K0640
Anti-Potassium Channel Kv11.1 (HERG) Extracellular−FITC antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-KCNH2, Anti-Voltage gated K+ channel subfamily H member 2, Anti-ether-a-go-go-related channel 1
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About This Item
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biological source
rabbit
Quality Level
conjugate
FITC conjugate
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
human
technique(s)
flow cytometry: 2-10 μg/mL using 1x106 human live cells
immunocytochemistry: 1:25 using intact live HEK-KV11.1 transfected cells
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... KCNH2(3757)
Related Categories
General description
Anti-Potassium Channel KV11.1 (HERG)- Extracellular-FITC (Voltage gated K+ channel subfamily H member 2, KCNH2, ether-a-go-go-related channel 1) is produced in rabbit using as immunogen the peptide AFLLKETEEGPPATEC corresponding to residues 430-445 of human KV11.1 (HERG). Anti-KV11.1 (HERG) antibody is directed against an extracellular epitope located between the S1 and S2 domains. The antibody is affinity purified on immobilized antigen and labeled with fluorescein isothiocyanate (FITC).
The gene Kv11.1, also referred to as KCNH2 (potassium voltage-gated channel subfamily H member 2), is mapped to human chromosome 7. The encoded voltage-activated potassium channel is a member of the ether-a-go-go (EAG) family.
Immunogen
peptide AFLLKETEEGPPATEC corresponding to residues 430-445 of human KV11.1 (HERG).
Application
Flow cytometry: a recommended working concentration of 2-10 μg per 1x106cells was determined using intact live human cells.
Biochem/physiol Actions
The gene Kv11.1, also referred to as HERG (human ether-a-go-go related gene), encodes the α-subunit of the rapid component of the delayed rectifier potassium channel. The third repolarization of the action potential of human cardiomyocytes is carried out by this protein. Mutations in this gene have been associated with type II hereditary long QT syndrome (LQT2). This disease is characterized by prolongation of the QT interval, abnormal T wave, torsade de pointes, syncope and sudden death caused by cardiac arrest.
Physical form
Lyophilized from phosphate buffered saline, pH 7.4, containing 1% BSA and 0.05% sodium azide.
Reconstitution
Reconstitute the lyophilized vial with 50 μL or 200 μL deionized water, depending on package size. Further dilutions should be made using a carrier protein such as BSA (1-3%).
Other Notes
Lyophilized powder can be stored intact at room temperature for several weeks. For extended storage, it should be stored at -20 °C or below. The reconstituted solution can be stored at 2-8 °C for up to 2 weeks. For longer storage, freeze in working aliquots. Avoid repeated freezing and thawing. Storage in “frost-free” freezers is not recommended. Centrifuge before use. Working dilution samples should be discarded if not used within 12 hours. The antibody is stable for at least 12 months when stored appropriately.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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[Progress in research on defective protein trafficking and functional restoration in HERG-associated long QT syndrome].
Fang P and Lian J
Zhonghua yi xue yi chuan xue za zhi (Chinese Journal of Medical Genetics), 33, 101-104 (2016)
Yu-Wen Cheng et al.
International journal of molecular sciences, 24(16) (2023-08-26)
KCNH2 loss-of-function mutations cause long QT syndrome type 2 (LQT2), an inherited cardiac disorder associated with life-threatening ventricular arrhythmia. Through whole-exome sequencing, we discovered a novel AGCGACAC deletion (S981fs) in the hERG gene of an LQT2 patient. Using a heterologous
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