SMAD6 Antibody
- Known as:
- SMAD6 Antibody
- Catalog number:
- BIN-004091-M09
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SMAD6 Antibody
Related genes to: SMAD6 Antibody
- Gene:
- SMAD6 NIH gene
- Name:
- SMAD family member 6
- Previous symbol:
- MADH7, MADH6
- Synonyms:
- HsT17432
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2015-08-26
Related products to: SMAD6 Antibody
Related articles to: SMAD6 Antibody
- Postoperative peritoneal adhesion (PPA) is a common complication following abdominal surgery and effective preventive strategies remain limited. The present study aimed to investigate the protective effect of aspirin against PPA in rats and to elucidate the underlying mechanism involving the transforming growth factor‑β1 (TGF‑β1)/Smad signaling pathway. A total of 32 male Sprague‑Dawley rats were randomly divided into the four following groups: Sham‑operated group, model group, low‑dose aspirin group (10 mg/kg) and high‑dose aspirin group (30 mg/kg). A PPA model was established by cecal wall abrasion. The aspirin‑treated groups received daily intragastric administration for 8 consecutive days post‑surgery. All animals were euthanized on day 8. Adhesion severity was assessed using the Nair scoring system; histopathological changes were examined by Masson's trichrome staining; the expression levels of proteins related to the TGF‑β1/Smad pathway and to markers of fibrosis were detected by western blot, immunohistochemical (IHC) and reverse transcription‑quantitative PCR (RT‑qPCR) analyses. In addition, rat primary peritoneal mesothelial cells (RPMCs) were treated with different concentrations of aspirin to evaluate the expression levels of the relevant proteins. The results indicated that compared with the model group, aspirin administration significantly reduced PPA scores. Histological examination revealed that aspirin treatment alleviated collagen deposition in adhesion tissues. The results derived from western blotting, IHC and RT‑qPCR analyses demonstrated that aspirin downregulated the expression levels of TGF‑β1, phosphorylated (p)‑Smad2/3, alpha smooth muscle actin (α‑SMA) and collagen type I, alpha 1 (COL1A1), and inhibited the phosphorylation of Smad2/3. Moreover, treatment of RPMCs with different concentrations of aspirin led to a dose‑dependent decrease in the protein expression levels of TGF‑β1, COL1A1, α‑SMA, p‑Smad2 and p‑Smad3, while simultaneously upregulating the expression levels of the endogenous inhibitory factor Smad6 in this pathway. In conclusion, the data demonstrated that aspirin effectively prevented the formation of PPA in rats by suppressing peritoneal fibrosis, an effect likely mediated via inhibition of the TGF‑β1/Smad signaling pathway. These findings suggest that aspirin is a promising candidate for the clinical prevention of PPA. - Source: PubMed
Publication date: 2026/07/03
Yan SiqiRen YuanLiu BingyanXiong PaiSun Yimin - This study aimed to evaluate the association between genetic polymorphisms in the BMP2, BMP4, RUNX2, and SMAD6 genes and the presence of severe external apical root resorption (EARR) in orthodontic patients undergoing orthognathic surgery. EARR represents a significant adverse outcome in orthodontic treatments, and genetic susceptibility may influence its occurrence. A cross-sectional study was conducted with 158 orthodontic patients treated with fixed appliances and mono or bimaxillary orthognathic surgery. Postoperative panoramic radiographs were used to assess severe EARR. Genomic DNA was extracted from buccal epithelial cells. Seven single-nucleotide polymorphisms (SNPs) in the target genes were genotyped using real-time PCR with TaqMan assays. Statistical analyses were performed with Chi-square or Fisher's exact tests. No significant associations were observed for polymorphisms in BMP2 (rs1005464, rs235768), BMP4 (rs17563), RUNX2 (rs59983488, rs1200425), or SMAD6 (rs2119261). However, a significant association was found for SMAD6 rs3934908 (p < 0.05), with the CC genotype more frequent in patients with severe EARR. No deviations from the Hardy-Weinberg equilibrium were observed. The findings suggest that the SMAD6 rs3934908 polymorphism may be associated with an increased susceptibility to severe EARR in orthodontic surgery patients. While most SNPs showed no association, these results contribute to understanding the genetic factors involved in EARR. Further studies with larger samples are needed to confirm these findings and explore gene-environment interactions. - Source: PubMed
