Purified anti-IDH2 Antibody, IDH2, KrMab-3,BioLegend,946002

This clone was tested for ICC using 4% PFA-fixed HepG2 cells permeabilized with either methanol or Triton X-100. While staining was observed with both methods, Triton X-100 permeabilization resulted in stronger staining.

Host

Mouse

Reactivity

Human, Mouse

Application

WB - Quality testedICC, IP - Verified

Platform ID

BAB055251611

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NamePurified anti-IDH2 Antibody, IDH2, KrMab-3
Cat. No.946002
HostMouse
RRIDAB_2894530 (BioLegend Cat. No. 946001)AB_2894530 (BioLegend Cat. No. 946002)
IsotypeMouse IgG2b, κ
ReactivityHuman, Mouse
ApplicationWB - Quality testedICC, IP - Verified
ClonalityMonoclonal
Clone NumberKrMab-3
Concentration0.5 mg/mL
TargetIDH2
ImmunogenSynthetic peptide corresponding to residues surrounding Ala174 of human IDH2 protein
PurityThe antibody was purified by affinity chromatography.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide
StorageThe antibody solution should be stored undiluted between 2°C and 8°C.
Regulatory StatusResearch Use Only

Scientific Background

Isocitrate dehydrogenase 2 (IDH2) is a mitochondrial enzyme that is directly involved in the TCA cycle. The primary role of IDH2 is to convert isocitrate to 2-ketoglutarate (α-KG). The mutated isoform of IDH2 has been reported in glioblastomas, AML, and other cancers. The gain of function mutation in IDH2 leads to the accumulation of oncometabolite 2-hydroxyglutarate (2HG), which competitively inhibits HIF Prolyl Hydroxylase 2 (PHD2). This results in the stabilization and accumulation of hypoxia-inducible factors (HIF). The downstream effects of this mutation promote epigenetic changes and impaired cellular differentiation.

Category Paths

Request a product

Please provide the required information below so that we can quickly source your products.