HEY1 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- HEY1 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00023462-T06
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- HEY1 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: HEY1 293T Cell Transient Overexpression Lysate(Denatured)
- 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 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: HEY1 293T Cell Transient Overexpression Lysate(Denatured)
- 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
Qu PengShi JiaoLi XueGu YaoLiu JunZhang HongyanZhou MingZhiMa CuiLi XinghuiTian WenjieLiang QiLi GangCheng Panke - Inducing the transition of tumor cells into normal hepatocyte-like cells represents a promising therapeutic strategy for hepatocellular carcinoma (HCC). However, safe and effective inducers are currently lacking, and the underlying mechanisms remain poorly understood. This study aimed to investigate whether tumor supernatant (Tsn) under mild hyperthermia conditions could induce the transition of HepG2 cells into normal hepatocyte-like cells and to elucidate the potential mechanisms involved. HepG2 cells were treated at 42.5 °C for 60 min, and the post-treatment tumor supernatant (42.5Tsn) was collected. Transcriptome sequencing was performed to identify differentially expressed genes (DEGs) between the 42.5Tsn and 37Tsn treatment groups. Compared with the 37Tsn group, 446 DEGs were identified in the 42.5Tsn group. These DEGs were enriched in pathways related to DNA damage repair, cell cycle arrest, and nuclear receptor signaling. Among the 33 core genes, tumor suppressor genes (BRCA1, PALB2, SLX4) were significantly upregulated, while nuclear transcription factors that maintain stemness, such as HEY1, were significantly downregulated. Tsn induced by mild hyperthermia demonstrates the potential to promote the transition of HepG2 cells toward normal hepatocyte-like cells while suppressing their metastatic potential. However, due to the complex composition of Tsn and the transcriptome-only level of this analysis, the specific active factors, causal regulatory mechanisms, and in vivo efficacy require further validation through component analysis, functional assays, and animal models. - Source: PubMed
Publication date: 2026/06/23
Zheng LiDing YihengMa YutingLi XinhaoQi JinshengLiu JianminLi Yanning - Liver development requires precise coordination of biochemical and biophysical cues to establish proper zonation and localized cell fate specification. However, there are limited models for studying the interactions between signaling pathways in defined microenvironmental contexts. Here, we employed complementary 2D microarray and 3D microwell platforms to systematically investigate how Wnt and YAP signaling pathways regulate hepatoblast differentiation and influence spatial patterning. siRNA-mediated knockdown of APC enhanced biliary marker expression and activated Notch signaling targets Hey1 and Hes1, while disrupting spatial organization patterns. YAP inhibition predominantly affected hepatocyte specification in 2D but dramatically inhibited biliary differentiation in 3D microtissues, revealing platform-dependent effects. Array culture analyses revealed that decreased cytoplasmic YAP levels, facilitated by YAP knockdown, were associated with a concomitant change in adherens junction protein expression. Collectively, the differential responses between 2D and 3D microtissue platforms are indicative of the context-dependence of intercellular interaction signals, with geometry-dependent effects influencing spatial distribution of differentiated cell types. Combinatorial pathway modulation demonstrated that Wnt and Notch signaling cooperatively regulate biliary fate, while YAP functions as a critical determinant through geometry-specific mechanisms. These findings highlight the application of engineered culture models for investigating the pathways that coordinate biochemical and biophysical signals during liver progenitor cell fate determination. - Source: PubMed
Publication date: 2026/06/11
Grenci BrockTsai ArianeZobus KatieUnderhill Gregory H