SMAD3 (phospho-Ser425) Antibody
- Known as:
- SMAD3 (phosphorilated-Ser425) Antibody
- Catalog number:
- abx000322
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- SMAD3 (phospho-Ser425) Antibody
Related genes to: SMAD3 (phospho-Ser425) 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 (phospho-Ser425) Antibody
Related articles to: SMAD3 (phospho-Ser425) Antibody
- During ischemia‒reperfusion injury (IRI), has been shown to alleviate inflammation and kidney damage. However, the function of the tubular epithelium-macrophage interaction mediated by in IRI-induced renal fibrosis is still unclear. - Source: PubMed
Publication date: 2026/05/18
Chen WuZhao ShengYang SongyuanYu WeiminRao TingZhou XiangjunRuan YuanZou FanCheng FanLi Wei - Plastic production has been increasing exponentially. Throughout their lifespan, plastics degrade into smaller particles that accumulate in our bodies and the environment. Recent studies found these plastic particles can cross the placental barrier and reach the fetus. However, the impact of plastic particles on placental function is still unknown. We hypothesized that nanoplastics would disrupt placental growth and function, specifically focusing on transforming growth factor beta (TGFβ) signaling. To understand the impact of plastic particles on the placenta, we orally exposed pregnant CD-1 mice to 50 nm or 200 nm polystyrene plastic particles from gestation day 8 to day 15 at a human-relevant concentration of 5 mg/kg/day. After euthanization on day 15, placenta and fetus weights were recorded, and tissues were prepared for histomorphology and gene expression analysis. We observed a statistically significant decrease in the area of the decidua in the placentas for the 200 nm treatment group and a borderline significant decrease in decidua area for the 50 nm treatment group compared to control. However, when we separated by sex, only the male decidua were significantly decreased in the 200 nm group. Gene expression analysis of key signaling factors in the TGFβ pathway identified increased expression of and , which may be suppressing prolactin and estrogen receptor signaling. Overall, both particle sizes disrupted placenta structure and signaling in a sex-dependent manner and may be acting as endocrine disruptors. - Source: PubMed
Publication date: 2026/05/26
Alahmadi HaninHarbolic AllisonDe Oliveira-Cordova ChristopherReynolds RaulleJojy MichellePotts CourtneyDoan SofiaMathur TanviIslam Mohammad SaifulAndrade Melisa JSmith QuintonStapleton Phoebe AMitra SomenathWarner Genoa R - Cisplatin (Cis) is a widely utilized chemotherapy drug for managing various cancers, but its efficacy is limited by nephrotoxicity, which frequently results in kidney fibrosis. Oxidative stress, inflammation, and the fibrotic transforming growth factor beta/small mothers against decapentaplegic (TGF-β/SMAD) pathway are among the underlying mechanisms. Long-term exposure to Cis causes apoptosis, extracellular matrix deposition, and fibrosis. Fluvoxamine (FLV), a selective serotonin reuptake inhibitor and sigma‑1 receptor agonist, lycopene (LYC), a carotenoid antioxidant, and their combination showed a novel protective influence on kidney fibrosis in male albino rats induced by administering Cis (7 mg/kg) by intraperitoneal (IP) injection once weekly for 4 weeks. FLV (5 mg/kg), LYC (10 mg/kg), and their combination were administered orally (PO) once daily for four weeks. Treatment reduced blood urea nitrogen (BUN), serum creatinine (S.cr), nuclear factor kappa B (NF-κB), microRNA-21 (miR-21) levels, and the pro-apoptotic response reflected by decreased Bcl-2-associated X protein (Bax) immunoreactivity while enhancing antioxidant activity. They also attenuated fibrosis markers, including TGF-β1, SMAD3, collagen I (Col-I), and alpha-smooth muscle actin (α-SMA). FLV and LYC effectively attenuated Cis-induced kidney fibrosis through antioxidant, antiapoptotic, and antifibrotic mechanisms. These findings may provide a new therapeutic approach to counter Cis-induced nephrotoxicity in clinical settings. - Source: PubMed
Publication date: 2026/06/04