Publication date: 2026/06/26
Schröder Ângela Graciela DeligaKuczera Milena SampaioAraujo Cristiano Miranda deFreitas Veridiana Pereira de Sá deMeger Michelle NascimentoSantos Katheleen Miranda DosScariot RafaelaKüchler Erika CalvanoBaratto-Filho Flares - Exome sequencing (ES) has improved Mendelian disease diagnosis, but in consanguineous populations, biallelic variants in typically dominant genes remain underrecognized. This study characterized their clinical and molecular features and explored pathway-level patterns of dual inheritance. Exome data from 1450 individuals analyzed between 2022 and 2024 were retrospectively reviewed. Biallelic variants were filtered in genes annotated as autosomal dominant in OMIM. A pathway-based analysis using Gene Ontology and STRING identified functionally related genes, and those showing both dominant and recessive inheritance were further evaluated with gnomAD constraint metrics to explore shared mechanisms. Five consanguineous families carried biallelic variants in genes typically associated with dominant inheritance, accounting for ~3.1% of all homozygous pathogenic variants. Mechanisms included hypomorphic effects (TERC, ASH1L), semidominant dosage sensitivity (LRP5), structural or positional effects (FBN1), and complete loss of function with pleiotropy (SMAD6). Pathway analysis revealed dosage-sensitive dynamics in telomere maintenance, extracellular matrix, Wnt/BMP signaling, and histone modification, supporting dual-inheritance behavior driven by gene dosage and functional impact. Our findings show that genes labeled autosomal dominant can also cause disease biallelically, reflecting a dosage-sensitive continuum. Including such analyses in diagnostic pipelines, especially in consanguineous populations, can refine understanding of inheritance in rare disorders. - Source: PubMed
Publication date: 2026/06/18
Taşdelen ElifcanTekbaş Umut CanKolkıran AbdulkerimÇetinkaya SemraKılıç MustafaSezer Abdullah - Osteosarcoma, the most common primary malignant bone tumor, predominantly affects adolescents and is characterized by high aggressiveness and early metastatic propensity. Chemoresistance and recurrence remain major clinical challenges, highlighting the urgent need for novel therapeutic targets and molecular mechanisms. - Source: PubMed
Publication date: 2026/05/12
Yang MengfanLiu PeiZhang HongjunTang XunHong XiangLiu YujiaoDeng MeichaoTu XiaolinShao Gaohai - The objective of this study was to analyse the genomic basis of litter size variability. We used 172 644 observations on the total number born (TNB) from 40 518 Large White sows. First, the variance components and heritability for TNB were estimated using ASReml. Then, based on those results, the log-transformed variance of residuals for TNB (LnVarTNB) was used to quantify phenotypic variability and estimate its variance components. Finally, both LnVarTNB and meanTNB (i.e., the average TNB per sow) were used in a genome-wide association study (GWAS) with whole-genome sequence data comprising 27 035 402 SNPs across all chromosomes from 40 509 Large White sows. The GWAS was performed in GCTA using a mixed-model approach. We investigated the genomic regions associated with both the meanTNB and its variability. Heritability estimates were 0.125 for TNB and 0.003 for LnVarTNB. GWAS revealed a prominent QTL for meanTNB on SSC1 (164.8 Mbp), highlighting SMAD3, SMAD6, and MAP2K1 as key candidate genes. In contrast, LnVarTNB was associated with 20 significant SNPs across multiple Sus scrofa chromosomes (SSC 1, 4, 6, 7, 11, and 13). These variants were characterised by low minor allele frequencies (MAFs), with a major cluster on SSC13 near the TFF3 and UMODL1 candidate genes. Genotypic analysis showed that specific heterozygous genotypes significantly reduced litter size with a slight reduction in meanTNB compared to the homozygotes. The genetic control of litter size variability is driven by rare variants that are often missed in lower-density analyses. The identified loci on SSC13 and SSC1 suggest that selection for "robustness" alleles can improve production stability and farm efficiency. These findings provide valuable genomic markers for future breeding programmes aimed at balancing high prolificacy with phenotypic uniformity. - Source: PubMed
Publication date: 2026/05/07
Cieleń GDerks M F LBoshove ASell-Kubiak E