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SMAD2 phosphorylates SMAD3. 24 / 24
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"Smad7 is an inhibitor of TGF-beta signaling by preventing Smad3 and/or Smad2 phosphorylation and recruitment of Smad2 and Smad3 complex (XREF_FIG)."
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"Both subunits of the receptor were equally expressed in the two cell types, overexpression of these receptor subunits did not modify the activation of PAI-1 SBE in myofibroblasts and, more important[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"U87MG cells were treated with miR-132 mimic, miR-132 inhibitor or corresponding controls, and western blotting was performed to detect the protein level of phosphorylated SMAD2 and phosphorylated SMAD[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR In renal fibroblasts relaxin prevents TGF- beta induced collagen synthesis by suppression of SMAD2 phosphorylation and complex formation of SMAD3."
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"The protein levels of alpha-smooth muscle actin (alpha-SMA), type 1 collagen (Col1), Smad2, Smad3, phosphorylated Smad2 (p-smad2), p-smad3 and Smad7 were assessed by Western blot analysis."
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"Following cytokine stimulation, cells were fixed and stained for flow cytometric detection of SMAD2 protein phosphorylated at Ser465/467 sites and the SMAD3 protein phosphorylated at Ser423/425 sites according to the manufacturer’s protocols (catalog # 562586, BD Biosciences) ."
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"We found that disruption of Smad2 induced smad3 phosphorylation and activity in cisplatin-treated TECs."
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"As indicated in xref and ( xref ), TGF-β1 treatment induced an increase in phosphorylated Smad2 and phosphorylated Smad3 (p-Smad3)."
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"Furthermore, both SMAD2 and SMAD3 are activated by phosphorylation, and our results support that patients whose TAFs exhibit a low (<1) pSMAD3/pSMAD2 ratio may be refractory to nintedanib and possibly to other antifibrotic drugs, whereas those with high (>1) pSMAD3/pSMAD2 ratio may elicit positive responses (where pSMAD2 and pSMAD3 refers to phosphorylated SMAD2 and SMAD3, respectively) (Figure 3D)."
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"Another interesting and novel observation of this study was the mutual amplification of effects such that knockdown of Smad2 or inhibition of Rac1 (without direct modulation of Smad3) enhanced growth inhibition, Smad3 specific transcriptional activity, and C-terminal phosphorylation of Smad3, while knockdown of Smad3 (without direct modulation of Smad2) enhanced both Smad2 specific responses such as cellular migration (this study) and Smad2 phosphorylation by TGF-beta [XREF_BIBR]."
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"HSP72 overexpression inhibited TGF-beta1-induced phosphorylation and nuclear translocation of Smad3 and p-Smad3, but not Smad2; these inhibitory effects required the PBD but not the NLS."
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"In addition, oridonin reduced the levels of Smad2, Smad3, Smad4, PAI-1 and the phosphorylation of Smad2 and Smad3 induced by TGF-beta1 in vitro."
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"In agreement, pretreatment of MCF-7 cells with 17-beta-estradiol resulted in a reduced phosphorylation of Smad2 and Smad3 as well as a diminished Smad2 and Smad3 gene reporter activity in response to TGF-beta."
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"Deletion of Smad2 did not prevent TGF-beta1-induced Smad3 phosphorylation (Supplemental Figure S4), TGF-beta1-induced collagen I and alpha-SMA expression, and loss of E-cadherin."
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"Smad2, Smad3, phosphorylated Smad3, and Smad4 were detected in all cases."
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"We analyzed the levels of both phosphorylated SMAD2 (pSMAD2) and phosphorylated SMAD3 (pSMAD3) in medial SMCs as a measure of downstream canonical TGFß signaling."
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"Of interest is that conditional deletion of SMAD2 enhanced renal fibrosis, because SMAD2 deficiency induced excess phosphorylation of SMAD3, resulting in the SMAD3 binding to a collagen promotor and auto-induction of TGF-β [56]."
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"In H-Smad7 cells, transient phosphorylation of Smad2 and continuous phosphorylation of Smad3 were induced in response to TGFbeta, whereas Smad3 RNA expression remained largely unchanged for up to 72 h (XREF_FIG, A and B)."
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"Western blot analysis shows that knockdown of Smad2 upregulated Smad3 phosphorylation, but overexpression of Smad2 suppressed Smad3 phosphorylation without altering total Smad3 protein in vitro (Figures xref A and B)."
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"In the present study, we observed that the TGF-beta1-induced phosphorylation of Smad2 and Smad3 and the TGF-beta1-induced increase in alpha-SMA production were partially dependent on Smad2 and Smad3 and were reversed by knockdown of both Smad2 and Smad3."
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"Antibodies were obtained from the following sources: the anti-Fibronectin (Santa Cruz, U.S.A), anti-Col1A1(Santa Cruz, U.S.A.), anti-Col3A1( Santa Cruz, U.S.A) and anti-α-SMA(Santa Cruz, U.S.A.), anti[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Smad2, Smad3, phosphorylated Smad3, and Smad4 were detected in all cases."
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"In contrast, Smad2 KO mice induce Smad3 phosphorylation and their binding to the collagen promoter, promoting transcriptional activity which is associated to fibrosis [94]."
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"Ghrelin up-regulates Smad7 at day 4, prevents Smad3 and/or Smad2 phosphorylation and recruitment of Smad2 and Smad3 complex which blocks betaTGFb activity, as shown in some organs 8), and thus, prevents fibrosis (see also XREF_FIG)."
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