MyD88 L265P antibody for lymphoma research

MyD88 is a critical adapter protein for TLR signaling. It supports the assembly of a signaling complex that includes IRAK1/4 and subsequently led to NFkB activation. A gain-of-function mutation L265P in MyD88 is preferentially complexed to BTK (a key component of BCR signalling) and strongly enhances NFκB and JAK-STAT3 signaling, thereby promoting B-cell proliferation and survival.

 

 

MyD88 L265P is one of the most common driver mutations found in B-cell lymphomas and associated with a poor prognosis. L265P mutation occurs frequently in 90% of Waldenström’s macroglobulinemia (WM), 50-80% of IgM monoclonal gammopathy of undetermined significance (IgM-MGUS), and 29% of diffuse large B-cell lymphomas (DLBCL) cases. To date MW and aggressive DLBCL with activated B-cell-like (ABC) subtype remain incurable. Tumor-specific MyD88 L265P mutation represents a useful prognostic marker and a promising target for new therapy approach.

arigo offers MyD88 L265P specific antibody and human IgM ELISA kit which are useful tool to detect L265P mutant and measure the elevated IgM level in B-cell lymphomas.

 

 

Targeting MyD88 L265P-oncogenic signaling

MyD88 L265P mutation promotes oncogenic signaling through activation of BTK, HCK, NFkB and JAK-STAT3. It attracts the interest in therapies by targeting BTK, IRAK1/4, and JAK. arigo offers research tools to examine NFkB and JAK-STAT3 activity. They are useful solutions to in vitro validate the efficacy of novel therapeutic agents.

 

 

Rabbit mAbs for B cells