CST, 8351S, NKCC1 (D13A9) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying NKCC1. Validated for Western Blotting,Immunoprecipitation,Immunofluorescence (Immunocytochemistry). Available in 2 sizes. Highly specific and rigorously validated in-house, NKCC1 (D13A9) Rabbit Monoclonal Antibody (CST #8351) is ready to ship. Product Usage Information Western Blotting: 1:2000 Immunoprecipitation: 1:50 Immunofluorescence (Immunocytochemistry): 1:100 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation, Immunofluorescence (Immunocytochemistry) Specificity / Sensitivity NKCC1 (D13A9) Rabbit Monoclonal Antibody recognizes endogenous levels of total NKCC1 protein. This antibody does not cross-react with NKCC2. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg80 of human NKCC1 protein. Background The electroneutral cation-chloride-coupled co-transporter (SLC12) gene family comprises bumetanide-sensitive Na /K /Cl (NKCC), thiazide-sensitive Na /Cl , and K /Cl (KCC) co-transporters. SLC12A1/NKCC2 and SLC12A2/NKCC1 regulate cell volume and maintain cellular homeostasis in response to osmotic and oxidative stress (1). The broadly expressed NKCC1 is thought to play roles in fluid secretion (i.e. salivary gland function), salt balance (i.e. maintenance of renin and aldosterone levels), and neuronal development and signaling (2-7). During neuronal development, NKCC1 and KCC2 maintain a fine balance between chloride influx (NKCC1) and efflux (KCC2), which regulates γ-aminobutyric acid (GABA)-mediated neurotransmission (3). Increased NKCC1 expression in immature neurons maintains high intracellular chloride levels that result in inhibitory GABAergic signaling; KCC2 maintains low intracellular chloride levels and excitatory GABAergic responses in mature neurons (4,5,8). Deletion of NKCC1 impairs NGF-mediated neurite outgrowth in PC-12D cells while inhibition of NKCC1 with bumetanide inhibits re-growth of axotomized dorsal root ganglion cells (6,7). Defective chloride homeostasis in neurons is linked to seizure disorders that are ameliorated by butemanide treatment, indicating that abnormal NKCC1 and NKCC2 expression or signaling may play a role in neonatal and adult seizures (9-12). NKCC1 is found as a homodimer or within heterooligomers with other SLC12 family members. This transport protein associates with a number of oxidative- and osmotic-responsive kinases that bind, phosphorylate, and activate NKCC1 co-transporter activity (13-16). In response to decreased intracellular chloride concentrations, Ste20-related proline-alanine-rich kinase (SPAK) phosphorylates NKCC1 to increase co-transporter activity and promote chloride influx (16-19). Oxidative stress response kinase 1 (OSR1) also phosphorylates and activates NKCC1 in response to oxidative stress (14). Alternate Names Basolateral Na-K-Cl symporter; BSC; BSC2; Bumetanide-sensitive sodium-(potassium)-chloride cotransporter 1; Bumetanide-sensitive sodium-(potassium)-chloride cotransporter 2; MGC104233; NKCC1; PPP1R141; protein phosphatase 1, regulatory subunit 141; S12A2; SLC12A2; solute carrier family 12 (sodium/potassium/chloride transporter), member 2; solute carrier family 12 (sodium/potassium/chloride transporters), member 2; Solute carrier family 12 member 2 Specification REACTIVITY: H SENSITIVITY: Endogenous MW (kDa): 160-200 Source/Isotype: Rabbit IgG