ArticleOncogene2007
A dual role for the API2 moiety in API2-MALT1-dependent NF-kappaB activation: heterotypic oligomerization and TRAF2 recruitment.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- The Paracaspase MALT1 in Cancer.Biomedicines · 2022Review
- Recent Advances in the Genetic of MALT Lymphomas.Cancers · 2021Review
- GRK2 suppresses lymphomagenesis by inhibiting the MALT1 proto-oncoprotein.The Journal of clinical investigation · 2020Article
- Inhibitory-κB Kinase (IKK) α and Nuclear Factor-κB (NFκB)-Inducing Kinase (NIK) as Anti-Cancer Drug Targets.Cells · 2018Review
- NF-κB Activation in Lymphoid Malignancies: Genetics, Signaling, and Targeted Therapy.Biomedicines · 2018Review
- First-line antibiotic therapy in Helicobacter pylori-negative low-grade gastric mucosa-associated lymphoid tissue lymphoma.Scientific reports · 2017Article
- NF-κB in Hematological Malignancies.Biomedicines · 2017Review
- Differing Requirements for MALT1 Function in Peripheral B Cell Survival and Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- API2-MALT1 oncoprotein promotes lymphomagenesis via unique program of substrate ubiquitination and proteolysis.World journal of biological chemistry · 2016Review
- Helicobacter pylori-negative gastric mucosa-associated lymphoid tissue lymphomas: A review.World journal of gastroenterology · 2015Review
- Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies.Oncogene · 2014Review
- The API2-MALT1 fusion exploits TNFR pathway-associated RIP1 ubiquitination to promote oncogenic NF-κB signaling.Oncogene · 2014Article
- Mechanism and specificity of the human paracaspase MALT1.The Biochemical journal · 2012Article
- Pathogenetic importance and therapeutic implications of NF-κB in lymphoid malignancies.Immunological reviews · 2012Review
- MALT1 protease: a new therapeutic target in B lymphoma and beyond?Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Review
- From MALT lymphoma to the CBM signalosome: three decades of discovery.Cell cycle (Georgetown, Tex.) · 2011Review
- Protease activity of the API2-MALT1 fusion oncoprotein in MALT lymphoma development and treatment.Future oncology (London, England) · 2011Review
- Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation.Science (New York, N.Y.) · 2011Article
- Antigen receptor signaling to NF-kappaB via CARMA1, BCL10, and MALT1.Cold Spring Harbor perspectives in biology · 2010Review
- IAPs: from caspase inhibitors to modulators of NF-kappaB, inflammation and cancer.Nature reviews. Cancer · 2010Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mucosa-associated lymphoid tissue (MALT) lymphoma is the most common extranodal lymphoid neoplasm. Chromosomal translocation t(11;18)(q21,q21) is found in 30% of gastric MALT lymphomas and is associated with a failure to respond to standard treatment and a tendency to disseminate. This translocation generates a chimeric protein composed of N-terminal sequences of Inhibitor of Apoptosis 2 (API2, also known as BIRC3 and cIAP2) fused to C-terminal sequences of MALT1. API2-MALT1 promotes cell survival and proliferation via activation of nuclear factor-kappaB (NF-kappaB). Here, we investigate the mechanism by which the API2 moiety contributes to NF-kappaB stimulation. We find that the API2 moiety mediates oligomerization of API2-MALT1 as well as interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2). Surprisingly, oligomerization does not occur via homotypic interaction; rather, the API2 moiety of one monomer interacts with the MALT1 moiety of another monomer. Further, the specific region of the API2 moiety responsible for mediating oligomerization is distinct from that mediating TRAF2 binding. Although deletion or mutation of the TRAF2 binding site does not inhibit oligomerization, it does lead to dramatically decreased NF-kappaB activation. Deletion of both TRAF2 binding and oligomerization regions results in near-complete loss of NF-kappaB activation. Thus, API2 moiety-mediated heterotypic oligomerization and TRAF2 binding both contribute to maximal API2-MALT1-dependent NF-kappaB stimulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.