biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
technique(s)
immunohistochemistry: 1:20- 1:50
immunogen sequence
RTPVVRPAHISAFLQDRPIPEWCGVQHIHLSPSHHSGSKAASLHW
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SDHD(6392)
General description
Succinate dehydrogenase complex subunit D (SDHD) gene encodes for a protein SDHD. It is a small sub unit of the cytochrome b, that is involved in the complex II of mitochondrial respiration. It is located at 11q23.1 on the human chromosome.
Immunogen
Succinate dehydrogenase complex subunit D recombinant protein epitope signature tag (PrEST)
Application
Anti-SDHD antibody produced in rabbit has been used in immunohistochemistry.
Biochem/physiol Actions
Mutation in this gene leads to paraganglioma and phaeochromocytoma.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Physical form
Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.
Other Notes
Corresponding Antigen APREST84465
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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In vivo detection of succinate by magnetic resonance spectroscopy as a hallmark of SDHx mutations in paraganglioma
Lussey L C, et al.
Clinical Cancer Research, 22(5), 1120-1129 (2016)
Risk assessment of maternally inherited SDHD paraganglioma and phaeochromocytoma
Burnichon N, et al.
Journal of medical Genetics, 54(2), 125-133 (2017)
Mélanie Menara et al.
The Journal of clinical endocrinology and metabolism, 100(2), E287-E291 (2014-11-19)
Pheochromocytomas (PCC) and paragangliomas (PGL) may be caused by a germline mutation in 12 different predisposing genes. We previously reported that immunohistochemistry is a useful approach to detect patients harboring SDHx mutations. SDHA immunostaining is negative in SDHA-mutated tumors only
Charlotte Lussey-Lepoutre et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 22(5), 1120-1129 (2015-10-23)
Germline mutations in genes encoding mitochondrial succinate dehydrogenase (SDH) are found in patients with paragangliomas, pheochromocytomas, gastrointestinal stromal tumors, and renal cancers. SDH inactivation leads to a massive accumulation of succinate, acting as an oncometabolite and which levels, assessed on
Analysis of the SDHD gene, the susceptibility gene for familial paraganglioma syndrome (PGL1), in pheochromocytomas
Aguiar R C T, et al.
The Journal of Clinical Endocrinology and Metabolism, 86(6), 2890-2894 (2001)
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