ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体

ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体 化学構造式
CAS番号.
化学名:
ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体
别名:
ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体
英語名:
Anti-Calcium Channel CaV3.2 (α1H) antibody produced in rabbit
英語别名:
Anti-Calcium Channel CaV3.2 (α1H) antibody produced in rabbit
CBNumber:
CB32100015
化学式:
分子量:
0
MOL File:
Mol file

ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体 物理性質

貯蔵温度 :
-20°C
外見 :
凍結乾燥粉末

安全性情報

ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体 価格

メーカー 製品番号 製品説明 CAS番号 包装 価格 更新時間 購入

ANTI-ANTI-CALCIUM CHANNEL CAV3.2 (Α1H) ウサギ宿主抗体 化学特性,用途語,生産方法

使用

Anti-Calcium Channel CaV3.2 (α1H) antibody produced in rabbit is suitable for western blotting at a dilution of 1:200 using lysate from the ND7/23 cell line.

一般的な説明

Calcium channel, voltage-dependent, T type, α1H subunit (CACNA1H) is a protein encoded by the CACNA1H gene in humans and is mapped to chromosome 16p13.3. The proteins are membrane protein machinery performing selective permeation of external calcium ions. The α1H channel is sensitive to mibefradil, a nondihydropyridine Ca2+ channel blocker. CACNA1H is abundantly expressed in both peripheral and central endings of the primary afferent neurons, regulating neuronal excitability and release of excitatory neurotransmitters.

Biochem/physiol Actions

Calcium channel, voltage-dependent, T type, α1H subunit (CACNA1H) plays an essential role in regulating neuronal excitability and network oscillations in the brain. Mutations in the gene are associated with various forms of idiopathic generalized epilepsy. Gaining-of-function mutation in CACNA1H increases seizure susceptibility by directly altering neuronal electrical properties and indirectly by changing gene expression. CACNA1H acts as an important mediator of Ca2+ entry near the resting membrane potential. It plays a pivotal role in processing of pain signals and may serve as a novel target for development of drugs for the treatment of intractable pain resistant to currently available analgesics. CACNA1H up-regulation is involved in the pathophysiology of inflammatory, neuropathic and visceral pain.

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