
IndraLab
Statements
reach
"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)."
reach
"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."
reach
"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]."
reach
"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 ."
reach
"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."
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 ."
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 ]."