Anti-IDH1 Rabbit Monoclonal Antibody

Overview

This product is an anti-IDH1 antibody for target detection and characterization. Key identifiers include host species: Rabbit; Monoclonal; clone 23I10; isotype IgG; reactivity: Human,Mouse,Rat. Reported application contexts include WB, IHC, IP (as provided in the source record). Boster Bio Anti-IDH1 Rabbit Monoclonal Antibody catalog # M00129-2. Tested in WB, IHC, IP applications. This antibody reacts with Human, Mouse, Rat.

Key elements and design rationale

• Target: IDH1 (E3 ubiquitin-protein ligase parkin).
• Antibody format: Monoclonal; clone 23I10; isotype IgG.
• Host: Rabbit.
• Species reactivity: Human,Mouse,Rat (confirm in your model system with appropriate controls).

This description is intended to help interpret the antibody design and the biological context of the target using the fields provided in the catalog record, alongside general experimental considerations.

Biological background

IDH1 (protein: P2X purinoceptor 1) is a commonly studied target in molecular and cellular biology. Functional context (as provided): Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins, such as BCL2, SYT11, CCNE1, GPR37, RHOT1/MIRO1, MFN1, MFN2, STUB1, SNCAIP, SEPT5, TOMM20, USP30, ZNF746 and AIMP2 (PubMed:10973942, PubMed:10888878, PubMed:11431533, PubMed:12150907, PubMed:12628165, PubMed:16135753, PubMed:21376232, PubMed:23754282, PubMed:23620051, PubMed:24660806, PubMed:24751536). Mediates monoubiquitination as well as 'Lys-6', 'Lys-11', 'Lys-48'-linked and 'Lys-63'-linked polyubiquitination of substrates depending on the context (PubMed:19229105, PubMed:20889974, PubMed:25621951). Participates in the removal and/or detoxification of abnormally folded or damaged protein by mediating 'Lys-63'-linked polyubiquitination of misfolded proteins such as PARK7: 'Lys-63'- linked polyubiquitinated misfolded proteins are then recognized by HDAC6, leading to their recruitment to aggresomes, followed by degradation (PubMed:17846173, PubMed:19229105). Mediates 'Lys-63'- linked polyubiquitination of a 22 kDa O-linked glycosylated isoform of SNCAIP, possibly playing a role in Lewy-body formation (PubMed:11590439, PubMed:11431533, PubMed:19229105, PubMed:11590439, PubMed:15728840). Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy (PubMed:20889974). Promotes the autophagic degradation of dysfunctional depolarized mitochondria (mitophagy) by promoting the ubiquitination of mitochondrial proteins such as TOMM20, RHOT1/MIRO1 and USP30 (PubMed:19029340, PubMed:19966284, PubMed:23620051, PubMed:24896179, PubMed:25527291). Preferentially assembles 'Lys-6'-, 'Lys-11'- and 'Lys-63'-linked polyubiquitin chains following mitochondrial damage, leading to mitophagy (PubMed:25621951). Mediates 'Lys-48'-linked polyubiquitination of ZNF746, followed by degradation of ZNF746 by the proteasome; possibly playing a role in the regulation of neuron death (PubMed:21376232). Limits the production of reactive oxygen species (ROS). Regulates cyclin-E during neuronal apoptosis. In collaboration with CHPF isoform 2, may enhance cell viability and protect cells from oxidative stress (PubMed:22082830). Independently of its ubiquitin ligase activity, protects from apoptosis by the transcriptional repression of p53/TP53 (PubMed:19801972). May protect neurons against alpha synuclein toxicity, proteasomal dysfunction, GPR37 accumulation, and kainate-induced excitotoxicity (PubMed:11439185). May play a role in controlling neurotransmitter trafficking at the presynaptic terminal and in calcium-dependent exocytosis. May represent a tumor suppressor gene. . Reported cellular localization context: Cytoplasm, cytosol . Nucleus. Endoplasmic reticulum. Mitochondrion . Mainly localizes in the cytosol. Co-localizes with SYT11 in neutrites. Co-localizes with SNCAIP in brainstem Lewy bodies. Mitochondrial localization gradually increases with cellular growth. Also relocates to dysfunctional mitochondria that have lost the mitochondrial membrane potential; recruitment to mitochondria is PINK1- dependent. Tissue expression notes (as provided): Highly expressed in the brain including the substantia nigra. Expressed in heart, testis and skeletal muscle. Expression is down-regulated or absent in tumor biopsies, and absent in the brain of PARK2 patients. Overexpression protects dopamine neurons from kainate-mediated apoptosis. Found in serum (at protein level). .

Research relevance and current trends

• Research context keywords from the source record include: Cell Biology,Metabolism,Mitochondrial Metabolism,Neurodegenerative Disease,Neurology Process,Neuroscience,Pathways and Processes,Proteasome / Ubiquitin,Proteolysis/Ubiquitin,Ring Finger E3 Ligase,Ubiquitin E3 Enzymes.
• Current studies often focus on connecting target abundance/localization to pathway perturbations across models, tissues, and cell states.
• Quantitative and multiplexed assays (e.g., imaging + immunoblot panels) are commonly used to compare phenotypes across conditions and time-courses.

Common research applications

• Western blotting (WB): assess relative target abundance across samples, treatments, or time-points.
• Immunohistochemistry (IHC): evaluate spatial distribution of target-positive staining in tissue architecture.
• Immunoprecipitation (IP): enrich target complexes for downstream immunoblot or interaction analyses.

Workflow ideas (metafield): Validate IDH1 antibody specificity using KO/KD control samples (WB/IF/IHC as appropriate), Detect IDH1 expression by Western blot in cell or tissue lysates, Detect IDH1 in FFPE tissue sections by immunohistochemistry, Enrich IDH1 by immunoprecipitation from lysates for downstream analysis

Notes for experimental interpretation

• Consider isoforms and post-translational modifications (PTMs) that may shift apparent molecular weight or epitope accessibility.
• Apparent molecular weight may vary by sample type and processing (observed MW: 47 kDa; calculated MW: 51641 MW).
• Control concepts: include appropriate negative controls (e.g., isotype, KO/KD samples) and orthogonal validation when feasible.

Additional product details (from the source record)

• Molecular weight (observed): 47 kDa
• Cellular localization (provided): Cytoplasm, cytosol . Nucleus. Endoplasmic reticulum. Mitochondrion . Mainly localizes in the cytosol. Co-localizes with SYT11 in neutrites. Co-localizes with SNCAIP in brainstem Lewy bodies. Mitochondrial localization gradually increases with cellular growth. Also relocates to dysfunctional mitochondria that have lost the mitochondrial membrane potential; recruitment to mitochondria is PINK1- dependent.
• Tissue details (provided): Highly expressed in the brain including the substantia nigra. Expressed in heart, testis and skeletal muscle. Expression is down-regulated or absent in tumor biopsies, and absent in the brain of PARK2 patients. Overexpression protects dopamine neurons from kainate-mediated apoptosis. Found in serum (at protein level). .

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