Anti-Kvbeta1.1 K+ Channel Antibody FL550 Conjugate (K9/40)
Our mouse Kvbeta1.1 K+ channel FL550 conjugate monoclonal antibody from NeuroMab is produced in-house from clone K9/40. It detects human, mouse, non-human primate, and rat Kvbeta1.1 K+ channel and is purified by Protein A chromatography. KO validated. Works in IHC, ICC.
Human, Mouse, Non-Human Primate, Rat
ICC, IHC
Mouse
SKU: 75-018-FL550
Ships: 1-5 business days
Product Details
Kvbeta1.1 K+ channel
Voltage-gated potassium channel subunit beta-1 or Kvβ1.1 is encoded by the gene KCNAB1. Kvß1.1 is a member of the potassium channel, voltage-gated, shaker-related subfamily. Alternative splicing of KCNAB1 allows for three distinct proteins to be made, Kvß1.1, Kvß1.2, and Kvß1.3. Each of these has a unique N terminus. Kvβ1.1 is a cytoplasmic subunit that modulates the characteristics of the membrane spanning, channel-forming alpha-subunits. Beta subunits can promote the closure of channels or enhance channel activity depending on the channel members. Kvß1 is predominantly expressed in brain and found in hippocampus, cerebral cortex, caudate putamen, colliculus and cerebellum. Diseases associated with this gene include Episodic Ataxia, Type 1 and Familial Temporal Lobe Epilepsy, 3
Purified by Protein A chromatography
Lot dependent: provided at 0.3-0.5 mg/mL
Monoclonal
K9/40
IgG2b
ICC, IHC
Mouse
Kcnab1 Kvb1
44 kDa
Synthetic peptide amino acids 7-28 (unique N-terminus) of rat Kv1.1 (TEHNLKSRNGEDRLLSKQSST; accession number NP_058999)
Rat
Human, Mouse, Non-Human Primate, Rat
AB_2939133
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 and conjugation of purified mAb. Purified mAbs are >90% specific antibody.
PBS with 0.09% azide
FL550 Ex: 550 nm, Em: 575 nm
Does not cross-react with Kvβ1.2, Kvβ1.3, Kvβ2
Each new lot of antibody is quality control tested by IHC on either rat or mouse brain and confirmed to give the expected staining pattern.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
United States
12 months from date of receipt
Akr8a8; Voltage-gated potassium channel subunit beta-1; mKv(beta1; EC 1.1.1.-; K(+ channel subunit beta-1; Kv-beta-1
P63143
UniProt Summary: Regulatory subunit of the voltage-gated potassium (Kv) Shaker channels composed of pore-forming and potassium-conducting alpha subunits and of regulatory beta subunits. The beta-1/KCNAB1 cytoplasmic subunit mediates closure of delayed rectifier potassium channels by physically obstructing the pore via its N-terminal domain and increases the speed of channel closure for other family members. Promotes the inactivation of KCNA1, KCNA2, KCNA4, KCNA5 and KCNA6 alpha subunit-containing channels. Displays nicotinamide adenine dinucleotide phosphate (NADPH)-dependent aldoketoreductase activity by catalyzing the NADPH-dependent reduction of a variety of endogenous aldehydes and ketones. The binding of NADPH is required for efficient down-regulation of potassium channel activity. Oxidation of the bound NADPH restrains N-terminal domain from blocking the channel, thereby decreasing N-type inactivation of potassium channel activity.
UniProt Summary: Regulatory subunit of the voltage-gated potassium (Kv) Shaker channels composed of pore-forming and potassium-conducting alpha subunits and of regulatory beta subunits. The beta-1/KCNAB1 cytoplasmic subunit mediates closure of delayed rectifier potassium channels by physically obstructing the pore via its N-terminal domain and increases the speed of channel closure for other family members. Promotes the inactivation of KCNA1, KCNA2, KCNA4, KCNA5 and KCNA6 alpha subunit-containing channels. Displays nicotinamide adenine dinucleotide phosphate (NADPH)-dependent aldoketoreductase activity by catalyzing the NADPH-dependent reduction of a variety of endogenous aldehydes and ketones. The binding of NADPH is required for efficient down-regulation of potassium channel activity. Oxidation of the bound NADPH restrains N-terminal domain from blocking the channel, thereby decreasing N-type inactivation of potassium channel activity.
16497
Shipped on ice packs
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