MKPSMilton Keynes Preparatory School (UK)
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Our data suggest that changes in the dose of MAPK phosphatases (MKPs) might dramatically affect the regulation of the MAPK module during T cell polarisation and stimulation at the inflammatory sites.
We did not detect mRNA of the atypical MKPs DUSP13, DUSP15, DUSP26, and DUSP27, the classical MKP DUSP9, the tensin homolog TPTE, the eyes absent EYA1, EYA2, and EYA4, and the myotubularin MTMR7.
Substantial changes in expression levels associated with Th1 polarisation were found in genes coding for regulators of the phosphorylation state of phosphoinositides (MTMs), the MAPK signalling module (MKPs), the actin cytoskeleton (Slingshots or SSHs), and the cell cycle (CDC25s and CDKN3) (Table 2).
Among the 9 out of 10 classical MKPs [8] whose expression was detected, DUSP1, DUSP2, DUSP4, DUSP7, and DUSP16 were found in the group of highly expressed PTPs (Figure 2).
The group of MKPs are characterised by sharing MAPK substrates.
Consistent with this complex scenario, Th1 polarisation and PI treatment of Thl cells induced dramatic changes in the expression profile of ERK-directed MKPs and, consequently, remarkable differences were found between naive and Thl restimulated cells (Thl-PI) (Figures 4(a) and 4(b)).
Dephosphorylation of activated ERK1/2 may be mediated by PP2A (protein phosphatase 2A) or by a family of recently described MAPK phosphatases (MKP) with dual specificity (Thr/Tyr).
This activation cascade can be downregulated by phosphatases, in particular by members of the MAPK phosphatase (MKP) family, which can remove phosphate groups from activated MAPK.
elegans JNK and p38 MAPK pathways is the MKP VHP-1, which negatively regulates these MAPK pathways by dephosphorylating KGB-1, PMK-1 and PMK-3.