추천 제품
생물학적 소스
rabbit
Quality Level
결합
unconjugated
항체 형태
affinity isolated antibody
항체 생산 유형
primary antibodies
클론
polyclonal
양식
lyophilized powder
종 반응성
human, mouse, rat
기술
immunocytochemistry: suitable
western blot: 1:200 using rat heart membranes
UniProt 수납 번호
배송 상태
dry ice
저장 온도
−20°C
타겟 번역 후 변형
unmodified
유전자 정보
human ... CACNA1C(775)
mouse ... Cacna1c(12288)
rat ... Cacna1c(24239)
특이성
Recognizes mouse Cav1.2, splice variants P22002-4 and P22002-5 of rat Cav1.2 and splice variant P15381-4 of rabbit Cav1.2.
면역원
peptide corresponding to residues 2-15 of human Cav1.2 (exon 1B). The sequence has 14/15 residues identical in mouse and rat.
생화학적/생리학적 작용
Calcium channel, voltage-dependent, L type, α1C subunit (Cav1.2) is a protein encoded by the CACNA1C gene in humans and belongs to the family of voltage-gated calcium channels. It serves as the key transducers of cell surface membrane potential changes into local intracellular calcium transients that initiate different physiological events. CACNA1C is a subunit of L-type voltage-dependent calcium channel. It is mapped to chromosome 12p13.3 and is implicated as a susceptibility gene for schizophrenia. CACNA1C is selectively expressed in human TH2 cells and blockage of Cav1.2 channel activation in TH2 cells may represent new strategies to treat allergic diseases in human subjects. Its increased activity is implicated in the pathogenesis of dementia and Alzheimer′s disease (AD).
표적 설명
Calcium Channel CaV1.2 (CACNA1C ) encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization.
물리적 형태
Lyophilized from phosphate buffered saline, pH 7.4, with 1% BSA and 0.05% sodium azide.
면책조항
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
이미 열람한 고객
Fanfan Zheng et al.
Schizophrenia research, 152(1), 105-110 (2013-12-21)
CACNA1C (12p13.3) has been implicated as a susceptibility gene for schizophrenia by several replicated genome wide association studies. While these results have been consistent among studies in European populations, the findings in East Asian populations have varied. To test whether
Monika A Davare et al.
Proceedings of the National Academy of Sciences of the United States of America, 100(26), 16018-16023 (2003-12-11)
An increase in Ca2+ influx through L-type Ca2+ channels is thought to contribute to neuronal dysfunctions that underlie senile symptoms and Alzheimer's disease. The molecular basis of the age-dependent up-regulation in neuronal L-type Ca2+ channel activity is largely unknown. We
Man Xu et al.
The Journal of biological chemistry, 278(42), 40837-40841 (2003-08-06)
Voltage-gated calcium (Ca2+) channels play a key role in the control of heart contraction and are essential for normal heart development. The Cav1.2 L-type calcium channel is the predominant isoform in cardiomyocytes and is essential for excitation-contraction coupling. Although the
Virginie Robert et al.
The Journal of allergy and clinical immunology, 133(4), 1175-1183 (2013-12-25)
In addition to calcium release-activated calcium channel/ORAI calcium channels, the role of voltage-gated calcium (Cav1) channels in T-cell calcium signaling is emerging. Cav1 channels are formed by α1 (CaV1.1 to CaV1.4) and auxiliary subunits. We previously demonstrated that mouse TH2
Sven Moosmang et al.
The EMBO journal, 22(22), 6027-6034 (2003-11-12)
Blood pressure is regulated by a number of key molecules involving G-protein-coupled receptors, ion channels and monomeric small G-proteins. The relative contribution of these different signaling pathways to blood pressure regulation remains to be determined. Tamoxifen-induced, smooth muscle-specific inactivation of
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