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Data suggest that Clock1a (show CLOCK Proteins) coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a (show CLOCK Proteins) alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a (show CLOCK Proteins) activates Smad3a promoter via its E-box1 element. (Clock1a (show CLOCK Proteins) = clock circadian regulator (show CLOCK Proteins) a; Nodal = nodal modulator 1 (show NOMO1 Proteins); Smad3a = SMAD (show SMAD1 Proteins) family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta (show TGFB1 Proteins) control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2 (show SMAD2 Proteins)/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2 (show SMAD2 Proteins)/3 signaling and embryonic patterning.
although the role of Smad (show SMAD1 Proteins) proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap (show TDP2 Proteins) provides insight into a novel Smad (show SMAD1 Proteins) partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2 (show SMAD2 Proteins)/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis
Data indicate that cardiac contractility modulation (CCM) therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-beta1 (show TGFB1 Proteins)/Smad3 signaling pathway in chronic heart failure .
study suggested that TGF-beta1/Smad3/smad7 is a major pathway which plays an important role in the regulation of the IUA and specific inhibitor of Smad3 (SIS3) may provide a new therapeutic strategy for IUA.
The results suggest that co-expression of active SMAD2 (show SMAD2 Proteins)/3 could enhance multiple types of transcription factors (TF)-based cell identity conversion and therefore be a powerful tool for cellular engineering.
The SMAD3 SNP rs12901499 GA genotype and G variant may increase the risk of hip osteoarthritis in Chinese Han patients.
We found that ITZ treatment was efficient in suppressing EMT (show ITK Proteins) and that the effect of ITZ was partially mediated by impaired TGF-b/SMAD2 (show SMAD2 Proteins)/3 signaling. The role of TGF-b/SMAD2 (show SMAD2 Proteins)/3 signaling in mediating the effect of ITZ was confirmed based on the results that recombinant TGF-b induced, but the TGF-b neutralizing antibody inhibited EMT (show ITK Proteins) as well as the invasion and migration of pancreatic cancer cells
Positive cooperativity of Smad3 and STAT3 (show STAT3 Proteins) during epithelial-mesenchymal transition [Review].
CXCL12 (show CXCL12 Proteins) activates the MEKK1 (show MAP3K1 Proteins)/JNK (show MAPK8 Proteins) signaling pathway, which in turn initiates SMAD3 phosphorylation, its translocation to nuclei, and recruitment of SMAD3 to the CTGF (show CTGF Proteins) promoter, which ultimately induces CTGF (show CTGF Proteins) expression in human lung fibroblasts.
SMAD2 (show SMAD2 Proteins)/3 interactome reveals that TGFbeta (show TGFB1 Proteins) controls m(6)A mRNA methylation in pluripotency
these results indicated that Bone marrow-derived mesenchymal stem cells -conditioned medium suppressed the epithelial-mesenchymal transition which might be associated with TGF-B1/Smad3. This study provides the theoretical basis for the research of the mechanisms responsible for pulmonary disease.
our findings demonstrated that thymoquinone suppressed the metastatic phenotype and reversed EMT (show ITK Proteins) of prostate cancer cells by negatively regulating the TGF-beta (show TGFB1 Proteins)/Smad2 (show SMAD2 Proteins)/3 signaling pathway. These findings suggest that thymoquinone is a potential therapeutic agent against prostate cancer which functions by targeting TGF-beta (show TGFB1 Proteins)
The present findings indicate that RACK1 (show GNB2L1 Proteins) silencing attenuates renal fibrosis by suppressing the activation of TGF-beta1 (show TGFB1 Proteins)/Smad3 signaling pathway in HK-2 (show HK2 Proteins) cells. Thus, RACK1 (show GNB2L1 Proteins) may serve as a novel regulator of renal fibrosis.
was found that treatment with iPSC-CM markedly reduced the proliferation of TGF-beta1 (show TGFB1 Proteins)-exposed cells, and the activities of TGF-beta1 (show TGFB1 Proteins), Smad-2 (show SMAD2 Proteins) and Smad-3. Accompanied by alterations in the expression of the indicated molecules, the lung structure of mice with PF was also markedly ameliorated.
