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Validated All-in-One™ qPCR Primer for MALT1(NM_006785.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene has been found to be recurrently rearranged in chromosomal translocation with two other genes - baculoviral IAP repeat-containing protein 3 (also known as apoptosis inhibitor 2) and immunoglobulin heavy chain locus - in mucosa-associated lymphoid tissue lymphomas. The protein encoded by this gene may play a role in NF-kappaB activation. Two alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq].
Gene References into function
- REVIEW: Genetic alterations involving MALT1 underlying the pathogenesis of MALT lymphoma
- Fuses with API2 and defines a distinctive clinicopathologic subtype in pulmonary extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue.
- translocations t(11;18)(q21;q21) and t(14;18)(q21;q32) represent the main structural aberrations involving MLT/MALT1 in MALT lymphomas, whereas true amplifications of MLT/MALT1 occur rarely in MZBCL
- copy numbers of API2-MALT1 do not reflect tumor cell proportions, and that the number of copies of API2-MALT1 in a tumor cell is different for each clinical sample.
- MALT1 chromosome rearrangements have a role in MALT gastric lymphomas in patients with Sjogren's syndrome
- Translocation breakpoint never exceeded 2.5% in B-cell lymphoma
- Detection of API2-MALT1 fusion transcripts is useful for evaluating the prognosis and clinical behavior of the MALT lymphoma.
- NF-kappa B signaling, once activated in a CD40-dependent immune response, is maintained and enhanced through deregulation of MALT1 or formation of an API2-MALT1 fusion.
- API2-MALT1 transcript was confirmed to be associated with the levels of apoptosis and API2 of MALT lymphoma.
- Taken together, our results strongly indicated that API2-MALT1 possesses a novel mechanism of self-activation by up-regulating its own expression in t(11;18)(q21;q21)-carrying MALT lymphomas.
- nucleocytoplasmic shuttling of MALT1 and BCL10 complex may indicate that these molecules are involved not only in the nuclear factor kappaB (NF-kappaB) pathway but also in other biologic functions in lymphocytes
- Study further supports the close interaction between the MALT1 and BCL10 proteins in the pathogenesis of MALT lymphomas.
- Common translocation in MALT lymphoma results in a fusion of the cIAP2 region on chromosome 11q21 with the MALT1 gene on chromosome 18q21.
- Chromosomal translocations leads to upregulation of either BCL10 or MALT1 or the generation of a fusion protein, cIAP2-MALT1.
- This study demonstrates that translocations involving MALT1, including IGH/MALT1, are uncommon in cutaneous MALT lymphomas and primary cutaneous DLBCL.
- MALT1-MAP4 fusion does not result in activation of NF-kappa B as with other MALT1-associated translocations.
- the t(11, 18)(q21;q21) translocation creating the c-IAP2.MALT1 fusion protein activates NF-kappaB independently of TRAF1 AND TRAF2 and contributes to human malignancy in the absence of signaling adaptors that might otherwise regulate its activity
- CARMA3/Bcl10/MALT1-dependent NF-kappaB activation mediates angiotensin II-responsive inflammatory signaling in hepatocytes.
- In vivo data indicate an effect of API2-MALT1 expression on the normal immune response of transgenic mice.
- Our results suggest that MALT1-specific translocations and FOXP1 rearrangements are not commonly involved in pathogenesis.
- careful observation for development of gastric carcinoma and disease progression is essential during follow-up of API2-MALT1-positive MALT lymphoma when patients decline second-line treatment.
- Upon T-cell activation, Malt1 is ubiquitinated, which is critical for the engagement of Carma1-Bcl10-Malt1 and IKK complexes, thereby directing T cell receptor signals to the NF-kappaB pathway.
- BCL10 and MALT1 might not only reflect the lymphocytic origin of H-RS cells, but autonomous activity of this crippled antigen receptor pathway might confer NFB activity and apoptosis resistance 9 at least in those cases of HL expressing wild-type IB.
- chromosome region 18q21 gain including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma
- Data show that the protein kinase C-responsive inhibitory domain of CARD11 functions in NF-kappaB activation to regulate the association of multiple signaling cofactors that differentially depend on Bcl10 and MALT1 for association.
- Caspase-8 undergoes limited activation upon antigenic stimulation, and this activation is dependent on the paracaspase MALT1.
- analysis of protein domains that mediate interaction between Bcl10 and MALT1
