Ask about this productRelated genes to: SMAD3 antibody
- Gene:
- SMAD3 NIH gene
- Name:
- SMAD family member 3
- Previous symbol:
- MADH3
- Synonyms:
- JV15-2, HsT17436
- Chromosome:
- 15q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2016-10-05
Related products to: SMAD3 antibody
Related articles to: SMAD3 antibody
- Somatic mutations in protein-coding genes and noncoding regulatory regions are the major drivers of cancer. Only a relatively small number of somatic noncoding mutations that are likely drivers have been described to date, including those in the promoters of the , and genes. The impact of these alterations can be profound by initiating, increasing, or abolishing gene expression. Promoter mutations in particular have been difficult to identify even from whole tumor genomes due to their high content of G and C nucleotides, which leads to loss of sequencing coverage in these regions. Therefore, the landscape of somatic drivers in gene promoters remains incomplete. Here, we present a hybrid capture assay optimized for >3000 promoters of cancer genes. We show that this assay allows for deep sequencing of challenging GC-rich promoter regions, enabling discovery of reliable point mutations, short insertions and deletions, copy number variants, and mutational signatures in cell line models as well as formalin-fixed, paraffin-embedded archival tissue samples. Our assay nominated candidate noncoding driver mutations in , and in breast cancer for future functional follow-up. - Source: PubMed
Publication date: 2026/05/04
Qi MeifangDave Preshita SanjayFrancis NicoleDeFelice MatthewPollock SamCorbitt HollyMitsiades Irene RinWang GengchaoFrere PaulFox AlanKhitrov GregoryPetersen CarolineLarkin KatieHamilton SusannaEllisen Leif WGulhan Doga CHidalgo-Miranda AlfredoLennon NiallCibulskis CarrieRheinbay Esther - As a precursor to creatine, guanidinoacetic acid (GAA) is widely recognized to enhance growth performance and flesh quality of animals, but the underlying molecular mechanism remains unclear. This study evaluated the effects of dietary GAA supplementation on growth performance, textural properties, and flavor constituents in gibel carp CAS V (, CAS V). A total of 300 healthy gibel carp (5.01 ± 0.13 g) at 42 d of age were assigned randomly to 12 tanks (3 replicates per group, 25 fish per replicate). Fish were fed with a basal diet supplemented with graded levels of GAA (0.00, 0.03%, 0.06%, and 0.12%) for 10 weeks. Results demonstrated that GAA supplementation significantly enhanced the specific growth rate (SGR) and crude protein content in gibel carp ( < 0.05). It also enhanced muscle physicochemical attributes by increasing water holding capacity and hardness, along with boosting glycogen content and free glutamate level ( < 0.05). Mechanistically, GAA promoted myofiber development by upregulating protein and gene expression of myogenic regulatory factors (MRFs), leading to increase myofiber density and a higher frequency of myofibers with diameters between 20 and 40 μm ( < 0.05). Furthermore, GAA facilitated collagen synthesis to improve muscle hardness by activating the transforming growth factor-beta 1 (TGF-β1)/mothers against decapentaplegic homolog (SMADs) signaling pathway, upregulating transcript levels of , , , and ( < 0.05). Additionally, GAA increased inosine monophosphate (IMP) content in muscle ( = 0.015), which was associated with enhanced expression of AMPD1 protein and upregulation of the , , and genes ( < 0.05). In conclusion, dietary GAA supplementation enhanced flesh quality of gibel carp via improving growth performance, nutrient deposition, texture characteristics, and flavor components. - Source: PubMed
Publication date: 2026/04/03
