HEY1 Over-expression Lysate Product
- Known as:
- HEY1 Over-expression Lysate Product
- Catalog number:
- GWB-DFB441
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- HEY1 Over-expression Lysate Product
Related genes to: HEY1 Over-expression Lysate Product
- 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 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: HEY1 Over-expression Lysate Product
- 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 - Gastric cancer, faced different therapeutic imperfections such as chemoresistance, dangerous side effects, and non-specificity of the treatments. Our aim in the present study was to investigate the potential of the Enhancer of Zeste Homolog 2 (EZH2) gene as a therapeutic target through analyzing its role in cell migration and regulation of Notch signaling pathway in gastric cancer. The overexpression and silencing studies of gene were performed in MKN-45 and AGS gastric cancer cell lines using pCMV3-ORF-HA and RNAi-Ready pSIREN-RetroQ Retroviral vectors, respectively. The cell migration was assessed using wound healing and closure assays. The effect of EZH2 overexpression and silencing on the Notch signaling pathway was evaluated using real-time PCR. The EZH2 expression was directly correlated with the increased rate of cell migration. Furthermore, increased expression of the majority of the Notch signaling pathway genes including , , , , , , and in MKN-45 and AGS cells. EZH2, as an upstream regulator, enhances the cell migration capacity and modulate expression of Notch signaling pathway gene in gastric cancer. EZH2 may be considered as a proper target for the treatment of gastric cancer. - Source: PubMed
Publication date: 2024/08/08
Ghazvini HosseinaliForghanifard Mohammad MahdiZarrinpour VajihehMirkalantari Shiva - Hepatocellular carcinoma (HCC), the most prevalent form of primary liver cancer, is driven by cancer stem cells (CSCs) and an immunosuppressive tumor microenvironment, which may underlie the limited efficacy of immune checkpoint blockade therapy. Here, we report that HEY1 plays a crucial role in sustaining HCC stemness and undergoes polyubiquitylation during liver CSC differentiation. Mechanistically, USP28 interacts with HEY1 and deubiquitinates its lysine 87 residue, thereby stabilizing HEY1 and enhancing the stem-like properties of liver cancer cells. Moreover, IKKβ phosphorylates HEY1 at serine 40, facilitating its interaction with USP28. Loss of USP28 reduces PD-L1 expression, increases effector cytokine production, and suppresses tumor growth in mice. Notably, combining a USP28 inhibitor with anti-PD-1 immunotherapy results in enhanced tumor regression and significantly prolonged overall survival in mouse tumor models. Collectively, these findings identify USP28 as a potential biomarker for stratifying patients likely to benefit from anti-PD-1/PD-L1 therapies in HCC. Furthermore, we uncover a previously unrecognized IKKβ-USP28-HEY1 signaling axis that governs HEY1 stability and cancer stemness, offering new opportunities for synergistic therapeutic strategies in HCC. - Source: PubMed
Publication date: 2026/05/26
Shao NaZhang LinShen GufangLv YangfanFang TianshuCao YaZhang QiongyiXu FengLiu Chungang - Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common monogenic cerebral small-vessel disease caused by NOTCH3 mutations, yet its pathogenic mechanisms remain incompletely understood due to limited disease models. The NOTCH3 R544C mutation is a prevalent hotspot in East Asian populations, but patient-derived iPSC models are lacking. Here, we generated an iPSC line from peripheral blood mononuclear cells of a middle-aged CADASIL patient carrying a heterozygous NOTCH3 c.1630C > T (p.Arg544Cys, R544C) mutation using a Sendai virus (SeV)-based reprogramming approach. The iPSCs exhibited typical morphology, normal 46, XY karyotype, expressed pluripotency markers (OCT4, NANOG, TRA-1-60, SSEA-4), and cleared SeV vectors after passaging. They differentiated into derivatives of all three germ layers, and STR analysis confirmed donor identity. Functionally, CADASIL iPSCs showed abnormal accumulation of the NOTCH3 extracellular domain (NOTCH3ECD) with unchanged NOTCH3 full-length and intracellular domain levels, and upregulation of canonical downstream genes HEY1, NRARP, and HES1, indicating activation of the NOTCH3 signaling pathway. This study establishes and characterizes a NOTCH3 R544C patient-derived iPSC line, providing a valuable model for investigating CADASIL pathogenesis and potential therapeutic strategies, with novel insights into early NOTCH3ECD accumulation and pathway activation. - Source: PubMed
Publication date: 2026/05/24
Sun RuihuaZhao ZhenxiangChe NingningLiu NingJi XiaoyiLi AnqiWang FengyuShang JunkuiZhang Jiewen