Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (Ab15895)
VDAC, VDAC1, Non-selective voltage-gated ion channel VDAC1, Outer mitochondrial membrane protein porin 1, Plasmalemmal porin, Porin 31HL, Porin 31HM, Voltage-dependent anion-selective channel protein 1, VDAC-1, hVDAC1, Non-selective voltage-gated ion channel VDAC2, VDAC-2, hVDAC2, Outer mitochondrial membrane protein porin 2, VDAC2, Non-selective voltage-gated ion channel VDAC3, VDAC-3, hVDAC3, Outer mitochondrial membrane protein porin 3
详细信息
特异性
This antibody detects VDAC1, VDAC2 and VDAC3.
背景信息
Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (ab15895) is a rabbit polyclonal antibody and is validated for use in ICC/IF, IHC-P, WB in human, mouse, rat samples. Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (ab15895) has been cited over 398 times in peer reviewed journals and is trusted by the scientific community. Abcam's high quality validation processes ensure Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (ab15895) has high sensitivity and specificity. Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (ab15895) has 33 independent reviews from customers. Anti-VDAC1/Porin + VDAC2 + VDAC3 antibody – Mitochondrial Loading Control (ab15895) specifically detects VDAC1/Porin; VDAC2; VCAD3 (UniProt ID: P21796; Molecular weight: 31kDa) and is sold in 100 µg and 250 µg selling sizes.
文献引用 (413)
Mitochondrial permeability transition pore desensitization by a novel dispiranic derivative prevents cardiac reperfusion injury.
一种新型双哌拉西林衍生物通过线粒体通透性转换孔脱敏来预防心脏再灌注损伤。
Synergistic Neurotoxicity of environmental Cadmium and Paraquat in Parkinsonism: Unveiling the Mito-ROS/OPA1/Caspase-3/GSDME-driven Apoptosis Axis.
环境镉和百草枯对帕金森病的协同神经毒性：揭示线粒体ROS/OPA1/Caspase-3/GSDME驱动的细胞凋亡轴。
Talin-tensin3 interactions regulate fibrillar adhesion formation and tensin3 phase separation.
Talin-tensin3 相互作用调节纤维粘附形成和 tensin3 相分离。
NAD+ and Sirt5 restore mitochondrial bioenergetics failure and improve locomotor defects caused by sucla2 mutations.
NAD+ 和 Sirt5 可恢复线粒体生物能量学功能障碍，并改善由 sucla2 突变引起的运动缺陷。
A shift in the cellular redox state redirects aspartate for export under glucose deprivation.
在葡萄糖缺乏的情况下，细胞氧化还原状态的改变会将天冬氨酸重新定向输出。
LPLAT10/LPEAT2 produces atypical phospholipids with an unsaturated FA at the sn-1 position.
LPLAT10/LPEAT2 产生非典型磷脂，其 sn-1 位具有不饱和脂肪酸。
Sex-dependent differences in bioenergetics of young mouse brain microvasculature: implications for oxygen-glucose deprivation and reoxygenation injury.
年轻小鼠脑微血管生物能量学的性别差异：对氧葡萄糖剥夺和再氧合损伤的影响。
A new subset of mitochondrial-derived vesicles perform inter-mitochondrial communications.
一类新的线粒体衍生囊泡进行线粒体间的通讯。
Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.
通过抑制电压依赖性阴离子通道靶向寻常型天疱疮中ST18介导的致病机制。
Metabolic adaptations direct cell fate during tissue regeneration
代谢适应在组织再生过程中指导细胞命运。
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