| First Author | Gehring T | Year | 2019 |
| Journal | Cell Rep | Volume | 29 |
| Issue | 4 | Pages | 873-888.e10 |
| PubMed ID | 31644910 | Mgi Jnum | J:298826 |
| Mgi Id | MGI:6488874 | Doi | 10.1016/j.celrep.2019.09.040 |
| Citation | Gehring T, et al. (2019) MALT1 Phosphorylation Controls Activation of T Lymphocytes and Survival of ABC-DLBCL Tumor Cells. Cell Rep 29(4):873-888.e10 |
| abstractText | The CARMA1/CARD11-BCL10-MALT1 (CBM) complex bridges T and B cell antigen receptor (TCR/BCR) ligation to MALT1 protease activation and canonical nuclear factor kappaB (NF-kappaB) signaling. Using unbiased mass spectrometry, we discover multiple serine phosphorylation sites in the MALT1 C terminus after T cell activation. Phospho-specific antibodies reveal that CBM-associated MALT1 is transiently hyper-phosphorylated upon TCR/CD28 co-stimulation. We identify a dual role for CK1alpha as a kinase that is essential for CBM signalosome assembly as well as MALT1 phosphorylation. Although MALT1 phosphorylation is largely dispensable for protease activity, it fosters canonical NF-kappaB signaling in Jurkat and murine CD4 T cells. Moreover, constitutive MALT1 phosphorylation promotes survival of activated B cell-type diffuse large B cell lymphoma (ABC-DLBCL) cells addicted to chronic BCR signaling. Thus, MALT1 phosphorylation triggers optimal NF-kappaB activation in lymphocytes and survival of lymphoma cells. |
