HEY1 Antibody
- Known as:
- HEY1 Antibody
- Catalog number:
- xw-8162
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HEY1 Antibody
Ask about this productRelated genes to: HEY1 Antibody
- Gene:
- HEY1 NIH gene
- Name:
- hes related family bHLH transcription factor with YRPW motif 1
- Previous symbol:
- -
- Synonyms:
- HESR-1, CHF2, HESR1, HRT-1, CHF-2, HERP2, bHLHb31
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2016-02-23
Related products to: HEY1 Antibody
Related articles to: HEY1 Antibody
- A receptive endometrium is essential for successful embryo implantation, yet its dynamic cellular and molecular features remain poorly understood due to limitations in current in vitro models. We aimed to establish a 3D co-culture endometrial model mimicking physiological conditions, characterizing its response to varied culture conditions using receptivity-associated gene expression profiling. Epithelial Ishikawa or RL95-2 cells were layered above stromal St-T1b cells separated by Matrigel and cultured in different media (growth factor-reduced, serum-containing standard, cytokine-supplemented and EGF-supplemented) or exposed to hormonal stimuli (E2, P4, cAMP) over a 10-day differentiation period. Our model effectively recapitulates the layered structure of the endometrium, as confirmed by scanning electron microscopy and immunofluorescence. Transcriptional analysis of fertility-associated markers revealed media- and cell line-dependent alterations of key receptivity markers; In standard media gene expression alterations occurred for HEY1 in both, but for HEY2 solely in the Ishikawa model and EDNRB only in the RL95-2 model, in cytokine-supplemented media for LIF and TAGLN in both models, while HPSE only in RL95-2 models and DPP4 and HEY1 only in Ishikawa models. Notably, the long-term hormonal treatment triggered a transcriptomic signature, especially in the RL95-2 model that closely correlates to the clinically determined one at the window of implantation (WOI). We conclude that our in vitro model reflects the phenotypic and transcriptional dynamics of the in vivo endometrium and responds distinctly to external stimuli. It serves as a robust platform to study endometrial receptivity mechanisms and holds potential for future applications in infertility and implantation research. - Source: PubMed
Publication date: 2026/09/23
Kyriakopoulou KonstantinaHeukamp Mariam AFranchi MarcoObermeyer UllaFuchs EvelinEspinoza-Sanchez NancyHellmold JohannaHanker LarsGötte MartinEl-Shorafa Heba M - Emerging evidence highlights the role of the gut microbiota in allergic asthma, with microbial metabolites mediating distal immune responses. This study investigated the protective efficacy of Lactiplantibacillus plantarum GUANKE and the mechanisms associated with dendritic cell (DC)-driven allergic airway inflammation (AAI). GUANKE conferred both prophylactic and therapeutic protection by attenuating airway hyperresponsiveness and Th2-driven inflammation while partially restoring regulatory T cell (Treg) population. Antibiotic depletion and fecal microbiota transfer indicated that GUANKE-mediated protection was associated with remodeling of the indigenous microbiota and microbiota-dependent restoration of circulating indole-3-acetic acid (IAA). Targeted serum metabolomics further revealed lower circulating IAA levels in patients with asthma than in healthy controls. Exogenous IAA reduced CX3CR1Ly6C monocytic precursors and pulmonary CD11b DC accumulation. These reductions were preserved after CD11c-specific aryl hydrocarbon receptor (AhR) deletion and accompanied by reduced JAK3-STAT3 signaling, lower STAT3 occupancy at the Jag1 promoter, and attenuation of the Jag1-Notch4-Hey1 axis. Pharmacological STAT3 activation or Jagged1-mediated Notch reactivation partially reversed the effects of IAA. Collectively, these findings link microbiota-associated IAA restoration to GUANKE-mediated protection and implicate STAT3-Jag1-Notch4 signaling in monocyte-to-DC differentiation during AAI. - Source: PubMed
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He YujiaMi JielanZhao ZhipingZhang XiaoYang ZhihanYue KunHuang YuanmingSong LiqiongWen XiaotingXu JianguoRen Zhihong - Particulate matter with an aerodynamic diameter ≤10 μm (PM10) is a major environmental pollutant implicated in chronic airway injury and remodeling. This study investigated the effects of chronic PM10 exposure on epithelial barrier integrity, cellular differentiation, surfactant expression, and inflammatory signaling in a human small airway epithelial air-liquid interface (ALI) model. - Source: PubMed
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Heo Mi HyeonSon Eun SukPark So YoungKo Ui WonPark Jeong-WoongJeong Sung HwanKyung Sun Young - Muscle stem cells (MuSCs) are the cellular source for the generation and regeneration of skeletal muscle. Proper muscle growth requires precise control over the differentiation and self-renewal of MuSCs. Signaling systems, such as bone morphogenetic proteins (BMPs) and Notch, suppress the myogenic differentiation of MuSCs. This allows the expansion of the progenitor pool necessary for muscle growth. To better understand the molecular mechanisms and target genes of BMPs during myogenesis, we examined the response of adult mouse MuSCs to BMP6. BMP6 stimulation of freshly isolated MuSCs suppressed myogenic differentiation. Short-term stimulation (one hour) rapidly increased the expression of classical BMP target genes, such as , as well as Notch pathway genes, including , , , and . We used Cleavage Under Targets and Tagmentation (CUT&Tag) to generate whole-genome binding profiles for pSMAD1/5/9 and SMAD4, which are transcriptional effectors of the BMP pathway. This method detected dynamic binding in promoters and regulatory elements of direct BMP targets, including Notch pathway genes. Our data demonstrate that BMP6 is a potent suppressor of MuSC differentiation and reveal that a subset of well-characterized anti-myogenic genes (i.e., and ) are shared targets of the BMP and Notch pathways. - Source: PubMed
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