ArticlePloS one2015
MALT1-ubiquitination triggers non-genomic NF-κB/IKK signaling upon platelet activation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The Role of the Proteasome in Platelet Function.International journal of molecular sciences · 2021Review
- Article
- Effect of ultrapure lipopolysaccharides derived from diverse bacterial species on the modulation of platelet activation.Scientific reports · 2019Article
- Mouse transient receptor potential channel type 6 selectively regulates agonist-induced platelet function.Biochemistry and biophysics reports · 2019Article
- Role of NF-κB in Platelet Function.International journal of molecular sciences · 2019Review
- SHARPIN at the nexus of integrin, immune, and inflammatory signaling in human platelets.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Z-VRPR-FMK can inhibit the growth and invasiveness of diffuse large B-cell lymphoma by depressing NF-κB activation and MMP expression induced by MALT1.International journal of clinical and experimental pathology · 2019Article
- CD40L Priming of Platelets via NF-κB Activation is CD40- and TAK1-Dependent.Journal of the American Heart Association · 2018Article
- Role of IκB kinase β in regulating the remodeling of the CARMA1-Bcl10-MALT1 complex.Biochemical and biophysical research communications · 2018Article
- Toll-Like Receptor 4 Signalling and Its Impact on Platelet Function, Thrombosis, and Haemostasis.Mediators of inflammation · 2017Review
- CXCL12 regulates platelet activation via the regulator of G-protein signaling 16.Biochimica et biophysica acta · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently shown that IKK complex plays an important non-genomic role in platelet function, i.e., regulates SNARE machinery-dependent membrane fusion. In this connection, it is well known that MALT1, whose activity is modulated by proteasome, plays an important role in the regulation of IKK complex. Therefore, the present studies investigated the mechanism by which IKK signaling is regulated in the context of the platelet proteasome. It was found that platelets express a functional proteasome, and form CARMA/MALT1/Bcl10 (CBM) complex when activated. Using a pharmacological inhibitor, the proteasome was found to regulate platelet function (aggregation, integrin activation, secretion, phosphatidylserine exposure and changes in intracellular calcium). It was also found to regulate thrombogenesis and physiologic hemostasis. We also observed, upon platelet activation, that MALT1 is ubiquitinated, and this coincides with the activation of the IKK/NF-κB-signaling pathway. Finally, we observed that the proteasome inhibitor blocks CBM complex formation and the interaction of IKKγ and MALT1; abrogates SNARE formation, and the association of MALT1 with TAK1 and TAB2, which are upstream of the CBM complex. Thus, our data demonstrate that MALT1 ubiquitination is critical for the engagement of CBM and IKK complexes, thereby directing platelet signals to the NF-κB pathway.
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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.