HEY1 Blocking Peptide, Blocking Peptides
- Known as:
- HEY1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-1335
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- HEY1 Blocking Peptide Peptides
Related genes to: HEY1 Blocking Peptide, Blocking Peptides
- 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 Blocking Peptide, Blocking Peptides
Related articles to: HEY1 Blocking Peptide, Blocking Peptides
- 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 - Successful implantation requires coordinated decidual differentiation of endometrial stromal cells. This study shows that anandamide treatment of decidualising cells is associated with reduced NOTCH1 activation and selective alterations in decidual, inflammatory and structural programs. - Source: PubMed
Publication date: 2026/08/17
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 - Papillary thyroid carcinoma (PTC) typically exhibits a favorable prognosis; however, lymph node and distant metastases continue to present significant clinical challenges. Plectin isoform 1d () contributes to myofiber integrity and is implicated in cytoskeletal organization and cancer cell motility, but its role in PTC progression is largely unknown. In this study, expression was examined by RT-PCR in three PTC cell lines (MDA-T32, MDA-T41, MDA-T120) and normal thyroid cells (Nthy-ori-3-1). CRISPR-Cas9-mediated knockdown (KD) of was performed in MDA-T41 cells, with KD efficiency confirmed by RT-qPCR. Cell proliferation and migration were assessed using EdU incorporation and wound-healing assays, respectively. RNA sequencing (RNA-seq) combined with RT-qPCR and Western blotting was employed to identify downstream targets. Accordingly, mRNA and total plectin protein levels were substantially elevated only in MDA-T41 cells. KD reduced proliferation by 6.6% and migration by 26%. Transcriptomic analysis revealed 170 differentially expressed genes, including significant downregulation of , , and . HEY1 downregulation was confirmed at both mRNA and protein levels. Although and were also downregulated following KD, mRNA expression varied across PTC cell lines, suggesting cell-line-specific regulation. Notably, was consistently upregulated at the mRNA level in all PTC cell lines, while HEY1 showed elevated expression at both the transcript and protein levels. Collectively, these findings indicate that enhances cell migration and may contribute to cellular processes associated with metastatic behavior in a subset of PTC cells, potentially through a HEY1-dependent mechanism. - Source: PubMed
Publication date: 2026/07/16
Gundesli HulyaBudak BetulArga Kazim Yalcin - The pathogenesis of myocardial ischemia-reperfusion (MI/R) injury is intricately linked to mitochondrial dysfunction occurring during both the ischemic and reperfusion phases. Through single-cell transcriptome analysis, we identified a subpopulation of HEY1-high expressing cardiomyocytes (HEY1 CMs) characterized by superior mitochondrial homeostasis. To leverage this, we isolated P5CS-type or ATP5B-type functional mitochondria from a ΔΨ-high subpopulation, which was obtained via membrane potential sorting following dual overexpression in HEY1 CMs, and subsequently encapsulated them within HEY1 CM-derived exosomes to achieve stable, targeted delivery. We designed a responsive microneedle patch based on local copper/iron ion dynamics to enable the stage-specific release of these mitochondria within the ischemic or reperfusion microenvironments. In a Bama minipig MI/R model, this system significantly ameliorated cardiac function, reduced infarct size, and attenuated cardiomyocyte death. Mechanistically, the therapeutic strategy enhanced mitochondrial structural integrity and energy metabolic function. This study establishes a responsive, stage-specific mitochondrial delivery platform, offering a promising strategy for the precision treatment of ischemic heart disease. - Source: PubMed
Publication date: 2026/06/10
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