SMAD6 monoclonal antibody (M03), clone 2A6
- Known as:
- SMAD6 mab (anti-) (M03), clonality 2A6
- Catalog number:
- H00004091-M03
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SMAD6 monoclonal antibody (M03) clone 2A6
Related genes to: SMAD6 monoclonal antibody (M03), clone 2A6
- Gene:
- CENPJ NIH gene
- Name:
- centromere protein J
- Previous symbol:
- MCPH6
- Synonyms:
- CPAP, BM032, LAP, LIP1, Sas-4, SASS4, SCKL4
- Chromosome:
- 13q12.12-q12.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-15
- Date modifiied:
- 2018-02-13
- Gene:
- CENPN NIH gene
- Name:
- centromere protein N
- Previous symbol:
- C16orf60
- Synonyms:
- FLJ13607, FLJ22660, BM039
- Chromosome:
- 16q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-20
- Date modifiied:
- 2015-08-24
- Gene:
- DONSON NIH gene
- Name:
- downstream neighbor of SON
- Previous symbol:
- C21orf60
- Synonyms:
- B17, C2TA, DKFZP434M035
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-18
- Date modifiied:
- 2017-03-30
- Gene:
- EAPP NIH gene
- Name:
- E2F associated phosphoprotein
- Previous symbol:
- C14orf11
- Synonyms:
- BM036, FLJ20578
- Chromosome:
- 14q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-18
- Date modifiied:
- 2016-02-26
- Gene:
- GOLGA2P5 NIH gene
- Name:
- GOLGA2 pseudogene 5
- Previous symbol:
- GOLGA2L1, GOLGA2B
- Synonyms:
- DKFZp434M0331
- Chromosome:
- 12q23.1
- Locus Type:
- pseudogene
- Date approved:
- 2006-01-27
- Date modifiied:
- 2018-04-26
Related products to: SMAD6 monoclonal antibody (M03), clone 2A6
Related articles to: SMAD6 monoclonal antibody (M03), clone 2A6
- The relatively low edible muscle yield and inconsistent flesh texture of red swamp crayfish limit its commercial value and highlight the need for effective nutritional interventions. Although L-carnosine has shown beneficial effects on muscle growth and quality in vertebrates, its nutritional functions and underlying mechanisms in crustaceans remain unclear. This study aimed to evaluate the effects of dietary L-carnosine on growth performance and muscle quality in red swamp crayfish (). A total of 324 red swamp crayfish, with an initial body weight of 6.19 ± 0.03 g, were randomly divided into 6 groups of three replicates and 54 crayfish per group (18 crayfish per replicate). Six experimental diets containing graded levels of L-carnosine (3.35, 59.28, 106.84, 222.20, 452.93, and 821.16 mg/kg) were fed for 8 weeks. Regression analysis revealed dose-dependent responses in multiple parameters. Weight gain rate, specific growth rate, protein efficiency ratio, protein deposition rate, muscle percentage, whole-body and muscle crude protein content, muscle textural properties (hardness and chewiness), hydroxyproline levels (alkaline-insoluble and total), myofiber density, small myofiber proportion (<50 μm), and total amino acid content exhibited quadratic trends ( < 0.05), with peak values observed in the 452.93 mg/kg group. Conversely, feed conversion ratio and large myofiber proportion (>70 μm) showed significant quadratic decreases ( < 0.05), reaching their lowest values at 452.93 mg/kg. Transcriptional analysis demonstrated that, compared with the 3.35 mg/kg L-carnosine group, the 452.93 mg/kg L-carnosine group significantly regulated genes involved in several key pathways: mTORC1 signaling (, , , , , and ), eIF2B-eIF2 signaling (), ubiquitin-proteasome system (, , , and ), autophagy-lysosomal system (, , , and ), TGFβ/Smads pathway (, , , , and ), and myogenic regulators (, , and ) ( < 0.05). These molecular modulations were consistent with observed phenotypic improvements. Overall, the findings demonstrated that a dietary L-carnosine level of 458.06 to 500.00 mg/kg, as determined by quadratic regression analysis, significantly enhances growth performance, feed utilization, muscle hardness and chewiness, and nutritive value in red swamp crayfish. - Source: PubMed
Publication date: 2026/08/05
