Invitrogen™ IRF8 Monoclonal Antibody (GW4CML3), eBioscience™

Description

Description: The GW4CML3 monoclonal antibody reacts with human and mouse interferon regulatory factor 8 (IRF8; ICSBP). IRF8 is a 50 kDa transcription factor that plays a critical role in the development of dendritic cells (DC). Specifically, IRF8 is essential in the development and differentiation of plasmacytoid DC (pDC) and CD8a+ DC. IRF8-/- mice are deficient in both pDC and CD8a+ DC populations. CD8a- DC are present in normal numbers in IRF8-/- mice but fail to mature upon Toll-like receptor signaling and are functionally impaired in response to in vivo microbial stimulation. IRF8 deficiency does not affect the frequency or viability of DC precursors and as a result retroviral IRF8 transduction restores pDC development from DC progenitors in IRF8-/- mice. Applications Reported: This GW4CML3 antibody has been reported for use in intracellular staining followed by flow cytometric analysis, and western blotting. (Fluorochrome conjugated GW4CML3 is recommended for use in intracellular flow cytometry). Applications Tested: This GW4CML3 antibody has been tested by western blot on lysates from stimulated normal human peripheral blood cells. This can be used at 1-5 μg/mL. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Purity: Greater than 90%, as determined by SDS-PAGE. Aggregation: Less than 10%, as determined by HPLC. Filtration: 0.2 μm post-manufacturing filtered.

IRF8 (interferon regulatory factor 8) is a transcriptional activator or repressor. It specifically binds to the upstream regulatory region of type I IFN and IFN-inducible MHC class I genes. IRF8 plays a negative regulatory role in cells of the immune system. It is involved in CD8+ dendritic cell differentiation by forming a complex with the BATF-JUNB heterodimer in immune cells. This leads to recognition of AICE sequence, an immune-specific regulatory element, followed by cooperative binding of BATF and IRF8 and activation of the genes. Mutations in the gene can result in immunodeficiencey 32A and 32B.