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
- Loeys-Dietz syndrome (LDS) is a heritable connective tissue disorder caused by pathogenic variants in genes of the transforming growth factor- (TGF-) signaling pathway. Although genotype-phenotype correlations have been suggested, comprehensive comparative data across LDS subtypes remain limited. Improved understanding of these correlations is essential to guide individualized surveillance and management strategies. - Source: PubMed
Publication date: 2026/09/06
Nabi Hussein AbdulDreher LukeHartnett JackCrossley AshleyEl Ghandour HusseinOsundiji MayowaEl Masry HichamAyoub ChadiShamoun Fadi EBaudhuin Linnea M - Neoadjuvant chemoradiotherapy followed by total mesorectal excision is standard for locally advanced rectal cancer, but response varies and current markers are insufficient. This study integrates public bulk RNA-seq data to identify predictive features of response. TRIM54 and PABPC4 were upregulated in the responder group, while ADSS1 and MGAT1 were upregulated in the non-responder group. ARMC2 was identified as a predictive biomarker upregulated in pathological complete response. Responder group showed enrichment of NK cells and CD4+ lymphocytes, while immune precursors were linked to poor outcome. Transcription factor analysis revealed SP1 and NFKB activations in the non-responder group and TCF15 in the responder group. SMAD3 and RDXANK were associated with complete regression, while MYC was dominant in incomplete regression. These findings provide insight into mechanisms underlying therapy response. To our knowledge, this is the first meta-analysis using high-throughput sequencing data, providing a valuable starting point for future rectal cancer research. - Source: PubMed
Publication date: 2026/09/07
Stanojevic AleksandraStroggilos RafaelMarinkovic MladenDjuric AnaStojanovic-Rundic SuzanaJankovic RadmilaCastellvi-Bel SergiFijneman Remond J AVlahou AntoniaZoidakis JeromeCavic Milena - IgA nephropathy (IgAN) is a progressive glomerular disease marked by mesangial IgA deposition, inflammation, podocyte injury, and fibrogenesis. Although understanding of its pathophysiology has advanced, effective disease-modifying therapies are still limited. Sarsasapogenin (SAR), a natural steroidal sapogenin, demonstrates anti-inflammatory, antioxidant, and antifibrotic properties by modulating signaling pathways such as NF-κB and TGF-β. The present study investigated the renoprotective effects of SAR in an experimental model of IgAN. IgAN was induced in Sprague-Dawley rats using bovine serum albumin (BSA), carbon tetrachloride (CCl), and lipopolysaccharide (LPS). SAR was administered at 60 mg/kg/day from week 7 through week 12. Renal function, histopathological changes (Oxford MEST-C classification), and immunohistochemical, ultrastructural, and molecular alterations were assessed. Induction of IgAN resulted in significant proteinuria, renal dysfunction, mesangial IgA deposition, and podocyte alterations, accompanied by increased expression of IL-6, TGF-β1, SMAD3, fibronectin, and α-SMA. Masson's trichrome staining did not reveal excessive collagen deposition, indicating early fibrogenic activity rather than established fibrosis. SAR treatment significantly reduced proteinuria and improved renal function, accompanied by decreased IL-6-mediated inflammation and reduced activation of the TGF-β1/SMAD3 pathway. SAR also preserved podocyte-associated proteins, including nephrin and podocin, and lowered pre-fibrotic markers. Ultrastructural analysis confirmed preservation of podocyte architecture, with reduced foot process fusion and mesangial matrix expansion. Overall, sarsasapogenin modulated multiple targets in experimental IgAN by reducing inflammation and early fibrogenesis while supporting podocyte integrity. These findings indicate that SAR is a promising therapeutic candidate for early IgAN, although further mechanistic and long-term studies are warranted. - Source: PubMed
Kumaş MeltemCanlar Akar DilekGül MehmetKaradaş ErkanKum Özşengezer SelenKulualp KadriYavuz OrhanYilmaz Osman - Keloids are pathological scars characterized by persistent fibroblast activation and excessive extracellular matrix (ECM) deposition. Cardamonin (CARD), a natural chalcone compound, has demonstrated anti-fibrotic effects; however, its role in keloid-associated fibrosis remains unclear. This study aimed to investigate the effects of CARD on human keloid fibroblasts (KFs) and the underlying molecular mechanisms. - Source: PubMed
Jin MeijingJing ChangzheLiu HongmeiLu BoJin ZhezhuPiao MinhaoJin ZhehuYuan Xinghua - Macrophage-Myofibroblast Transition (MMT) is a process in which macrophages, under the influence of specific factors such as transforming growth factor-beta 1 (TGF-β1) within a fibrotic microenvironment, gradually lose their original immune phenotype and acquire the biological characteristics of myofibroblasts. This transition involves changes in cell morphology, protein expression, and function, representing an important mechanism in the development and progression of tissue fibrosis. The TGF-β1/Smad3 signaling pathway, as a central regulator of fibrosis, plays a key role in MMT by modulating cell proliferation, differentiation, and the synthesis and degradation of extracellular matrix. Recent studies have identified MMT as a newly recognized form of phenotypic switching that contributes significantly to fibrosis in multiple organs, including the heart, lungs, liver, and kidneys. Experimental evidence has confirmed that the TGF-β1/Smad3 pathway directly regulates critical steps in MMT, thereby promoting the progression of fibrosis. However, the specific molecular targets and detailed mechanisms underlying this regulation remain incompletely understood and require further investigation. Elucidating the regulatory network of this pathway may offer new strategies for early intervention and targeted therapy in clinical diseases with fibrosis. However, direct evidence for MMT in human myocardial fibrosis remains limited, and its relative contribution compared to other sources of myofibroblasts requires further elucidation. - Source: PubMed
Publication date: 2026/08/05
Zou Ming-RuiHuang KangZhao Shuai-ShuaiWu BoHong XinZhou Xue-Liang