BCL10 Human
Description
BCL10 is fused to a 24 amino acid His-tag at N-terminus & purified by proprietary chromatographic techniques.
Product Specs
Product Science Overview
BCL10 was first identified due to its involvement in mucosa-associated lymphoid tissue (MALT) lymphomas. The protein consists of 233 amino acids and contains a caspase recruitment domain (CARD), which is essential for its function in signaling pathways.
BCL10 is primarily involved in the adaptive immune response. It acts as a mediator in the signaling cascade that leads to the activation of NF-κB. This pathway is crucial for the proper functioning of B and T cells, which are essential components of the adaptive immune system.
- Signal Transduction: BCL10 is a part of the CARMA1-BCL10-MALT1 (CBM) complex, which is activated upon antigen receptor stimulation in B and T cells. This complex then activates the IκB kinase (IKK) complex, leading to the phosphorylation and degradation of IκB proteins, and the subsequent release and activation of NF-κB.
- Immune Response: Through the activation of NF-κB, BCL10 plays a vital role in the immune response, including the production of cytokines and the proliferation and survival of immune cells.
Mutations and translocations involving the BCL10 gene have been implicated in various lymphomas, particularly MALT lymphomas. These genetic alterations can lead to the constitutive activation of NF-κB, promoting uncontrolled cell growth and survival, which are hallmarks of cancer.
- MALT Lymphomas: BCL10 was initially identified due to its involvement in MALT lymphomas. Translocations involving BCL10 can lead to its overexpression, contributing to the development of these lymphomas.
- Other Lymphomas: Besides MALT lymphomas, alterations in BCL10 have also been observed in other types of B-cell lymphomas, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukemia (CLL).
Given its central role in the NF-κB signaling pathway, BCL10 is a potential target for therapeutic intervention in lymphomas and other diseases involving dysregulated NF-κB activity. Inhibitors targeting components of the CBM complex or downstream effectors of NF-κB signaling are being explored as potential treatments.
