J.A., et al. 2014. Hyperkalemic hypertension–associated cullin 3 promotes WNK signaling by degrading KLHL3. The Journal of clinical investigation, 124(11), pp.4723-4736.
25113964 not listed Chávez -Canales, M., et al. 2014. WNK-SPAK-NCC cascade revisited: WNK1 stimulates the activity of the Na-Cl cotransporter via SPAK, an effect antagonized by WNK4. Hypertension, 64(5), pp.1047-1053.
24799612 not listed Terker, A.S., et al. 2014. Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension. Hypertension, 64(1), pp.178-184.
24231659 1:5000 Picard, N., et al. 2014. . Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension. Journal of the American Society of Nephrology, 25(3), pp.511-522.
22651238 not listed Komers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21963515 not listed Hoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
21907141 not listed McCormick, J.A., et al. 2011. A SPAK isoform switch modulates renal salt transport and blood pressure. Cell metabolism, 14(3), pp.352-364.
21896937 not listed McCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.
Western Blot: Rat
PMID Dilution Publication
373189901:1000Zietara, A, et al. 2023. Kir7.1 Knockdown and Inhibition Alter Renal Electrolyte Handling But Not the Development of Hypertension in Dahl Salt-sensitive Rats. American Journal of Physiology. Renal Physiology, F177-F187.
37082243not listedCai, L., et al. 2023. Dietary Sodium Enhances the Expression of SLC4 Family Transporters, IRBIT, L-IRBIT, and PP1 in Rat Kidney: Insights Into the Molecular Mechanism for Renal Sodium Handling. Frontiers in Physiology, 1154694.
35466690 1:1000 Kravtsova, O., et al. 2022. SGLT2 inhibition effect on salt-induced hypertension, RAAS, and Na+ transport in Dahl SS rats. American Journal of Physiology, 322(6), ppF692-F707.
34904226 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.
32830328 1:500 Fu, Y., et al. 2020. Geniposide in Gardenia jasminoides var. radicans Makino modulates blood pressure via inhibiting WNK pathway mediated by the estrogen receptors. Journal of Pharmacy and Pharmacology.
31608673 1:1000 Frame, A.A., et al. 2019. Sympathetic regulation of NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats. American Journal of Physiology-Renal Physiology, 317(6), pp.F1623-F1636.
28931751 not listed Palygin, O., et al. 2017. Essential role of K ir 5.1 channels in renal salt handling and blood pressure control. JCI Insight, 2(18).
22651238 not listed Komers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21896937 not listed McCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.

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