Li XinyuanLiu YangyangXie ShouqiZhang JianminGao WeihuaJiang MingDong LixuePeng DiCheng KeHuang FengTian Juan - Esophageal atresia/tracheoesophageal fistula (EA/TEF) are congenital malformations of the foregut, and we identified two EA/TEF patients with two variants in the BMP/TGFβ repressor SMAD6. We investigated the function of SMAD6 in tracheoesophageal development using two orthogonal approaches in Xenopus embryos, both resulting in foregut malformations including EA/TEF. We then used human Pluripotent Stem Cell-derived foregut epithelium and mesenchyme to explore the separate roles of SMAD6 in these germ layers. CRISPR-mediated disruption of human SMAD6 caused an increase in BMP signaling in foregut epithelium and mesenchyme consistent with its role as a BMP repressor. Loss of SMAD6 caused patterning defects in both tissue types; SMAD6-/- endoderm shows increased expression of distal gut tube markers and SMAD6-/- mesenchyme shows increased expression of ventral and posterior markers including markers of cardiac and liver mesenchyme lineages. Furthermore, SMAD6-/- mesenchyme had decreased ability to form CD31-positive endothelial cells. Our results demonstrate that SMAD6 is required for foregut development and that rare variants in this gene are likely causative for foregut malformations in EA/TEF patients. - Source: PubMed
Publication date: 2026/08/14
Pagan VivienRankin Scott AEdwards Nicole AThorner KonradXie ShangqianChung Wendy KShen YufengZorn Aaron MWells James M - The therapeutic potential of selective PAD4 inhibitors such as GSK484 in mitigating adverse cardiac remodeling remains to be established. This study tested the hypothesis that PAD4 inhibition by GSK484 alleviates doxorubicin (DOX)-induced myocardial fibrosis in mice by modulating the expression of fibrosis-related biomarkers. - Source: PubMed
Publication date: 2026/08/13
Al-U'datt Doa'a G FTashtush AyssarAl-U'datt MuhammadTranchant Carole CAl-Masaed SaraJaradat Saied - Thoracic aortic dissection (TAD) associates with a high mortality rate. Treatment options are limited and mainly consist of surgical repair at critical aortic diameters as current pharmacological interventions are unable to stop disease progression. Despite the existence of different mouse models for thoracic aortic aneurysm (TAA) and TAD, the underlying disease mechanisms remain elusive. In humans, loss-of-function of SMAD3 or SMAD6 increases the risk for TAA. We therefore targeted both ohnologs of smad3 and smad6 in zebrafish in order to further investigate their contribution to aortic homeostasis. We found an increased diameter of the ventral aorta in smad3a;smad3b double knockout (smad3a/b DKO) zebrafish larvae, while smad6a;smad6b (smad6a/b DKO) zebrafish larvae have a reduced aortic diameter. Smad3a/b DKO survive normally to adulthood, but smad6a/b DKO die before the age of 8 months due to dissections and ruptures in the ventral aorta. Smad6a/b DKO zebrafish also show hypoplasia of the aortic arches and the distal part of the ventral aorta. Surprisingly, the smad3a;smad3b;smad6a;smad6b quadruple knockout (qKO) zebrafish model has normal survival and a milder vascular phenotype compared to the smad6a/b DKO. RNA sequencing of zebrafish larvae indicates upregulation of pathways related to melanogenesis, ribosome, blood vessel development and carboxylic acid transport, and downregulation of negative regulation of endopeptidase activity and immune system. Transcriptomic data of damaged aorta compared with healthy control aorta identifies significant differences in oxidative phosphorylation, mitochondrial function, extracellular matrix and the citrate cycle. In conclusion, data from our novel zebrafish models of thoracic aortic dissection and rupture indicate that SMAD3 function has an important modifying effect on the severe aortic manifestations induced by loss of SMAD6. - Source: PubMed
Publication date: 2026/08/12
Vanhooydonck MichielVerlee MaximSilva Marta SantanaPottie LoreBoel AnnekatrienVan Impe MatthiasDe Saffel HannaCaboor LisaBonnin AnneSegers PatrickDe Clercq AdelbertGansemans YannickVan Nieuwerburgh FilipSyx DelfienWillaert AndySips PatrickCallewaert Bert - 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