E2a (show TCF3 Proteins) is necessary to drive transcription of Smad2 (show SMAD2 Proteins)/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
HSP70 (show HSP70 Proteins) indirectly interacted with Smad3.
Activin A (show INHBA Proteins) and overexpression of SMAD2 (show SMAD2 Proteins)/3 significantly promoted expressions of porcine NANOG (show NANOG Proteins) and OCT4 (show POU5F1 Proteins),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (show NANOG Proteins)/OCT4 (show POU5F1 Proteins) expression.
Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition
SP1 (show SP1 Proteins) and SMAD3 are required for high glucose-induced p21(WAF1 (show CDKN1A Proteins)) gene transcription in LLC-PK1 (show PKLR Proteins) cells.
Cav-3 (show CAV3 Proteins) and Smad3 may be involved in the occurrence and development of viral myocarditis.
In pancreata of mice and rats, TGFB (show TGFB1 Proteins) promotes peripheral nociceptive sensitization via a direct effect on primary sensory neurons mediated by intra-neuronal SMAD3.
We provide the evidence that over-expression of miR (show MLXIP Proteins)-145 could inhibit osteoclast differentiation, at least partially, by decreasing Smad3 expression
Activin signaling through SMAD2 (show SMAD2 Proteins)/3 in retinal progenitor cells regulates expression of transcription factors involved in cell type determination and promotes photoreceptor lineage specification.
conclude that VDD promotes tumor growth in the context of Smad3 disruption, potentially through regulation of TLR7 (show TLR7 Proteins) expression and beta-catenin (show CTNNB1 Proteins) activation
SMAD3 is regulated by miR (show MLXIP Proteins)-489 in pulmonary fibrosis.miR-489 suppresses fibroblast differentiation by targeting Smad3.
Alendronate (ALN)-augmented IL-1beta production and cell death require Smad3 and ASC activation, and SIS3 and anti-ASC antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN
CRP (show CRP Proteins) is pathogenic in type-2 diabetes (T2DN). CRP (show CRP Proteins) may promote CD32b- NF-kappaB (show NFKB1 Proteins) signaling to mediate renal inflammation; whereas, CRP (show CRP Proteins) may enhance renal fibrosis in T2DN via CD32b-Smad3-mTOR (show FRAP1 Proteins) signaling.
A Smad3-PTEN regulatory loop controls proliferation and apoptotic responses to TGF-beta (show TGFB1 Proteins) in mouse endometrium.
These findings indicate that both systemic factors and intrinsic properties of skin cells contribute to enhanced wound healing and less inflammatory reaction observed in Smad3 knock-out mice.
Data show that the transcription factor Smad3 (Smad3) gene was expressed ubiquitously in 11 bovine tissues and displayed different expression patterns between muscle and adipose tissue.
the present work provides evidence supporting a functional role of SMAD2 (show SMAD2 Proteins)/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2 (show SMAD2 Proteins)/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta (show TGFB1 Proteins) signalling that incorporates elements of previous models together with crosstalking between Smad1 (show SMAD1 Proteins)/5/8 and Smad2 (show SMAD2 Proteins)/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 Proteins).
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein functions as a transcriptional modulator activated by transforming growth factor-beta and is thought to play a role in the regulation of carcinogenesis.
MAD homolog 3
, MAD homolog 3a
, MAD, mothers against decapentaplegic homolog 3
, SMA- and MAD-related protein 3
, SMAD, mothers against DPP homolog 3
, mad homolog JV15-2
, mad protein homolog
, mothers against DPP homolog 3
, mothers against decapentaplegic homolog 3
, SMAD 3
, TGF beta response effector Smad3
, TGF-beta response effector Smad3
, Smad 3
, MAD (mothers against decapentaplegic, Drosophila) homolog 3
, SMAD family member 3