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
1-2 business days
Price:
Sale price$374.00

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
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: Mouse
PMID Dilution Publication
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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