Smad1 (Phospho_Ser465) Antibody
- Known as:
- Smad1 (Phospho_Ser465) Antibody
- Catalog number:
- E011321-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Smad1 (Phospho_Ser465) Antibody
Ask about this productRelated genes to: Smad1 (Phospho_Ser465) Antibody
- Gene:
- SMAD1 NIH gene
- Name:
- SMAD family member 1
- Previous symbol:
- MADH1
- Synonyms:
- MADR1, JV4-1
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2015-09-02
Related products to: Smad1 (Phospho_Ser465) Antibody
Related articles to: Smad1 (Phospho_Ser465) Antibody
- Preeclampsia (PE) is a major hypertensive disorder of pregnancy and a leading cause of maternal and perinatal mortality and morbidity worldwide. Aberrant placental development, characterized by shallow trophoblast invasion and incomplete remodeling of maternal spiral arteries, remains central to PE pathogenesis. In PE, tissue transglutaminase (TGM2) is dysregulated in the placenta, contributing to vascular dysfunction, inflammation, and impaired trophoblast differentiation, yet the upstream regulatory signals remain unknown. Bone morphogenetic protein 7 (BMP7) is abundantly expressed at the maternal-fetal interface and implicated in vascular homeostasis, but its role in regulating trophoblast function, especially related to PE pathogenesis, remains undefined. Here, single-cell transcriptomic profiling of placental tissues revealed coordinated downregulation of BMP7 and upregulation of TGM2 in PE relative to normotensive controls. Functional assays in immortalized and primary human trophoblasts demonstrated that BMP7 promotes trophoblast migration and invasion by suppressing TGM2 expression through the ALK2/3-SMAD1/5/9-SMAD4 pathway. Trophoblast organoid models further demonstrated the anti-invasive role of TGM2 in trophoblast differentiation during early placentation. In vivo, an adenovirus-expressing sFlt-1 (Ad sFlt-1)-induced PE mouse model showed increased placental Tgm2 expression, while recombinant BMP7 administration ameliorated PE-like symptoms. Although the protective effects of BMP7 in vivo are likely mediated by mechanisms beyond TGM2 alone, together these findings identify the BMP7-TGM2 axis as an important trophoblast-regulatory mechanism in PE and support BMP7 as a potential therapeutic candidate. - Source: PubMed
Publication date: 2026/07/11
Ding QiaoqiaoLiu MingxiZhao BinbinSu YaxinZhong YingKlein CameronYan JunhaoLeung Peter C KChen Zi-JiangWei DaiminLi Yan - ERK1/2 play crucial roles in diverse cellular processes, yet their functions and underlying mechanisms in human embryonic stem cells (hESCs) remain incompletely defined. Here, we generate hESC lines with graded ERK1/2 activities and demonstrate that moderate ERK1/2 activation, with intact kinase activity and nuclear localization capacity, is optimal for sustaining the primed pluripotency state. Specifically, ERK1/2 hyperactivation induces mesendoderm differentiation, whereas their depletion drives trophoblast-like differentiation. Mechanistically, ERK1/2 govern pluripotency primarily through directly controlling key transcription factors (e.g., MYC, ZIC2, and FOS) and crosstalking with Hippo and BMP signaling pathways. Additionally, ERK1/2 preserve the homeostasis of the MYC-Ac-CoA-H3K27ac axis and constrain the CDK1-EZH2-H3K27me3 axis, thereby activating pluripotency genes and repressing trophoblast lineage genes. Collectively, this study systematically deciphers direct and indirect regulatory functions of ERK1/2 in hESCs, revealing a holistic regulatory network, in which ERK1/2 act as a central hub, to govern pluripotency of primed hESCs. - Source: PubMed
Publication date: 2026/07/09
Zhou YifanZhao HanzhiShao MinLu WeixuanJiao HuiyuanLi LingjieJin Ying - Biological age (BA) has emerged as a promising integrative indicator of physiological state and welfare, but its use within aquaculture remains underdeveloped. Previous genome-wide analysis in gilthead sea bream revealed skeletal muscle markers with inverse age-related expression and methylation patterns. Specifically, psmd2, ramp1, sirt1 and smad1 were up-regulated and hypomethylated with age, while atp1a2, bmp1, calcrl, col5a1, spred2 and thrb exhibited down-regulation coupled with hypermethylation. Here we assessed the responsiveness of this gene set across multiple aquaculture-relevant challenges using a real-time PCR array. Environmental stressors (e.g. increased temperature and high stocking density with low O concentration) induced transcriptional profiles resembling muscle gene-expression patterns of older individuals. Conversely, cold exposure and nutritional interventions, including restricted feeding and feed supplementation with bioactive protein hydrolysates, microalgae meal with a PUFA-rich lipid source, or fat emulsifiers promoted signatures aligned with those observed in younger animals. Although the direct reversal of stress-induced aging signatures was not tested, results indicate that dietary interventions elicit opposing transcriptional patterns, highlighting potential strategies to mitigate environmentally mediated aquaculture stress through targeted nutrition. These findings provide preliminary evidence of a potential relationship between BA and aquaculture stressors in farmed fish, underpinning a genomics-based framework for welfare assessment and adaptive management. - Source: PubMed
Publication date: 2026/07/09
Naya-Català FernandoGasperini AliceCarbonero-Acín BeatrizCalduch-Giner JosepBelenguer ÁlvaroPérez-Sánchez Jaume - Does 3'-phosphoadenosine 5'-phosphosulfate synthase 2 (PAPSS2)-mediated sulfation contribute to defective decidualization in patients with recurrent implantation failure (RIF), and what are the underlying mechanisms? - Source: PubMed
Publication date: 2026/07/09
Zi DuoDeng WanyingZhang XiaoliLi YunfeiLiang JunzhiHu JiaCao RuizheGao WenhuiZuo NaChen HaoLi Da - During genetic screening for radioulnar synostosis (RUS), we identified variants in individuals who also exhibited pectus excavatum (PE). This study aimed to investigate the association between variants and non-syndromic paediatric PE. - Source: PubMed
Publication date: 2026/07/06
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