Anti-KCNK18/TRESK antibody
Description
Application Data
Description
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An antibody raised against KCNK18/TRESK, a two-pore domain potassium channel with a key role in regulating neuronal excitability.
Application Data
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Data Sheet Data Sheet Data Sheet Material Safety Data Sheet (MSDS)Catalogue number crb2005677 Antibody Anti-KCNK18/TRESK antibody Antigen Peptide KLH conjugated synthetic peptide crb1200886 Protein ID UniProtKB - Q7Z418 Aliases Potassium channel subfamily K member 18, TWIK-related individual potassium channel, TWIK-related spinal cord potassium channel, KCNK18, TRESK, TRIK Cross-Reactivity Human Host Species Rabbit Antibody Type Polyclonal Concentration 0.4 mg/ml Glycine (R1G), 0.1 mg/ml TEA (R1T), 0.2 mg/ml Glycine (R2G) Target KCNK18/TRESK Family Two-pore domain potassium channel (TC 1.A.1.8) family Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References Dobler et al., (2007). TRESK two-pore-domain K+ channels constitute a significant component of background potassium currents in murine dorsal root ganglion neurones. J. Physiol. 585: 867. Doi: 10.1113/jphysiol.2007.145649.
Guo et al., (2014). Over-expression of TRESK K(+) channels reduces the excitability of trigeminal ganglion nociceptors. PLoS One., 9(1): 87029. doi: 10.1371/journal.pone.0087029.
Weir et al., (2019). The Role of TRESK in Discrete Sensory Neuron Populations and Somatosensory Processing. Front. Mol. Neurosci., 12(170): 1. doi: 10.3389/fnmol.2019.00170.
TRESK (TWIK-related spinal cord K+ channel) functions as an outward rectifying potassium channel that generates K+ outward rectifier currents and sets resting membrane potential through operation as a background potassium channel. Activation is caused by the G-protein coupled receptor pathway, with calcium signals directly activating the channel via calcineurin.
TRESK has a prominent role in activating in vivo pain pathways and increased neuron excitability and is abundantly expressed in trigeminal and dorsal root ganglion neurons. Mutations in the KCNK18 gene have been associated with familial and sporadic migraines.