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JNK activates SMAD3. 15 / 15
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"However, JNK can also activate the M2 phenotype transcription factor SMAD3 [XREF_BIBR]."

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"JNK pathway mediates TGFβ-induced EMT in keratinocytes. xref Further it was shown that activation of Smad3 by JNK is necessary to mediate TGFβ -induced EMT. xref "

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"P38 MAPK and c-Jun N-terminal kinase (JNK) can activate Smad 3 [ xref , xref ] and p38 MAPK also strengthens interaction between Smad3 and coactivators [ xref ]."

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"P38 MAPK and c-Jun N-terminal kinase (JNK) can activate Smad 3 [XREF_BIBR, XREF_BIBR] and p38 MAPK also strengthens interaction between Smad3 and coactivators [XREF_BIBR]."

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"In this study, we found that blockade of KCa3.1 inhibited the activation of Smad2, Smad3 and Erk1/2 signaling pathways, but not p38 and JNK MAPK pathways, indicating that KCa3.1 plays an important role involving Smad2, Smad3 and ERK1/2 in kidney myofibroblast activation by TGF-beta1."

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"Furthermore, ERS and JNK pathway inhibition decreased the expression levels of TGF-beta and Smad3 pathway signals in cells incubated with TM."

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"Smad3 itself is activated by phosphorylation at the C-terminus (pSmad3C) or at the linker domain (pSmad3L) through TGF-beta type I receptor or TGF-beta-dependent c-Jun N-terminal kinase."

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"In addition, this pathway can be deregulated in the context of active RAS signaling, through JNK mediated SMAD3 signaling [XREF_BIBR]."

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"Furthermore, IFNgamma reduced JNK phosphorylation, which tightly was associated with decreased phosphorylation of downstream factors c-Jun and Smad3 and decreased binding activity of c-Jun and Smad3 in the preprpET-1 promoter."

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"This finding supports the postulate that JNK mediated Smad3 linker region phosphorylation is an important mechanism by which reduced eNOS expression promotes renal fibrosis."

"JNK-mediated phosphorylation of Smad3 outside the -SSXS motif enhances Smad3 nuclear translocation and potentiates transcriptional activation independent of Smad3 phosphorylation by T_RI."

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"It is possible, therefore, that JNK is activating both NF-kB and AP-1 as well as Smad3 which can then possibly bind SP-1 or AP-1 along with NF-kB and PEA-3 and enhance promoter activity."

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"Then JNK mediated linker phosphorylation of Smad3 inactivated cytostatic Smad3 signaling and facilitated hepatocarciongenesis [XREF_BIBR]."

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"Smad3 is normally activated by TGF-beta, but JNK, via the linker phosphorylation pathway, also enables Smad3 to induce HSC proliferation [XREF_BIBR, XREF_BIBR]."

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"XREF_BIBR Further it was shown that activation of Smad3 by JNK is necessary to mediate TGFbeta -induced EMT."