HEY1 Antibody
- Known as:
- HEY1 Antibody
- Catalog number:
- xw-8162
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HEY1 Antibody
Related 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
- 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
Publication date: 2026/09/04
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
Publication date: 2026/08/19
Lange Birthe Katrin AlexandraPolydorou IoannaHuryn ViktoriiaGeorgieva Angelina MYou ShanshanMüller ThomasMorales-Gonzalez SusanneBrandt BettinaBirchmeier CarmenAmthor HelgeSchuelke Markus - To investigate the role of integrin-associated adhesion signalling in Jagged1-driven osteogenic differentiation and to determine the specific contribution of integrin β3 (ITGβ3). - Source: PubMed
Publication date: 2026/08/17
Kornsuthisopon ChatvadeeChansaenroj AjjimaPhothichailert SuphalakGedik BetulZhang ChengfeiNowwarote NunthawanYuan QuanSilvio Lucy DiOsathanon Thanaphum - In brief: Successful implantation requires coordinated decidual differentiation of endometrial stromal cells. This study shows that anandamide treatment of decidualizing cells is associated with reduced neurogenic locus notch homolog protein 1 (NOTCH1) activation and selective alterations in decidual, inflammatory, and structural programs. Abstract: Decidualization of endometrial stromal cells is essential for human embryo implantation and pregnancy maintenance. The endocannabinoid system (ECS), particularly anandamide (AEA), has been implicated in endometrial receptivity, but the mechanisms through which AEA influences decidualization have been only partially elucidated. This study investigates the effects of AEA during decidualization of immortalized human endometrial stromal cells (HESCs), focusing on the neurogenic locus notch homolog protein 1 (NOTCH1) pathway, inflammatory mediators, cell-cycle arrest/senescence-associated markers, and cytoskeletal remodelling. Expression was analysed by quantitative real-time PCR, western blot, and immunofluorescence. Anandamide treatment during decidualization selectively reduced forkhead box O1 (FOXO1) and insulin-like growth factor binding protein 1 (IGFBP1), without affecting prolactin (PRL); homeobox A10 (HOXA10) was reduced during decidualization but was not further modified by AEA. Anandamide also attenuated NOTCH1 activation and reduced HES-related family bHLH transcription factor with YRPW motif 1 (HEY1) expression. Given the role of NOTCH signalling in cellular plasticity and cytoskeletal organization, NOTCH1/HEY1 attenuation after AEA exposure was accompanied by changes in snail family transcriptional repressor 1 (SNAI1), vimentin organization, and N-cadherin distribution. Consistent with the inflammatory component of stromal decidualization, decidualized HESCs showed increased interleukin-1 beta (IL1B), IL-8/C-X-C motif chemokine ligand 8 (CXCL8/IL-8), and prostaglandin-endoperoxide synthase 2/cyclooxygenase-2 (PTGS2/COX-2), whereas AEA reduced selected inflammatory mediators. Analysis of cyclin-dependent kinase inhibitor 1A (CDKN1A/p21) and cyclin-dependent kinase inhibitor 2A (CDKN2A/p16) suggested a short-term senescence-associated response, with AEA attenuating p21 expression. These findings suggest that AEA interferes with transcriptional and structural pathways critical for decidualization, highlighting a potential role of ECS-NOTCH1 crosstalk in implantation failure and endometrial dysfunction. - Source: PubMed
Carriero IleniaLacconi ValentinaBianco ClaudiaBertani NicoleStamme CamillaGasperi ValeriaMassimiani MicolTicconi CarloMaccarrone MauroLa Sala GinaCampagnolo Luisa - Patients with kidney stones (KS) often have an increased risk of atherosclerosis (AS). Because endothelial dysfunction (ED) is closely associated with AS, its role in KS remains unclear. This study aimed to examine the roles and mechanisms of AS-related ED genes in KS. Three datasets (GSE73680, GSE117518, and GSE132651) were analyzed. Differential expression analysis was conducted to identify differentially expressed genes (DEGs). To identify potential biomarkers, least absolute shrinkage and selection operator (LASSO) regression analysis and expression validation were conducted. Further analyses including GeneMANIA, gene set enrichment analysis (GSEA), examination of biomarkers within immune cells and subcellular localization analysis, molecular regulatory network analysis, tissue specificity analysis, and competing endogenous (ceRNA) network analysis were employed to comprehensively explore the functions and regulatory mechanisms of the identified biomarkers. Moreover, drug prediction analysis was conducted. Finally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) was proceeded to verify the expression levels of the biomarkers. A total of 22 DEGs associated with KS and AS were identified. Lasso regression selected 4 candidate biomarkers (MMP10, UCHL1, NEK2, and HEY1), among which UCHL1 and NEK2 were validated as key biomarkers. GeneMANIA and GSEA analyses uncovered the potential involvement of these biomarkers in cell adhesion molecules, focal adhesion, and lysosome pathways. Analysis of immune cells and subcellular localization provided insight into the biological functions and intracellular distribution of the biomarkers. Transcription factor regulatory network and ceRNA network analyses elucidated potential upstream regulatory mechanisms. Drug prediction analysis identified 17 potential drugs, including pazopanib and palbociclib, that may target NEK2. RT-qPCR demonstrated that NEK2 was significantly overexpressed in KS samples. This study identified biomarkers associated with KS and AS and comprehensively analyzed their molecular regulatory networks. These findings provide novel understandings of the molecular mechanism underlying KS and lay the foundation for future personalized treatment and drug development. - Source: PubMed
Publication date: 2026/08/04
Li AinaLiu ChenjingLiu XiangshenChen LeiWang DongZhu Changyan