Anti-Slo2.2/Slack K+ Channel Antibody (N3/26)

Our Anti-Slo2.2/Slack K+ channel mouse monoclonal primary antibody from NeuroMab is produced in-house from hybridoma clone N3/26. It is KO validated, detects human, marine mollusk, mouse, and rat Slo2.2/Slack K+ channel, and is purified by Protein A chromatography. It is great for use in IHC, ICC, WB.



SKU: 75-051

Volume: 100 µL
Price:
Sale price$385.00
Ships: 1-2 business days

Product Details

Slo2.2/Slack K+ channel
Potassium channel subfamily T member 1 or -KCNT1/Slo2.2/Slack K+ channel is encoded by the gene KCNT1. Slo2.2 is a member of the the voltage-gated ion channel (vic) superfamily, and the KCNT protein family, which is made of KCNT1 and KCNT2. Slo2.2 functions as an outwardly rectifying potassium channel subunit to contribute to ion conductance and signaling pathways. Slo2.2 can be activated by high intracellular sodium or chloride levels. Slo2.2 is expressed at the membrane in many areas of the brain, brainstem, spinal cord, spleen and liver. Mutations in this gene cause the early-onset epileptic disorders
Purified by Protein A chromatography
1 mg/mL
Monoclonal
N3/26
IgG1
ICC, IHC, WB
Mouse
Kcnt1 Slack
140 kDa
Fusion protein amino acids 1168-1237 of rat Slo2.2 (accession number NP_068625) produced recombinantly in E. Coli
Human, Mouse, Rat
AB_2131855
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography. Purified mAbs are >90% specific antibody.
10 mM Tris, 50 mM Sodium Chloride, 0.065% Sodium Azide pH 7.4
WB: 1:1000
IHC: 1:400
ICC: 1:250
Unconjugated
No cross-reactivity reported
Each new lot of antibody is quality control tested by western blot on rat whole brain lysate and confirmed to stain the expected molecular weight band.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
United States
24 months from date of receipt
Shipped on ice packs
Potassium channel subfamily T member 1 (Sequence like a calcium-activated potassium channel subunit)

