NCC Antibody: Biotin

The Na⁺-Cl⁻ co-transporter (NCC), primarily expressed in the distal convoluted tubule of the kidney, is a thiazide-sensitive transporter critical for sodium and chloride reabsorption. While traditionally studied in renal physiology and hypertension, emerging evidence suggests that NCC may also play a role in neurodegenerative disease through its influence on systemic electrolyte balance and neuronal excitability. NCC is activated by phosphorylation and regulated by signaling pathways involving SGK1 and WNK kinases. Dysregulation of NCC activity can alter extracellular potassium and sodium levels, indirectly affecting neuronal membrane potential and synaptic transmission. Additionally, NCC expression has been detected in non-renal tissues, including the lens and possibly the brain, suggesting broader physiological roles. In neurodegenerative contexts, electrolyte imbalance and altered ion transport are known contributors to neuronal dysfunction and glial activation. NCC-mediated sodium handling may influence neuroinflammatory responses and oxidative stress, particularly in conditions such as Alzheimer’s disease and vascular dementia. Furthermore, thiazide diuretics targeting NCC have been associated with cognitive effects, underscoring the transporter’s potential relevance in brain health. Understanding NCC’s extrarenal functions may reveal novel mechanisms linking ion transport to neurodegeneration and offer new therapeutic avenues for modulating neuronal homeostasis.

NCC, SLC12A3, SCYL1, CKb10, MCP-4, MGC17134, NCC-1, NCC1, SCYA13, CK-beta-10, Monocyte chemoattractant protein 4, Monocyte chemotactic protein 4, New CC chemokine 1, Small inducible cytokine A13, Small inducible cytokine subfamily A (Cys-Cys) member 13, Chemokine (C-C)

1 µg/ml of SPC-402 was sufficient for detection of NCC3 in 10 µg of rat kidney tissue lysate by colorimetric immunoblot analysis using Goat anti-rabbit IgG:HRP as the secondary antibody.

1. Vallon V., Schroth J, Lang F, Kuhl D and Uchida S. (2009) Am J Physiol Renal Physiol. 297 (3) : F704-712. 2. Tiwari S., et al. (2009) Am J Nephrol. 30 (6) : 554-562. 3. Chee K.N., Vorontsova I., Lim J.C., Kistler J. and Donaldson P.J. (2010) Mol Vis. 16:800-812.