SMAD6 Antibody (monoclonal) (M08)
- Known as:
- SMAD6 Antibody (mab) (M08)
- Catalog number:
- AT3947a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SMAD6 Antibody (monoclonal) (M08)
Related genes to: SMAD6 Antibody (monoclonal) (M08)
- Gene:
- ANAPC15 NIH gene
- Name:
- anaphase promoting complex subunit 15
- Previous symbol:
- C11orf51
- Synonyms:
- HSPC020, DKFZP564M082, APC15
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-06
- Date modifiied:
- 2015-09-11
- Gene:
- KIAA0100 NIH gene
- Name:
- KIAA0100
- Previous symbol:
- -
- Synonyms:
- DKFZp686M0843, MGC111488, BCOX1, CT101, BCOX, FMP27
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-22
- Date modifiied:
- 2019-04-12
- 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
- Gene:
- TMEM184B NIH gene
- Name:
- transmembrane protein 184B
- Previous symbol:
- C22orf5
- Synonyms:
- HS5O6A, DKFZP586A1024, FM08
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2016-10-05
Related products to: SMAD6 Antibody (monoclonal) (M08)
Related articles to: SMAD6 Antibody (monoclonal) (M08)
- The current evidence suggests that the formation of pulp stones (PS) has a genetic background. Therefore, the present study aimed to evaluate the association between PS in orthodontically treated patients and single nucleotide polymorphisms (SNPs) in the mineralization-related genes ( [, , , and [). - Source: PubMed
Publication date: 2026/08/06
Hemming Danielde Mattos de Araujo Bianca MarquesKirschneck ChristianScariot RafaelaPerin Camila PaivaSousa-Neto Manoel DFonseca-Souza GabrielaMattos Natanael Henrique RibeiroMeger Michelle NascimentoBaratto-Filho FlaresKüchler Erika Calvano - This study aimed to evaluate the association between single nucleotide polymorphisms (SNPs) in endochondral development-related genes and cranial base 3D phenotypes. - Source: PubMed
Publication date: 2026/07/21
Marañón-Vásquez Guido ArtemioTirre de Souza Araújo MônicaCarlos de Oliveira Ruellas AntônioMatsumoto Mírian Aiko NakaneChávez Alejandro David AvalosFigueiredo Marciode Oliveira Fernandes ThaísAntunes Lívia Azeredo AlvesLagravère Vich ManuelScariot RafaelaFlores-Mir CarlosKirschneck ChristianDos Santos Antunes LeonardoKüchler Erika Calvano - Juvenile idiopathic arthritis (JIA) is a complex rheumatic disease that is influenced by environmental and genetic factors. Linkage studies and genome-wide association studies have identified genes that contribute to the risk of developing JIA but are limited in their ability to identify disease-risk variants of large effect. Penetrant, heritable risk variants can be detected in high-risk families, but such cases are uncommon due to the low prevalence of JIA. This study utilizes whole-genome sequencing of 23 multiplex families, the largest such cohort to date, to discover variants and genes relevant to JIA pathogenesis. Pathogenic variants in NOD2 associated with Blau syndrome, an ultra-rare Mendelian inflammatory disorder, are the most recurrent variants in the cohort, consistent with previous reports that milder presentations of Blau syndrome are oftentimes misdiagnosed as JIA. For the first time, however, rare variants in ACVR1 and SMAD6, integral components of the Bone Morphogenic Protein (BMP) pathway, are found to be associated with JIA. Identified ACVR1 variants map to critical protein domains. AlphaFold modeling predicts that the ACVR1 interaction with its inhibitor OGT is disrupted by these variants, indicating that the patient-mutated protein has a gain-of-function phenotype. Drosophila melanogaster expressing either a wild-type or patient-mutated version of ACVR1 exhibit embryonic lethality, with the mutant exhibiting 1.4-fold greater lethality than wild-type. The combination of family-based cohorts for gene discovery, AI-based computational tools, and animal model studies for tests of variant function underscores shared disease pathogenesis between JIA and monogenic disorders of immunity and connective tissue. - Source: PubMed
Publication date: 2026/07/17
Avery Cecile NHernandez Edgar JKazuko Sandy GBohnsack John FSudman MarcPrahalad SampathRadmall KaitlinHersh Aimee OLetsou AntheaJorde Lynn B - Young-onset lung cancer is enriched for never-smoking and oncogene-driven tumors, yet its inherited genetic basis remains poorly defined. We performed germline whole-genome sequencing in 251 young-onset lung cancer cases (median age 37), which we jointly analyzed with never-smoking cases (n=196; median age 68) and cancer-free controls (n=1,883). We identified enrichments of rare deleterious coding variants across 55 cancer-related gene sets, including signaling and genes implicated by prior lung cancer GWAS. Exome-wide analyses of rare coding variants affirmed as a penetrant lung cancer predisposition gene (odds ratio [OR]=36.1, p=1.02×10 ) and discovered two novel exome-wide significant tumor subtype-dependent associations: in cases with fusion-driven tumors (p=1.39×10 ) and in fusion-negative tumors (p=2.05×10 ). Structural variants contributed distinct risk, with enrichment in constrained, lung-expressed genes (OR=5.79, p=5.8×10 ) and very large germline deletions being markedly enriched in cases with fusion-driven tumors. Polygenic risk scores for lung cancer were inversely correlated with rare variant burden, consistent with additive risk from rare and common variants. Collectively, these findings delineate a complex germline architecture underlying susceptibility and molecular subtype in young-onset lung cancer. - Source: PubMed
Publication date: 2026/07/10
LoPiccolo JaclynCollins Ryan LFields NoahNakagawa CarterTaraszka KodiWang XinanSu LiKoeller Diane RSchwartz Alison LevinePollaci Alicia CharlestonYoung Sarah MWilliamson Victoria GAvila Jose AVoligny EmmaNguyen TomPangilinan Andy JErwin Richard MGitlitz Barbara JNovello SilviaOxnard Geoffrey RChukwueke Ugonma NBrastianos Priscilla KAizer Ayal AHatabu Mizuki NishinoFlorez NarjustHaigis Kevin MVan Allen Eliezer MNieva Jorge JGarber Judy EChristiani David CJänne Pasi AGusev Alexander - 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