Synthesized peptide derived from human BCL-10 (Phospho-Ser138)

This antibody detects endogenous levels of BCL-10 (Phospho-Ser138) at Human, Mouse,Rat.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):SNsDE

BCL10 CIPER CLAP

BCL-10 (Phospho-Ser138)

B-cell lymphoma/leukemia 10 ;
B-cell CLL/lymphoma 10 ;
Bcl-10 ;
CARD-containing molecule enhancing NF-kappa-B ;
CARD-like apoptotic protein ;
hCLAP ;
CED-3/ICH-1 prodomain homologous E10-like regulator ;
CIPER ;
Cellular homolog of vCARMEN ;
cCARMEN ;
Cellular-E10 ;
c-E10 ;
Mammalian CARD-containing adapter molecule E10 ;
mE10 ;

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],

Disease:A chromosomal aberration involving BCL10 is recurrent in low-grade mucosa-associated lymphoid tissue (MALT lymphoma). Translocation t(1;14)(p22;q32). Although the BCL10/IgH translocation leaves the coding region of BCL10 intact, frequent BCL10 mutations could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions.,Disease:Defects in BCL10 are involved in various types of cancer.,Function:Promotes apoptosis, pro-caspase-9 maturation and activation of NF-kappa-B via NIK and IKK. May be an adapter protein between upstream TNFR1-TRADD-RIP complex and the downstream NIK-IKK-IKAP complex. Is a substrate for MALT1.,PTM:Phosphorylated. Phosphorylation results in dissociation from TRAF2 and binding to BIRC2/c-IAP2.,similarity:Contains 1 CARD domain.,subcellular location:Appears to have a perinuclear, compact and filamentous pattern of expression. Also found in the nucleus of several types of tumor cells.,subunit:Self-associates by CARD-CARD interaction and forms a tight complex with MALT1. Interacts with other CARD-proteins such as CARD9, CARD10, CARD11 and CARD14. Binds caspase-9 with its C-terminal domain. Interacts with TRAF2 and BIRC2/c-IAP2.,tissue specificity:Ubiquitous.,

Cytoplasm, perinuclear region . Membrane raft . Appears to have a perinuclear, compact and filamentous pattern of expression. Also found in the nucleus of several types of tumor cells. Colocalized with DPP4 in membrane rafts. .

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>>C-type lectin receptor signaling pathway ;
>>T cell receptor signaling pathway ;
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