SMC-392
KCC2 Antibody, Clone N1/12
Cannot supply to this region.
- SKU:
- SMC-392
- Additional Names:
- KCC2, KCC 2, rKCC2, hKCC2, SLC12A5, S12A5, KIAA1176, Solute carrier family 12 member 5, Solute carrier family 12 (potassium chloride transporter) member 5, Potassium chloride transporter 5, Electroneutral potassium-chloride cotransporter 2, Electroneutral potassium chloride cotransporter 2, Furosemide-sensitive K-Cl cotransporter, Furosemide sensitive K Cl cotransporter, K-Cl cotransporter 2, Neuronal K-Cl cotransporter, Neuronal K Cl cotransporter, Erythroid K Cl cotransporter 2, Potassium
- Application:
- IHC, WB, IF, ICC, IP
- Concentration:
- 1 mg/ml
- Species Reactivity:
- Rat
- Purification:
- Protein G Purified
- Storage Conditions:
- -20[o]C
- Supplier:
- StressMarq Biosciences
- Host:
- Mouse
- Reactivities:
- Human, Mouse, Rat
- ABP:
- IMP-GEN-2015-06 < 10% Serum <100ml
- Buffer:
- PBS pH7.4, 50% glycerol, 0.09% sodium azide
- Immunogen:
- Fusion protein amino acids 932-1043 corresponding to rat KCC2
- Clone:
- N1/12 (Formerly sold as S1-12)
- Uniprot:
- Q63633
- Synonyms:
- electroneutral potassium-chloride cotransporter 2;furosemide-sensitive K-Cl cotransporter;K-Cl cotransporter 2;Kcc2;neuronal K-Cl cotransporter;neuronal-specific K-Cl cotransporter;solute carrier family 12 (potassium-chloride transporter), member 5;solute carrier family 12 member 5
- Extra Details:
- KCC2 (potassium-chloride cotransporter 2) is a neuron-specific member of the cation-chloride cotransporter family, essential for maintaining low intracellular chloride concentrations. By leveraging potassium gradients, KCC2 facilitates chloride extrusion, enabling hyperpolarizing GABAergic inhibition-a cornerstone of neuronal stability and synaptic precision. Highly expressed throughout the central nervous system, KCC2 is enriched at inhibitory synapses, particularly in the spinal cord and brain. Its function is critical for establishing the inhibitory tone required for proper motor control, sensory processing, and cognitive function. Disruption of KCC2 activity alters chloride homeostasis, leading to depolarizing GABA responses and impaired inhibitory signaling. Animal studies have demonstrated that KCC2 deficiency results in severe neurological phenotypes, including motor dysfunction, epilepsy, and anxiety-like behaviors. These findings underscore KCC2's pivotal role in maintaining excitatory-inhibitory balance and highlight its relevance in the pathogenesis of neurodegenerative and neurodevelopmental disorders. In conditions such as Alzheimer's disease, amyotrophic lateral sclerosis (ALS), and traumatic brain injury, KCC2 downregulation contributes to neuronal hyperexcitability and excitotoxicity. As a result, KCC2 has emerged as a promising therapeutic target. Pharmacological and genetic strategies aimed at enhancing KCC2 function are being actively explored to restore inhibitory signaling and protect against neurodegeneration. KCC2's central role in chloride regulation, synaptic inhibition, and disease progression positions it as a key focus in neuroscience and neurotherapeutic research.
- Shipping Conditions:
- Blue Ice