Abu-Risha Sally ESokar Samia SMousa Mai AEl-Shitany Nagla AElsisi Alaa E - This study aimed to investigate the therapeutic potential of Colivelin in modulating the cross-talk between the IL-6/JAK2/STAT3 and TGF-β/SMAD2/SMAD3 signaling pathways and its downstream effects on retinal apoptosis in an in vitro AMD model. An in vitro AMD model was established in ARPE-19 human RPE cells using a sublethal combination of lipopolysaccharide and hydrogen peroxide. Apoptosis was quantified via Tali® image cytometry. Gene expression profiling was performed by qRT- PCR. Protein expressions were assessed by Western blot. Formal mediation analysis was employed to quantify pathway-specific mechanistic contributions. The AMD model exhibited significant upregulation of hypoxia-related genes (HIF-1α, VEGF, MMP3, MMP9), pro-inflammatory cytokines (IL-6, TNF-α), and pro-apoptotic markers (BAX, p53, Caspase- 3), accompanied by markedly elevated ROS levels and reduced cell viability. Low-dose Colivelin (1 µM) significantly enhanced STAT3 phosphorylation, restored antioxidant gene expression (GSS, CAT, SOD2), suppressed hypoxia-associated gene expression, and substantially reduced TGF-β receptor, SMAD2, and SMAD3 expression at both transcriptional and protein levels. Formal mediation analysis revealed that 91-98% of Colivelin's anti-apoptotic effect at the therapeutic dose was mediated through STAT3-driven suppression of TGF-β/SMAD2/3 signaling, rather than through direct STAT3 transcriptional activity on apoptotic target genes. Conversely, high-dose Colivelin (10 µM) paradoxically activated SMAD2/3-independent pro-apoptotic cascades, demonstrating a dose- dependent biphasic response. This study provides the first formal mechanistic evidence that Colivelin exerts its cytoprotective effects in AMD primarily through a STAT3 → SMAD2/3 suppression axis. Low-dose (1 µM) Colivelin demonstrated superior and broader therapeutic efficacy compared to Bevacizumab by simultaneously modulating oxidative stress, hypoxia, angiogenesis, and apoptotic signaling pathways. These findings establish Colivelin as a promising multi-target therapeutic candidate for AMD, with its therapeutic window defined by the capacity of STAT3 activation to selectively suppress TGF-β/SMAD-driven apoptotic signaling without engaging compensatory pro-death mechanisms. Rigorous pharmacokinetic optimization and in vivo validation are warranted to advance Colivelin toward clinical translation. - Source: PubMed
Publication date: 2026/06/04
Güçlü HandeDoğanlar ZeynepŞambel Aykutlu MerveKöse GizemDoğanlar Oğuzhan - Voice disorders affect nearly 20 million Americans and cost more than $13 billion annually. Vocal fold (VF) fibrosis, a major cause of chronic dysphonia, disrupts normal vocal fold vibration by replacing the flexible extracellular matrix with stiff fibrotic tissue. Although TGF-β drives fibrosis, it also activates intrinsic negative feedback mechanisms, including SMAD7 induction and SMAD3 downregulation, to restrain excessive signaling. Broad inhibition of TGF-β or canonical SMAD signaling may disrupt these protective feedback loops and impair normal tissue homeostasis. An ideal anti-fibrotic strategy should differentially target the pro-fibrotic output of TGF-β. Here, we show YAP/TAZ inhibition selectively suppresses pro-fibrotic TGF-β signaling in VF fibroblasts. Pharmacologic inhibition of YAP/TAZ blocked TGF-β-induced fibroblast activation and fibrotic gene expression, while only modestly affecting canonical SMAD feedback responses. Integrated RNA-seq and ChIP-seq analyses demonstrated YAP/TAZ primarily regulate non-canonical TGF-β signaling and pro-fibrotic transcriptional programs. In a rat model of VF fibrosis, YAP/TAZ inhibition reduced nuclear YAP/TAZ localization and attenuated scar formation. Together, these findings identify YAP/TAZ inhibition as a promising therapeutic strategy for VF fibrosis and other fibrotic diseases. - Source: PubMed
Publication date: 2026/05/21
Nakamura RyosukeBing RenjieWeber HannahYoshimatsu MasayoshiGartling GaryGarabedian Michael JBranski Ryan C