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KCNV2 Rabbit pAb (bs-16921R)  
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產品編號 bs-16921R
英文名稱 KCNV2 Rabbit pAb
中文名稱 電壓門控鉀通道Kv8.2抗體
別    名 KCNV2; KCNV2_HUMAN; KV11.1; Kv8.2; MGC120515; Potassium channel subfamily V member 2; Potassium voltage-gated channel subfamily V member 2; RCD3B; Voltage-gated potassium channel Kv8.2; Voltage-gated potassium channel subunit Kv8.2.  
研究領域 細胞生物  神經生物學  通道蛋白  
抗體來源 Rabbit
克隆類型 Polyclonal
克 隆 號
交叉反應 Human,Mouse (predicted: Rat,Rabbit,Pig,Cow,Chicken,Dog,Horse)
產品應用 IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=2μg/Test
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 62 kDa
檢測分子量
細胞定位 細胞膜 
性    狀 Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human KCNV2: 131-230/545 <Extracellular>
亞    型 IgG
純化方法 affinity purified by Protein A
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
產品介紹 Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium voltage-gated channel subfamily V. This member is identified as a 'silent subunit', and it does not form homomultimers, but forms heteromultimers with several other subfamily members. Through obligatory heteromerization, it exerts a function-altering effect on other potassium channel subunits. This protein is strongly expressed in pancreas and has a weaker expression in several other tissues. [provided by RefSeq, Jul 2008]

Function:
Potassium channel subunit. Modulates channel activity by shifting the threshold and the half-maximal activation to more negative values.

Subunit:
Heteromultimer with KCNB1, KCNC1 and KCNF1. Does not form homomultimers.

Subcellular Location:
Cell membrane. Has to be associated with KCNB1 or possibly another partner to get inserted in the plasma membrane. Remains intracellular in the absence of KCNB1.

Tissue Specificity:
Detected in lung, liver, kidney, pancreas, spleen, thymus, prostate, testis, ovary and colon.

DISEASE:
Defects in KCNV2 are the cause of cone dystrophy retinal type 3B (RCD3B) [MIM:610356]; also called cone dystrophy with night blindness and supernormal rod responses KCNV2-related. RCD3B is a rare form of cone dystrophy associated with supernormal rod responses. The disorder is characterized by reduced visual acuity, photoaversion, night blindness, and abnormal color vision. At an early age, the retina shows subtle depigmentation at the macula and, later, more obvious areas of atrophy.

Similarity:
Belongs to the potassium channel family. V (TC 1.A.1.2) subfamily. Kv8.2/KCNV2 sub-subfamily.

SWISS:
Q8TDN2

Gene ID:
169522

Database links:

Entrez Gene: 169522 Human

Entrez Gene: 240595 Mouse

Omim: 607604 Human

SwissProt: Q8TDN2 Human

SwissProt: Q8CFS6 Mouse

Unigene: 624689 Human

Unigene: 660831 Human

Unigene: 269759 Mouse



產品圖片
Tissue/cell: human colon carcinoma; 4% Paraformaldehyde-fixed and paraffin-embedded; Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-KCNV2 Polyclonal Antibody, Unconjugated(bs-16921R) 1:500, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Blank control(blue): Hepg2 Cells(fixed with 2% paraformaldehyde (10 min)). Primary Antibody: Rabbit Anti-KCNV2/FITC Conjugated antibody (bs-16921R /FITC), Dilution: 3μg in 100 μL 1X PBS containing 0.5% BSA; Isotype Control Antibody: Rabbit IgG/FITC(orange) ,used under the same conditions.
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