IndraLab

"Due to smoking and the anatomical location of the SCC in the proximal airways, which allows for greater exposure to cigarette smoke particles, cigarette smoke condensates selectively increase SMAD3 promoter methylation, exposing SCC-TAFs to stronger epigenetic suppression of SMAD3."

"This result suggests that the histotype-specific regulation of lung cancer tumour fibrosis is mediated by differential levels of SMAD3 promoter methylation in TAFs."

"Among them, SMAD3 methylation in the neonates with maternal asthma was strongly and positively associated with neonatal production of cord blood mononuclear cell-derived IL-1β, an innate inflammatory mediator."

"Another study demonstrated that EZH2-mediated methylation of SMAD3 at K53/K333 can drive cancer metastasis [ xref ]."

"Moreover, we evaluated the impact of SMAD3 methylation expression on the survival prognosis using the GSCA database."

"Augmented methylation of SMAD3 in cord blood mononuclear cells of newborns, which was associated with the inflammatory regulator IL-1b, determined whether or not the subjects, all with asthmatic mothers, would develop asthma by age 9 [ xref ]."

"The results were rather promising, demonstrating that high SMAD3 methylation expression tended to predict a more favorable prognosis in nearly all statistically significant prognostic analyses (Fig.  xref C, Supplementary Fig. 3SD-G)."

"It was shown that the reduced fibrosis and nintedanib response in SCC-TAFs compared to ADC-TAFs was associated with increased promoter methylation of SMAD3."

"Further researches are needed to elucidate the potential function of SMAD3 methylation in different cancers."

"Unlike EDARADD , no prognostic information was observed in SMAD3 or CHI3L1 methylation status in the same data sets (, available at Carcinogenesis Online)."

"Smad3 methylation by EZH2 promotes its activation and tumor metastasis."

"EZH2 triggers SMAD3 methylation to promote the interaction between SMAD3 and its cell membrane locator, maintaining SMAD3 phosphorylation of TGFβ receptors and facilitating breast cancer metastasis. xref EZH2 also induces ribosomal synthesis overactivation and ribosomal DNA instability by silencing PHACTR2-AS1 to accelerate breast cancer metastasis. xref EZH2 induces methylation of lysine K362 in ERG, which is beneficial for DNA binding and increases ERG transcriptional activity, thereby enhancing the invasiveness of ERG fusion prostate cancer. xref , xref EZH2 silences primary cilia genes and activates the Wnt pathway to promote melanoma metastasis. xref "

"SMAD3 methylation mediated by EZH2 promotes SMAD3 phosphorylation by TGF-β receptors and is correlated with hyperactivation of TGF-β/SMAD3 signaling and promotion of EMT and metastasis in breast cancer."

"EZH2 triggers SMAD3 methylation to promote the interaction between SMAD3 and its cell membrane locator, maintaining SMAD3 phosphorylation of TGFβ receptors and facilitating breast cancer metastasis."

"Other studies indicated that increased EZH2 expression abnormally increased SMAD3 methylation, thereby activating SMAD3."

"We also confirmed that PRMT5 interacted with Smad3 in TGF-β-stimulated cardiac fibroblasts using IP-WB analysis (Fig.  xref ) and found that Smad3 was not methylated by PRMT5 in vitro (Supplementary Fig.  xref )."

"We also confirmed that PRMT5 interacted with Smad3 in TGF-β-stimulated cardiac fibroblasts using IP-WB analysis (Fig. 3e) and found that Smad3 was not methylated by PRMT5 in vitro (Supplementary Fig. 12)."

"This finding naturally raises the question of whether PRMT5 also directly methylates and thereby activates Smad3, but we have shown that this is not the case, as the in vitro methylation assay carried out in this study revealed that Smad3 was not methylated by PRMT5."

"This finding naturally raises the question of whether PRMT5 also directly methylates and thereby activates Smad3, but we have shown that this is not the case, as the in vitro methylation assay carried out in this study revealed that Smad3 was not methylated by PRMT5."

"Yang et al. pointed out that the Salvia miltiorrhiza and Carthamus tinctorius extract (SCE) prevents myocardial fibrosis and adverse remodeling after MI by suppressing histone methylation of the SMAD3 and its transcription in cardiac fibroblasts [ xref ]."

"To our knowledge, the relationship between histone methylations of Smad3, both H3K4me3 and H3K36me3, and fibrosis has not yet been reported in heart disease but has been previously investigated, mainly in cancer [ xref ] and fibrosis of other organs [ xref ]."

"Yang et al. pointed out that the Salvia miltiorrhiza and Carthamus tinctorius extract (SCE) prevents myocardial fibrosis and adverse remodeling after MI by suppressing histone methylation of the SMAD3 and its transcription in cardiac fibroblasts [XREF_BIBR]."

"Because SMYD2 mainly methylates the H3K36 histone demethylase in the SMAD3 gene body , we performed a ChIP assay using an anti-H3K36 dimethylation antibody."

"Thus, SMYD2 knockdown reduced the methylation of its direct target, SMAD3, via a consequent reduction in H3K4 monomethylation."

"Interestingly, lower methylation of CpG sites in SMAD3 , a transcription factor known to directly upregulate miR-21 ( xref ), was also found in the chemotherapy- versus non-chemotherapy treated patients."

"MSP analysis and Sequenom MassARRAY analysis from 81 ACS samples, 74 stable coronary artery disease samples, and 53 healthy samples confirmed that the reference results of the HumanMethylation450 array significantly corrected the differential CpG methylation of SMAD3 ."

"It was shown that the reduced fibrosis and nintedanib response in SCC-TAFs compared to ADC-TAFs was associated with increased promoter methylation of SMAD3."

"Exposure to cigarette smoke particles and condensation of these particles in the proximal airways enhance SMAD3 promoter methylation leading to SMAD3 suppression ."

"When comparing 4+ to 0-2 organochlroides detected in PD patient’s blood samples, the top 5 hits included hypermethylation of cg09677945 (DNAJC15) and cg15723784 (SMAD3) and hypomethylation cg12456927 (Intergenic), cg02598807 (AP2A2) and cg11667387 (CNNM2)."

"When comparing 4+ to 0-2 organochlroides detected in PD patient’s blood samples, the top 5 hits included hypermethylation of cg09677945 (DNAJC15) and cg15723784 (SMAD3) and hypomethylation cg12456927 (Intergenic), cg02598807 (AP2A2) and cg11667387 (CNNM2)."

"Additionally, YTHDC1 promotes the nuclear export of methylated SMAD family member 3 (SMAD3) mRNA, affecting its protein production and leading to enhanced EMT and promoting lung metastasis of triple‐negative breast cancer (TNBC) cells [105]."

"Therefore, Smad3 gene hypomethylation may be caused by long-term exposure to allergen sources; an increase in levels of TGF-beta, an upstream factor of Smad3; or interactions between these two factors."

"When comparing 4+ to 0-2 organochlroides detected in PD patient’s blood samples, the top 5 hits included hypermethylation of cg09677945 (DNAJC15) and cg15723784 (SMAD3) and hypomethylation cg12456927 (Intergenic), cg02598807 (AP2A2) and cg11667387 (CNNM2)."

"When comparing 4+ to 0-2 organochlroides detected in PD patient’s blood samples, the top 5 hits included hypermethylation of cg09677945 (DNAJC15) and cg15723784 (SMAD3) and hypomethylation cg12456927 (Intergenic), cg02598807 (AP2A2) and cg11667387 (CNNM2)."