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SMAD2 activates SMAD4. 31 / 34
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"ADAM12 has been shown to upregulate the expression and stability of TGF-βRII, promote the phosphorylation of the Smad2 protein, enhance the binding ability of the Smad2/3 complex to Smad4, and subsequently activate the TGF-β signaling pathway [50]."

sparser
"We have previously demonstrated that phosphorylated Smad2 can activate the Wnt/β-catenin signaling pathway independently of Smad4 [ xref ]."

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"Through analyzing the publicly available algorithms, including TargetScan, miRWalk, and miRanda, we found that several components of TGF-beta signaling, including SMAD2, SMAD4, and TGFBRI, may be potential targets of miR-582-3p, and SMAD2, SMAD4, TGFBRI, and TGFBRII for miR-582-5p (XREF_SUPPLEMENTARY A-S4C)."

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"Ligand binding and recruitment of TβRI activates its kinase that phosphorylates the carboxy-terminal serine residue of SMAD2 (SMAD Family Member 2) or SMAD3 (SMAD Family Member 3), which induces oligomerization of SMAD2 or SMAD3 with SMAD4 (SMAD Family Member 4), resulting in nuclear translocation for transcriptional activation or repression of target genes."

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"Smad2 reversed, whereas Smad3 further enhanced, the inhibitory effect of Smad4 on Eomes-luc activity (XREF_FIG B)."

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"Overexpression of Smad3 and Smad4, but not Smad2, induced rat and murine FSHbeta gene expression [XREF_BIBR, XREF_BIBR, XREF_BIBR]; however, Smad2 overexpression was shown to be low in LbetaT2 cells [XREF_BIBR, XREF_BIBR]."

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"Activated TGF-β signals through the TGF-β receptor to phosphorylate Smad2 and Smad3, which leads to the formation of a Smad complex with Smad4."

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"Along with the positive correlation between pAMPK and nuclear pSMAD2/SMAD4 in IHC, the Western blot result puts forward the idea that pAMPK overexpression phosphorylates SMAD2 and subsequently activates pSMAD2/SMAD4 in ccRCC."

sparser
"Since Smad2 must activate Smad4 to regulate the Smad downstream pathway, as expected, the deletion of Smad2 in LCs also displayed the interruption of long-term LC repopulation and the lower expression of EpCAM and CD24 on the long-term LCs, while short-term LCs were unaffected."

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"Following increased production in the infarcted and border regions, TGF-β1 binds to TGF-β receptor on the cell membrane and phosphorylates mothers against the decapentaplegic homolog 2 (SMAD2) and SMAD3, allowing these to bind SMAD4 to form a complex in which SMAD7 functions as an inhibitory molecule [11]."

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"Overexpression of Smad2 increases endogenous Smad4 and TGF-beta 1 expression while heterozygous loss of Smad2 reduces their expression levels, suggesting a concerted action of Smad2 and -4 in regulating TGF-beta signaling during skin development."

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"In contrast, TGFβ synergizes with IL-6 to induce the differentiation of IL-17A-producing Th17 cells , driven in part by STAT3 attenuation of the SMAD3–SMAD4-mediated suppression of TCR signalling , and SMAD2–SMAD3 reversal of the SMAD4–SKI–SKIL-mediated transcriptional repression of RORγt ."

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"Activated TβRI kinase phosphorylates the carboxy-terminal serine residue of the mothers against DPP Homolog proteins SMAD2 or SMAD3, which induces oligomerization of SMAD2 or SMAD3 with SMAD4, and DNA binding of the complex to mediate transcriptional activation or repression of target genes."

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"Phosphorylation of Smad2 or Smad3 by the type I TGFβ receptor induces association with Smad4."

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"The active form of TGF-β1 binds to the type II TGF-β1 receptor (TβRII) and further binds to the type I TGF-β1 receptor (TβRI) and induces the phosphorylation of the SMAD2/SMAD3 complex, which activates SMAD4."

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"TGF- β mediated phosphorylation of mothers against decapentaplegic homolog 2 and 3 (SMAD2/3) enables complex formation with SMAD4 [156] ."

eidos
"Since Smad2 must activate Smad4 to regulate the Smad downstream pathway , as expected , the deletion of Smad2 in LCs also displayed the interruption of long-term LC repopulation and the lower expression of EpCAM and CD24 on the long-term LCs , while short-term LCs were unaffected ."

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"Since Smad2 must activate Smad4 to regulate the Smad downstream pathway, as expected, the deletion of Smad2 in LCs also displayed the interruption of long-term LC repopulation and the lower expression of EpCAM and CD24 on the long-term LCs, while short-term LCs were unaffected."

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"Smad activation independent of TGFb signalling In endothelial cells, a MAPKKK, MEKK1, was shown to stimulate phosphorylation of Smad2, and moreover, increased interaction of Smad2 with Smad4.72 The Sm[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"That overexpression of Smad3 and Smad4, but not Smad2, decreased Galectin-3 promoter activity, while Smad3 silencing inhibited the promoter activity clearly indicated that the Galecin-3 promoter activity was responsive to Smad3."

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"Our results revealed that knockdown of Smad2 could inhibit Smad4 and Foxp3."

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"Both TGF-beta1 and activin A, but not BMP-7, increased the phosphorylation of Smad2, induced nuclear translocation of Smad2, Smad3, and Smad4, and inhibited thyrocyte cell growth as well as TSH stimulated cAMP response."

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"Thyrocyte growth is inhibited by TGF-beta1 factor (encoded by Tgfb1), which increases the phosphorylation of SMAD2 and induces the nuclear translocation of SMAD2, SMAD3, and SMAD4 ."

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"We have demonstrated that PR-619 suppressed UUO induced upregulation of Smad4 but not TGF-beta receptors, Smad2, or Smad3."

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"The phosphorylation of Smad2 and Smad3 induces complex formations with Smad4."

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"The activation of TGF-β receptors potentiates the phosphorylation of Smad2 and Smad3, which leads to the formation of hetero-oligomeric complexes with Smad4."

sparser
"For instance, phosphorylated Smad-2 can activate the Wnt/β-catenin signaling pathway independently of Smad-4 through p300 [ xref ]."

reach
"This causes phosphorylation of SMAD2 and SMAD3, two transcription factors that then bind to and activate SMAD4."

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"Furthermore, KLF10 overexpression enhanced the TGFbeta induced Smad2 phosphorylation and increased the transcription of Smad2, but not Smad3 or Smad4 [XREF_BIBR]."

sparser
"It is generally suggested that TGF- β 1 induces cell apoptosis via canonical Smad signaling (figure xref (D)), where TGF- β RI and TGF- β RII form a complex in the presence of TGF- β 1 and activates Smad2 and Smad3, which in turn activates Smad4 and thereby mediating programmed cell death via activating pro-apoptotic genes such as caspase 9 [ xref ]."

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"In this process, TGF-β1 can lead to activation of the canonical Smad pathway involving phosphorylation of Smad2 and Smad3 proteins which together with Smad4 can activate EMT- and CSC-associated transc[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"