AI Article Synopsis
- CARMA1 is a key regulator of NF-kappaB activation in lymphocytes and works together with Bcl10 to manage NF-kappaB signaling triggered by T-cell receptor (TCR) stimulation.
- Research identifies calmodulin-dependent protein kinase II (CaMKII) as a crucial player in this signaling pathway, particularly as it redistributes to the immune synapse during T-cell activation.
- CaMKII not only promotes NF-kappaB activation but also phosphorylates CARMA1, which strengthens CARMA1's interaction with Bcl10, highlighting a new role for CaMKII in TCR signaling.
Article Abstract
CARMA1 is a central regulator of NF-kappaB activation in lymphocytes. CARMA1 and Bcl10 functionally interact and control NF-kappaB signaling downstream of the T-cell receptor (TCR). Computational analysis of expression neighborhoods of CARMA1-Bcl10MALT 1 for enrichment in kinases identified calmodulin-dependent protein kinase II (CaMKII) as an important component of this pathway. Here we report that Ca(2+)/CaMKII is redistributed to the immune synapse following T-cell activation and that CaMKII is critical for NF-kappaB activation induced by TCR stimulation. Furthermore, CaMKII enhances CARMA1-induced NF-kappaB activation. Moreover, we have shown that CaMKII phosphorylates CARMA1 on Ser109 and that the phosphorylation facilitates the interaction between CARMA1 and Bcl10. These results provide a novel function for CaMKII in TCR signaling and CARMA1-induced NF-kappaB activation.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592706 | PMC |
| http://dx.doi.org/10.1128/MCB.02469-05 | DOI Listing |
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