Product Specific References for Applications and Species

Immunocytochemistry: Mouse
PMID Dilution Publication
38457342not listedWu, J, et al. 2024. Disease-causing Slack potassium channel mutations produce opposite effects on excitability of excitatory and inhibitory neurons. Cell Reports, 113904.
Immunocytochemistry: Marine Mollusk
PMID Dilution Publication
231151701:1000Zhang, Y., et al. 2012. Regulation of neuronal excitability by interaction of fragile X mental retardation protein with slack potassium channels.. Journal of Neuroscience, 15318-15327.
Immunocytochemistry: Rat
PMID Dilution Publication
289829741:250Gururaj, S., et al. 2017. Protein kinase A-induced internalization of Slack channels from the neuronal membrane occurs by adaptor protein-2/clathrin-mediated endocytosis. Journal of Biological Chemistry, 19304-19314.
270915441:50Bansal, V., et al. 2016. Na(+) -Activated K(+) Channels in Rat Supraoptic Neurones. Journal of Neuroendocrinology, .
234668071:200Cervantes, B., et al. 2013. Identity, expression and functional role of the sodium-activated potassium current in vestibular ganglion afferent neurons.. Neuroscience, 163-175.
194038312.6ug/mlChen, H., et al. 2009. The N-terminal domain of Slack determines the formation and trafficking of Slick/Slack heteromeric sodium-activated potassium channels.. Journal of Neuroscience, 5654-5665.
Immunohistochemistry: Mouse
PMID Dilution Publication
382893381:100Yuan, T, et al. 2024. Coupling of Slack and NaV1.6 sensitizes Slack to quinidine blockade and guides anti-seizure strategy development. Elife, RP87559.
378893661:200Wu, J, et al. 2024. Interaction Between HCN and Slack Channels Regulates mPFC Pyramidal Cell Excitability in Working Memory Circuits. Molecular Neurobiology, 2430-2445.
356267301:500Zhou, F., et al. 2022. Slack Potassium Channels Modulate TRPA1-Mediated Nociception in Sensory Neurons. Cells, .
353595691:400Liu, Y., et al. 2022. The Slack Channel Deletion Causes Mechanical Pain Hypersensitivity in Mice. Frontiers in Molecular Neuroscience, 811441.
353468321:400Gertler, T.S., et al. 2022. KNa1.1 gain-of-function preferentially dampens excitability of murine parvalbumin-positive interneurons. Neurobiology of disease, 105713.
338178751:100-1:200Ehinger, R., et al. 2021. Slack K+ channels attenuate NMDA‐induced excitotoxic brain damage and neuronal cell death.. The FASEB Journal, e21568.
334016891:400Lu, R., et al. 2021. Functional Coupling of Slack Channels and P2X3 Receptors Contributes to Neuropathic Pain Processing. International Journal of Molecular Sciences, 405.
265879661:400Rizzi, S., et al. 2016. Differential distribution of the sodium-activated potassium channels slick and slack in mouse brain.. Journal of Comparative Neurology, 2093-2116.
291242161:200Rizzi, S., et al. 2015. Identification of potential novel interaction partners of the sodium-activated potassium channels Slick and Slack in mouse brain. Biochemistry and Biophysics Reports, 291-298.
256096271:400Lu, R., et al. 2015. Slack channels expressed in sensory neurons control neuropathic pain in mice.. Journal of Neuroscience, 1125-1135.
Immunohistochemistry: Rat
PMID Dilution Publication
238725941:1000Huang, F., et al. 2013. TMEM16C facilitates Na(+)-activated K+ currents in rat sensory neurons and regulates pain processing.. Nature Neuroscience, 1284-1290.
234668071:200Cervantes, B., et al. 2013. Identity, expression and functional role of the sodium-activated potassium current in vestibular ganglion afferent neurons.. Neuroscience, 163-175.
Immunoprecipitation: Human
PMID Dilution Publication
382893385ugYuan, T, et al. 2024. Coupling of Slack and NaV1.6 sensitizes Slack to quinidine blockade and guides anti-seizure strategy development. eLife, .
Immunoprecipitation: Mouse
PMID Dilution Publication
382893385ugYuan, T, et al. 2024. Coupling of Slack and NaV1.6 sensitizes Slack to quinidine blockade and guides anti-seizure strategy development. eLife, .
2912421640ugRizzi, S., et al. 2015. Identification of potential novel interaction partners of the sodium-activated potassium channels Slick and Slack in mouse brain. Biochemistry and Biophysics Reports, 291-298.
Western Blot: Mouse
PMID Dilution Publication
391028311:600Roslan, A., et al. 2024. Slack K+ channels confer protection against myocardial ischemia/reperfusion injury. Cardiovascular Research, .
361736838ug/mlBurbano, L.E., et al. 2022. Antisense Oligonucleotide Therapy for KCNT1 Encephalopathy. JCI Insight, e146090.
353595691:1000Liu, Y., et al. 2022. The Slack Channel Deletion Causes Mechanical Pain Hypersensitivity in Mice. Frontiers in Molecular Neuroscience, 811441.
353595691:1000Liu, Y., et al. 2022. The Slack Channel Deletion Causes Mechanical Pain Hypersensitivity in Mice. Frontiers in Molecular Neuroscience, 811441.
351973181:1000Zhang, Q., et al. 2022. The Slack Channel Regulates Anxiety-like Behaviors via Basolateral Amygdala Glutamatergic Projections to Ventral Hippocampus. The Journal of Neuroscience, 3049-3064.
308608701:500Pryce, K.D., et al. 2019. Magi-1 scaffolds NaV1.8 and Slack KNa channels in dorsal root ganglion neurons regulating excitability and pain. FASEB, 7315-7330.
28982974not listedGururaj, S., et al. 2017. Protein kinase A-induced internalization of Slack channels from the neuronal membrane occurs by adaptor protein-2/clathrin-mediated endocytosis. Journal of Biological Chemistry, 19304-19314.
289437561:1000Tomasello, D.L., et al. 2017. Slick (Kcnt2) Sodium-Activated Potassium Channels Limit Peptidergic Nociceptor Excitability and Hyperalgesia. Journal of Experimental Neuroscience, .
265879661:3000Rizzi, S., et al. 2016. Differential distribution of the sodium-activated potassium channels slick and slack in mouse brain.. Journal of Comparative Neurology, 2093-2116.
291242161:3000Rizzi, S., et al. 2015. Identification of potential novel interaction partners of the sodium-activated potassium channels Slick and Slack in mouse brain. Biochemistry and Biophysics Reports, 291-298.
26559620not listedMartinez-Espinosa, P.L., et al. 2015. Knockout of Slo2.2 enhances itch, abolishes KNa current, and increases action potential firing frequency in DRG neurons.. Elife, e10013.
256096271:500Lu, R., et al. 2015. Slack channels expressed in sensory neurons control neuropathic pain in mice.. Journal of Neuroscience, 1125-1135.
22145034not listedWojtovich, A.P., et al. 2011. SLO-2 is cytoprotective and contributes to mitochondrial potassium transport.. PLoS One, e28287.
26845140not listedWojtovich, A.P., et al. 2016. Cardiac Slo2.1 Is Required for Volatile Anesthetic Stimulation of K+ Transport and Anesthetic Preconditioning.. Anesthesiology, 1065-1076.
Western Blot: Rat
PMID Dilution Publication
289437561:1000Tomasello, D.L., et al. 2017. Slick (Kcnt2) Sodium-Activated Potassium Channels Limit Peptidergic Nociceptor Excitability and Hyperalgesia. Journal of Experimental Neuroscience, .
283666651:2000Evely, K.M., et al. 2017. The Phe932Ile mutation in KCNT1 channels associated with severe epilepsy, delayed myelination and leukoencephalopathy produces a loss-of-function channel phenotype. Neuroscience, 65-70.
270915441:500Bansal, V., et al. 2016. Na(+) -Activated K(+) Channels in Rat Supraoptic Neurones. Journal of Neuroendocrinology, .
26721627not listedGururaj, S., et al. 2016. Slack sodium-activated potassium channel membrane expression requires p38 mitogen-activated protein kinase phosphorylation.. Neuropharmacology, 279-289.
238725941:1000Huang, F., et al. 2013. TMEM16C facilitates Na(+)-activated K+ currents in rat sensory neurons and regulates pain processing.. Nature Neuroscience, 1284-1290.
20962237not listedNuwer, M.O., et al. 2010. PKA-induced internalization of slack KNa channels produces dorsal root ganglion neuron hyperexcitability.. Journal of Neuroscience, 14165-14172.

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