Recent studies have begun to demonstrate unique functions of the different isoforms, with p38α being implicated as the key isoform involved in CNS inflammation. Interestingly, there is also emerging evidence that two downstream substrates of p38 may have opposing roles, with MK2 being pro-inflammatory and MSK1/2 being antiinflammatory.
Activated p38 can directly activate transcription factors or can act indirectly via two downstream kinases MK2 and MSK1/2.
The expression of p38 and MK2 are each reliant on the other, as loss of MK2 causes a decrease in the amount of total p38 .
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