Wang YuZhang YanWu LiyunLi ChaoyueChen QiaozhenHan DongLiu HaokunZhang ZhiminXie ShouqiJin Junyan - Thirteen previously undescribed and structurally diverse sesquiterpenoids-comprising seven cadinane-type (1a, 1b, 2a, 2b, 3a, 3b, and 4), two eremophilane-type (8a and 8b), two eudesmane-type (9 and 10), one tricyclic (12), one guaiane-type (13), along with eight known analogues (5-7, 11, and 14-17) were isolated from the fruits of Alpinia oxyphylla. The structures of the thirteen sesquiterpenoids, including their relative and absolute configurations, were determined through their NMR, HRESIMS, and ECD spectroscopic data. Eight compounds (1b, 2a, 3a, 3b, 5, 8a, 8b, and 11) were found to have significant anti-renal fibrosis activity by inhibiting the expression of extracellular matrix components (Fibronectin and Collagen I) and α-SMA in TGF-β1 induced NRK-52e cells. Compounds 1b and 8b displayed significant inhibitory activity towards three markers of renal fibrosis in a dose-dependent manner in three types of TGF-β1 induced kidney cells (NRK-52e, NRK 49f, and HCK-8). RNA-seq analysis and target protein validation displayed that the anti-renal fibrosis activity of 1b was related to modulation of the NF-κB P65/IκBα signaling pathway, and simultaneously showed relative correlation to the inhibition of Smad3 phosphorylation. These results suggested that NF-κB P65/IκBα and TGF-β1/Smad3 signaling pathways were collectively mediated for the biological activity of 1b, revealing the potential of sesquiterpenoids derived from the fruits of A. oxyphylla as novel agents for the prevention and treatment of renal fibrosis. - Source: PubMed
Publication date: 2026/05/03
Lu Bo-TaoLiu Xiao-NingFang Hong-BinZhu Yue-TongZheng Yu-ZhongCheng Yong-XianWang Yan-Zhi - Liver fibrosis is an abnormal wound-healing response. Neuraminidase 1 (NEU1) is a sialidase that has been reported to be involved in the development of cancers and metabolic diseases. However, the role of NEU1 in liver fibrosis remains unreported. This study explored the potential role of NEU1 in liver fibrosis. - Source: PubMed
Zhang YueSong YuanNie YuanZhu XuanLi Bi-MinHuang Chenkai - Diabetic cardiomyopathy (DCM) features progressive fibrotic remodeling, but the shared molecular circuitry connecting diabetes mellitus (DM) to cardiomyopathy (CM) remains unclear. We integrated three DM- and three CM-related Gene Expression Omnibus (GEO) datasets and corrected batch effects with sva, verified by violin plots, principal component analysis (PCA), and silhouette coefficients computed on all common genes (DM: 0.9489 to -0.1016; CM: 0.9693 to -0.045; PC1/PC2 inter-batch differences abolished after normalization). Differential expression analysis identified 2562 DM Differentially expressed genes (DEGs) and 1414 CM DEGs, and their intersection yielded 91 common DEGs (51 upregulated, 40 downregulated). Protein-protein interaction (PPI) analysis prioritized 25 hub genes, whose enrichment profiles implicated insulin resistance/insulin signaling and adrenergic signaling in cardiomyocytes. TRRUST-based inference further defined a regulatory network centered on seven key genes (, , , , , , and ). To nominate a candidate target of oxymatrine (OMT), we performed docking and molecular dynamics (MD) simulations for representative complexes; OMT showed the most stable interaction with LTBP1, maintaining a consistently short pocket distance (~0.2 nm), the highest contact frequency, and the lowest MM/PBSA binding free energy (-15.32 kcal/mol), with favorable contributions dominated by van der Waals and nonpolar solvation terms. In primary cardiac fibroblasts (CFs), high glucose (HG, 30 mM glucose) induced proliferative and profibrotic activation, whereas OMT (0.4-0.8 mM) reduced HG-driven proliferation without detectable toxicity below 1.2 mM, suppressed FN, collagen I/III, and α-SMA expression, and inhibited migration. OMT also normalized HG-induced cell-cycle skewing by restoring G0/G1-phase occupancy and reducing S-phase entry, with effects comparable to metformin. Finally, HG increased LTBP1 expression and upregulated SMAD3/SMAD4, while OMT attenuated LTBP1 induction and suppressed downstream TGF-β/SMAD activation. Together, these data integrate cross-dataset transcriptomics with mechanistic validation to position LTBP1 as a putative antifibrotic node targeted by OMT, supporting inhibition of the LTBP1/TGF-β/SMAD axis as a candidate strategy to counter DCM-associated fibrosis. - Source: PubMed
Publication date: 2026/04/13
Tian LianqingGan ShiquanDu YouqiLong ChaowenChang ChuruiShen Xiangchun