抗OPA1抗体 | Anti-OPA1 Antibody

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	Western Blot: OPA1 Antibody [NB110-55290] - Total protein from Human HeLa cells, Mouse MEF cells and Rat Brain was separated on a 7.5% gel by SDS-PAGE, transferred to PVDF membrane and blocked in 5% non-fat milk in TBST. The membrane was probed with 2.0 ug/ml anti-OPA1 in 1% blocking buffer. Precision Plus Protein All Blue molecular weight markers (BioRad) were detected with 1 ug/ml Anti-Blue Marker antibody (NBP2-33376). The protein ladder was detected with an anti-mouse HRP secondary antibody and OPA1 with an anti-rabbit HRP secondary antibody using chemiluminescence.
	Immunohistochemistry: OPA1 Antibody [NB110-55290] - Staining in prostatic smooth muscle and glandular epithelium. Human Prostate 40X magnification.
	Western Blot: OPA1 Antibody [NB110-55290] - Detection of OPA1 protein in post-nuclear extracts of mouse embryonic fibroblasts.
	Western Blot: OPA1 Antibody [NB110-55290] - analysis of OPA1 in porcine retinal pigment epithelium lysate using anti-OPA1 antibody. Image from verified customer review.
	Simple Western: OPA1 Antibody [NB110-55290] - Simple Western lane view shows a specific band for OPA1 in 0.5 mg/ml of MEF lysate. This experiment was performed under reducing conditions using the 12-230 kDa separation system.

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Background

OPA1 (optic atrophy-1) is a member of dynamin family of large GTPases and is a major player in fusion of the inner mitochondrial membrane and maintenance of cristae architecture, events which are orchestrated through oligomerization of differentially processed forms of OPA1. It exists as a single-pass membrane protein in the mitochondrion inner membrane as well as in soluble forms in mitochondrion intermembrane space, and is expressed in retina, brain, testis, heart, skeletal muscles etc. It binds with PARL and interacts with CHCHD3 as well as IMMT (preferentially with soluble OPA1 forms). Proteolytic processing in response to intrinsic apoptotic signals may lead to disassembly of OPA1 oligomers and release of the caspase activator cytochrome C (CYCS) into mitochondrial intermembrane space. OPA1 form S1: inactive form produced by cleavage at S1 position by OMA1 following stress conditions that induce loss of mitochondrial membrane potential, leading to negative regulation of mitochondrial fusion. Defects in OPA1 have been linked to optic atrophy type 1 (OPA1) and dominant optic atrophy plus syndrome (DOA+).

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