Abcam, ab308511, Anti-CHCHD10 antibody [EPR26966-33] - BSA and Azide free

Size: 100µg / 1mg
Rabbit Recombinant Monoclonal CHCHD10 antibody. Carrier free. Suitable for WB, IHC-P, ICC/IF, Flow Cyt (Intra), IP and reacts with Human, Rat samples.
Key facts
Host species:Rabbit,
Clonality:Monoclonal,
Clone number:EPR26966-33,
Isotype:IgG,
Carrier free:Yes,
Reacts with:Human, Rat,
Applications:Flow Cyt (Intra), IHC-P, WB, ICC/IF, IPSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:The exact immunogen used to generate this antibody is proprietary information.

Product details:
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
Conjugation ready
Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications.
Use our
conjugation kits
for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Compatibility
This product is compatible with the Maxpar
Antibody Labeling Kit from Fluidigm, without the need for antibody preparation. Maxpar
is a trademark of Fluidigm Canada Inc.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein A, Storage buffer-pH: 7.2 - 7.4Constituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
The CHCHD10 protein also known as coiled-coil-helix-coiled-coil-helix domain containing 10 is a mitochondrial protein with a molecular weight of approximately 14 kDa. It is specifically localized within the intermembrane space of mitochondria and is expressed in various tissues with high levels in the brain heart and skeletal muscles. CHCHD10 plays a role in maintaining mitochondrial structure and function contributing to the stability and regulation of mitochondrial cristae.
Biological function summary
The CHCHD10 protein participates in mitochondrial processes that regulate cellular energy production and apoptosis. It is part of a complex network within mitochondria interacting with other proteins to support mitochondrial DNA maintenance and oxidative phosphorylation. Its presence helps maintain cellular homeostasis by preventing mitochondrial dysfunction which can otherwise trigger oxidative stress and cellular damage.
Pathways
CHCHD10 is integral in the maintenance of mitochondrial quality control and respiratory pathways. It is involved in the mitochondrial inner membrane organizing system (MINOS) complex that is important for organizing and stabilizing mitochondrial membrane structure. CHCHD10 also interacts with proteins like OPA1 and CHCHD2 which are important for mitochondrial dynamics and energy regulation demonstrating its key role in these pathways.
CHCHD10 mutations are linked to conditions like amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The interaction between CHCHD10 and other mitochondria-related proteins like SOD1 and TDP-43 highlights its role in the pathogenesis of these neurodegenerative diseases. These mutations lead to mitochondrial dysfunction which contributes to the degeneration of motor neurons in ALS and the degeneration of frontal and temporal lobes in FTD.