Affinity purified from pooled serum. Learn more.

NCC (Thr53) Antibody

Rabbit Polyclonal Antibody

Catalog #: p1311-53 Categories: , , Datasheet:

$119.00$380.00

  • SizePrice
Clear
Pooled Serum
Formulation:
Affinity Purified from Pooled Serum
Species Tested:
Human, Mouse, Rat
Expected Reactivity:
Guinea Pig, Hamster
Applications:
WB 1:1000-1:6000IHC 1:100-1:10,000 Don't see your application?
Host Species:
Rabbit Polyclonal
Molecular Weight:
~160 kDa
Cite This Antibody:
PhosphoSolutions Cat# p1311-53, RRID:AB_2650477
Antigen/Purification: ExpandCollapse

Phosphopeptide corresponding to amino acid residues surrounding the phospho-Thr53 of mouse NCC.

The antibody is prepared from pooled rabbit serum by affinity purification via sequential chromatography on phospho- and dephosphopeptide affinity columns.

Biological Significance: ExpandCollapse

The thiazide-sensitive sodium chloride cotransporter, NCC, is the major NaCl transport protein in the distal convoluted tubule (DCT) and plays an important role in maintaining blood pressure (Rosenbaek et al., 2014, Feng et al., 2015). Phosphorylation of NCC at Thr-53, Thr-58, and Ser-71 is an essential mediator of NCC function (Rosenbaek et al., 2014). 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).

Synonyms: ExpandCollapse

• FLJ96318 antibody
• Na Cl cotransporter antibody
• Na Cl symporter antibody
• Na-Cl symporter antibody
• NaCl electroneutral thiazide sensitive cotransporter antibody
• NCCT antibody
• SLC12A3 antibody
• S12A3_HUMAN antibody
• slc12a3 antibody
• Solute carrier family 12 (sodium/chloride transporters) member 3 antibody
• Solute carrier family 12 member 3 antibody
• Thiazide sensitive Na Cl cotransporter antibody
• Thiazide sensitive sodium chloride cotransporter antibody
• Thiazide-sensitive sodium-chloride cotransporter antibody
• TSC antibody

Storage

100 µl in 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg BSA per ml and 50% glycerol. Adequate amount of material to conduct 10-mini Western Blots.

Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.

Product Specific Protocols

Western Blotting

Click here to view our protocols page for Western blotting and lysate preparation.

Product Specific References for Applications and Species

Immunohistochemistry: Human | Mouse | Rat

Western Blot: Human | Mouse | Rat


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
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
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.

  • 5 – Excellent (publishable, performed ideally)
  • 4 – Good (publishable, would use again)
  • 3 – Average (publishable, might use again)
  • 2 – Poor (unpublishable, signal inconclusive)
  • 1 – No signal (unpublishable)
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