MAB13170
抗-Cav1.2钙通道抗体，克隆L57/46
clone L57/46, from mouse
别名:
calcium channel, voltage-dependent, L type, alpha 1C subunit1, voltage-gated calcium channel alpha subunit Cav1.2, calcium channel, L type, alpha 1 polypeptide, isoform 1, cardic muscle, calcium channel, cardic dihydropyridine-sensitive, alpha-1 subunit,
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所有图片(2)
About This Item
UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41
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生物来源
mouse
质量水平
抗体形式
purified immunoglobulin
抗体产品类型
primary antibodies
克隆
L57/46, monoclonal
种属反应性
mouse, human
种属反应性（根据同源性预测）
rabbit (based on 100% sequence homology), rat (based on 100% sequence homology)
技术
immunohistochemistry: suitable
western blot: suitable
同位素/亚型
IgG2bκ
NCBI登记号
UniProt登记号
运输
wet ice
靶向翻译后修饰
unmodified
基因信息
human ... CACNA1C(775)
rabbit ... Cacna1C(100101555)
一般描述
该基因可编码电压依赖性钙通道的α-1亚基。钙离子通道在膜极化时介导钙离子流入细胞。α -1亚基由24个跨膜片段组成，并形成离子进入细胞的孔。钙通道由α -1、α -2/ δ、β和γ亚基按1:1:1:1的比例组成。每一种蛋白质都有多种亚型，有的由不同的基因编码，有的是转录物选择性剪接的结果。由该基因编码的蛋白质与二氢吡啶结合并被二氢吡啶抑制。该基因的许多替代转录剪接变体已被观察到，但尚未完全表征。
特异性
该抗体可识别胞质结构域的Cav1.2钙通道。
免疫原
表位：细胞质结构域
重组蛋白，对应于C端附近细胞质结构域的兔Cav1.2钙通道。
应用
免疫组化分析： 该抗体的1:300稀释液已显示可检测人肾脏组织中的Cav1.2钙通道。
研究子类别
离子通道 & 转运蛋白
离子通道 & 转运蛋白
研究类别
神经科学
神经科学
该抗Cav1.2钙通道抗体，克隆L57/46经验证可用于WB、IH中Cav1.2钙通道的检测。
质量
通过蛋白质印迹法在小鼠脑组织裂解物中进行评价。
蛋白质印迹分析：2 µg/mL的该抗体可在10 µg小鼠脑组织裂解液中检测到Cav1.2钙通道。
蛋白质印迹分析：2 µg/mL的该抗体可在10 µg小鼠脑组织裂解液中检测到Cav1.2钙通道。
目标描述
在约240 kDa处观察到
外形
形式：纯化
纯化的小鼠单克隆IgG2bκ，溶于含0.1 M Tris-甘氨酸（pH 7.4，150 mM NaCl）和0.05％叠氮化钠的缓冲液中。
蛋白G纯化
储存及稳定性
自收到之日起，在2-8°C条件下可稳定保存1年。
分析说明
对照
小鼠脑组织裂解液
小鼠脑组织裂解液
其他说明
浓度：请参考批次特异性浓缩物的检验报告。
免责声明
除非我们的产品目录或产品附带的其他公司文档另有说明，否则我们的产品仅供研究使用，不得用于任何其他目的，包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。
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储存分类代码
12 - Non Combustible Liquids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Elizabeth J Akin et al.
The Journal of general physiology, 155(11) (2023-09-13)
Pulmonary arterial (PA) smooth muscle cells (PASMC) generate vascular tone in response to agonists coupled to Gq-protein receptor signaling. Such agonists stimulate oscillating calcium waves, the frequency of which drives the strength of contraction. These Ca2+ events are modulated by
Jia Li et al.
FEBS letters, 596(24), 3145-3158 (2022-08-04)
Cardiomyopathies are ascribed to a variety of etiologies, present with diverse clinical phenotypes, and lack disease-modifying treatments. Mounting evidence implicates dysregulated activin receptor signaling in heart disease and highlights inhibition of this pathway as a potential therapeutic target. Here, we
Christine Y Ivashchenko et al.
American journal of physiology. Heart and circulatory physiology, 305(6), H913-H922 (2013-07-09)
Human-induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs) have been recently derived and are used for basic research, cardiotoxicity assessment, and phenotypic screening. However, the hiPS-CM phenotype is dependent on their derivation, age, and culture conditions, and there is disagreement as to
Christopher J Garland et al.
Science signaling, 10(486) (2017-07-06)
Vascular smooth muscle contraction is suppressed by feedback dilation mediated by the endothelium. In skeletal muscle arterioles, this feedback can be activated by Ca2+ signals passing from smooth muscle through gap junctions to endothelial cells, which protrude through holes in
Dianaly T Au et al.
Arteriosclerosis, thrombosis, and vascular biology, 38(11), 2651-2664 (2018-10-26)
Objective- Mutations affecting contractile-related proteins in the ECM (extracellular matrix), microfibrils, or vascular smooth muscle cells can predispose the aorta to aneurysms. We reported previously that the LRP1 (low-density lipoprotein receptor-related protein 1) maintains vessel wall integrity, and smLRP1-/- mice
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