IndraLab

Statements


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"Protein phosphatase PPM1A, which was identified to negatively regulate the activin signaling pathway, can dephosphorylate phospho-SMAD2 and enable SMAD2 to relocate back to the cytoplasm and terminate signal transduction [XREF_BIBR]."
| PMC

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"In this study, we found that miR-582-3p targeted SMAD2, SMAD4, and TGFBRI, and miR-582-5p directly inhibited SMAD2, TGFBRI, and TGFBRII."

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"Besides, we also found that p21-activated kinase 2 (PAK2) can directly phosphorylate Smad2 at Ser417, which interferes with the TβRI-Smad2 association and thus blocks TGF-β-induced Smad2 activation and signaling [93]."

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"Besides, we also found that p21 activated kinase 2 (PAK2) can directly phosphorylate Smad2 at Ser417, which interferes with the TbetaRI-Smad2 association and thus blocks TGF-beta-induced Smad2 activation and signaling [XREF_BIBR]."

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"To evaluate if PI3K activation was dependent on SMAD2 activation, we assessed if the phosphorylated p85 subunit of PI3K was affected by inhibition of native SMAD2 by DN-SMAD2 after TGFβ treatment."

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"Besides, we also found that p21-activated kinase 2 (PAK2) can directly phosphorylate Smad2 at Ser417, which interferes with the T RI-Smad2 association and thus blocks TGF--induced Smad2 activation and signaling [93] ."

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"These results demonstrate that inhibiting TGF-beta signaling with SB-431542 blocks phosphorylation of Smad2 and Smad3 and prevents nuclear translocation of p-Smad2 and p-Smad3, which ultimately interrupts bladder smooth muscle formation."

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"Smad2 phosphorylation at the linker region inhibits the nuclear accumulation of Smad2 without interfering with the TGF-beta-induced phosphorylation of its COOH-tail."

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"Activation of Ca2 +/calmodulin-dependent protein kinase II (CamKII) also results in Smad2, Smad3 and Smad4 phosphorylation inhibiting TGF-beta-induced nuclear import and transcriptional activity of Smad2, and affecting Smad heteromerization [XREF_BIBR]."

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"Each dose of losartan after bilateral cavernous nerve injury significantly attenuated the up-regulated expression of fibronectin (p < 0.01), pSMAD2 (p < 0.05) and thrombospondin-1 (p < 0.05), and up-regulated total SMAD2 (p < 0.05)."

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"Smad2 phosphorylation at the linker region inhibits nuclear accumulation of Smad2 without interfering with TGF-beta-induced phosphorylation of its COOH-tail."

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"Recent data from myeloma cells found that phosphorylation of Smad2 at the T8 site by CDK2 prevented Smad2 from linking with the co-Smad, Smad4, thus inhibiting Smad dependent transcriptional activity."

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"To determine if TGFβ-induced PTEN suppression was dependent on SMAD2, we assessed PTEN expression while native SMAD2 was inhibited by DN-SMAD2."

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"On the contrary, the overexpression of Smad2 attenuated this process, indicating a protective mechanism of Smad2 in TGF-mediated fibrosis (Meng et al., 2010)."