Rabbit polyclonal to Smad6, Host Rabbit
- Known as:
- Rabbit pab Smad6, Host Rabbit
- Catalog number:
- YF-PA13016
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Rabbit polyclonal Smad6 Host
Related genes to: Rabbit polyclonal to Smad6, Host Rabbit
- 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
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guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: Rabbit polyclonal to Smad6, Host Rabbit
- 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 - Investigation of in utero, tissue-specific molecular pathways contributing to prenatal programming of childhood-onset asthma is needed to develop effective, targeted prevention strategies. We aimed to examine the relationship between predicted gene expression in placenta and childhood-onset asthma and to compare relationships between childhood- and adult-onset asthma. Asthma genome-wide association study published summary statistics were obtained from the UK Biobank and published placental gene expression quantitative trait loci were obtained from the Rhode Island Child Health Study. We used S-PrediXcan to evaluate and compare associations between placental predicted gene expression and childhood- and adult-onset asthma and to determine whether signals were placenta-specific. Among 8,038 tested placental predicted expression-asthma associations, we identified 56 (0.7%) genes only significantly associated with childhood-onset asthma, 12 (0.1%) genes only significantly associated with adult-onset asthma, and 18 (0.2%) shared genes. Predicted expression of several genes (ACTL9, AMN, C9orf38, C11orf30, CTSE, EFCAB13, EIF4E1B, FN1, GLS2, IL6, IVL, LZIC, MAN2A2, MEGT1, RACGAP1, SMAD6, SPATA5, TMEM25, VTI1B, WDR19) was not significantly associated with childhood- or adult-onset asthma in any non-placental tissue, suggesting that the associations may be placenta-specific. This study identified alterations in predicted expression of placental genes associated with transcriptional pathways critical to the development of asthma. We identified unique and shared pathways, particularly related to immune regulation, associated with childhood- and adult-onset. This expands our understanding of the fetal origins of asthma, highlights the placenta as an informative tissue in understanding asthma pathogenesis, and identifies target genes to prioritize for future functional studies. - Source: PubMed
Publication date: 2026/05/13
Jasper Elizabeth AMcKennan Christopher GThompson Emma ESchoettler NathanGebretsadik TebebHellwege Jacklyn NEdwards Todd LOber CaroleVelez Edwards Digna RHartert Tina VSnyder Brittney M - Autism spectrum disorder (ASD) shows a consistent sex bias, yet how sex shapes de novo variant (DNV) risk across coding and noncoding sequence remains unclear. I analyzed DNVs in > 41,000 parent–child sequenced trios from three ASD family-based cohorts and compared DNV characteristics and enrichment patterns in males and females. Notably, these trios included individuals with ASD as well as those without ASD. I developed a new sex-aware DNV caller (HAT-FLEX) and thoroughly evaluated each candidate DNV using an additional tool introduced in this study, SNOW, to generate a high-confidence callset. - Source: PubMed
Publication date: 2026/04/24
Turner Tychele N