Bcl-10 / Biotin /
Product Details
| Description | BCL10, NT (BCL10, CIPER, CLAP, B Cell lymphoma/leukemia 10, B Cell CLL/lymphoma 10, CARD-containing molecule enhancing NF-kappa-B, CARD-like apoptotic protein, CED-3/ICH-1 prodomain homologous E10-like regulator, Cellular homolog of vCARMEN, Cellular-E10, Mammalian CARD-containing adapter molecule E10) (Biotin) Pab | |
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| Conjugate | Biotin | |
| Clone | ||
| Target Species | Human | |
| Applications | ELISA, IF, WB, IHC | |
| Supplier | US Biological | |
| Catalog # | Sign in to view product details, citations, and spectra | |
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About Bcl-10
This gene was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain containing proteins including CARD9, 10, 11 and 14, which are thought to function as upstream regulators in NF-kappaB signaling. This protein is found to form a complex with MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and this protein are thought to synergize in the activation of NF-kappaB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2016]
This gene was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain containing proteins including CARD9, 10, 11 and 14, which are thought to function as upstream regulators in NF-kappaB signaling. This protein is found to form a complex with MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and this protein are thought to synergize in the activation of NF-kappaB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2016]
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