BCL10 (NM_003921) Human Tagged ORF Clone Lentiviral Particle

CAT#: RC208752L4V

Lenti ORF particles, BCL10 (mGFP-tagged) - Human B-cell CLL/lymphoma 10 (BCL10), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Human Tagged ORF Clone Lentiviral Particle
• Tag: mGFP
• Symbol: BCL10
• Synonyms: c-E10; CARMEN; CIPER; CLAP; IMD37; mE10
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-mGFP-P2A-Puro
• ACCN: NM_003921
• ORF Size: 699 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(RC208752).
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.

Reference Data

• RefSeq: NM_003921.3
• RefSeq Size: 3118 bp
• RefSeq ORF: 702 bp
• Locus ID: 8915
• UniProt ID: O95999
• Cytogenetics: 1p22.3
• Domains: CARD
• Protein Families: Druggable Genome
• Protein Pathways: B cell receptor signaling pathway, T cell receptor signaling pathway
• MW: 26.3 kDa
• Gene Summary: 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]