Anti-VDAC1/Porin + VDAC2 antibody [EPR10852(B)] - Mitochondrial Loading Control (Ab154856)
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
详细信息
背景信息
What is this antibody validated in? Anti-VDAC1/Porin + VDAC2 antibody [EPR10852(B)] - Mitochondrial Loading Control (ab154856) is a rabbit recombinant monoclonal antibody and is validated for use in Western Blot (WB), Immunohistochemistry (IHC-P), Immunohistochemistry (IHC-Fr), Immunocytochemistry/immunofluorescence (ICC/IF) and Flow Cytometry (Intra) in Human, Mouse, Rat samples. What is the molecular weight of VDAC1/Porin? Anti-VDAC1/Porin + VDAC2 [EPR10852(B)] - Mitochondrial Loading Control (ab154856) is often used as a loading control in Western blot. It specifically detects a band for VDAC1/Porin (UniProt: P21796) at a molecular weight of 31kDa. Trusted by the scientific community Anti-VDAC1/Porin + VDAC2 [EPR10852(B)] - Mitochondrial Loading Control (ab154856) was first used in a scientific publication in 2012 and has been cited over 90 times in peer-reviewed journals. Specificity confirmed The specificity of Anti-VDAC1/Porin + VDAC2 antibody [EPR10852(B)] - Mitochondrial Loading Control (ab154856) has been confirmed by Western blot testing in VDAC1 Knockout HAP1 cell line, ab255444. Other related products We have a range of other formats of antibody clone [EPR10852(B)] also available for your convenience: ab154856, HRP - ab185063, Carrier free - ab240128, PE - ab317896, APC - ab317934, Alexa Fluor® 488 - ab317974, Alexa Fluor® 594 - ab318015, Alexa Fluor® 555 - ab318057, Alexa Fluor® 647 - ab318099, Alexa Fluor® 750 - ab321135 Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents. What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies. Trial sizes available! Test your antibody or perform pre-screening before committing to a larger quantity. Sold in 20µl. Discover our selection of trial-size antibodies.
文献引用 (118)
Regulation of mitochondrial ROS by C15ORF48 in a basal cell subpopulation contributes to chemotherapy resistance in TNBC.
基底细胞亚群中 C15ORF48 对线粒体 ROS 的调节导致 TNBC 产生化疗耐药性。
Mitochondrial DNA release via VDAC1 in keratinocytes: a key driver of innate immunity and vitiligo pathogenesis.
角质形成细胞中通过 VDAC1 释放线粒体 DNA：先天免疫和白癜风发病机制的关键驱动因素。
Voltage-dependent anion channel 1 oligomerization regulates PANoptosis in retinal ischemia-reperfusion injury.
电压依赖性阴离子通道 1 寡聚化调节视网膜缺血再灌注损伤中的 PANoptosis
Kynurenic Acid/GPR35 Signaling Protects the Infarcted Heart by Suppressing Macrophage mtDNA-Triggered cGAS-STING Activation.
犬尿酸/GPR35 信号通过抑制巨噬细胞 mtDNA 触发的 cGAS-STING 激活来保护梗死的心脏。
p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.
p53 与 VDAC1 相互作用，调节其表达水平和寡聚状态，从而激活细胞凋亡。
Nitrogen cavitation enables rapid and high-yield preparation of functional cell-membrane-derived vesicles.
氮气空化技术能够快速、高产地制备功能性细胞膜衍生囊泡。
Selective antagonism of adenosine A2A receptor reduces hypobaric hypoxia-induced neuroinflammation by inhibiting cGAS-STING pathway.
选择性拮抗腺苷 A2A 受体可通过抑制 cGAS-STING 通路来减轻低压缺氧引起的神经炎症。
Boosting energy metabolism and biosynthesis in diverse organisms by a common bacterial salvage lipoylation protein.
一种常见的细菌补救性脂酰化蛋白能够促进多种生物体的能量代谢和生物合成
Genome-Wide CRISPR/Cas9 Screening Identifies the COMMANDER Recycling Complex as a Key Player in EV Uptake
全基因组 CRISPR/Cas9 筛选发现 COMMANDER 回收复合物是 EV 吸收的关键参与者。
Hsp90Â C-terminal domain inhibition enhances ferroptosis by disrupting GPX4-VDAC1 interaction to increase HMOX1 release from oligomerized VDAC1 channels.
Hsp90 C 端结构域抑制通过破坏 GPX4-VDAC1 相互作用来增强铁死亡，从而增加 HMOX1 从寡聚化的 VDAC1 通道中的释放
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