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
- 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 - Craniofacial malformations such as orofacial clefts affect ~1 in 700 births; 40-60% lack clear genetic etiology, and many exhibit asymmetry and variable expressivity unexplained by classical Sonic Hedgehog (SHH) morphogen gradient models. We investigated whether integrated molecular modules linking morphogen signaling with metabolic stress responses may better account for craniofacial developmental outcomes. - Source: PubMed
Publication date: 2026/04/08
Gramatikoff KosiStoykov MiroslavHörmann KarlMilkov Mario - Decidualization is essential for embryo implantation and maintenance of pregnancy, during which quiescent endometrial stromal fibroblasts proliferate and differentiate into decidual stromal cells. Emerging evidence indicates that epigenetic regulators, including histone modifications, play critical roles in uterine receptivity, implantation, and stromal cell decidualization. Our previous study demonstrated that loss of histone deacetylase 3 (HDAC3) impairs endometrial receptivity and decidualization, resulting in female infertility. However, the genome-wide transcriptomic alterations responsible for defective decidualization in loss of HDAC3 remain unclear. In this study, uterine-specific Hdac3 knockout (PgrHdac3; Hdac3) mice exhibited decidual defects following 3 days of artificial decidualization. RNA sequencing analysis of uteri from control and Hdac3 mice revealed widespread dysregulation of genes and pathways associated with decidualization. Pathway analysis identified significant alterations in RHOA, AMPK-NOTCH1-HEY1, and oxidative stress-induced senescence signaling, implicating dysregulation of cytoskeletal remodeling, cellular metabolism, and oxidative stress responses in the HDAC3-mediated decidual response. Notably, expression of Limk1, Prkag1, and Cbx2 for key regulators of these pathways was significantly reduced in Hdac3 mice compared with controls. These findings demonstrate that HDAC3 is a key regulator of the transcriptional and signaling networks required for successful decidualization. Collectively, our study provides a comprehensive transcriptomic profile of HDAC3-deficient uteri and uncovers key molecular mechanisms underlying impaired decidualization, thereby advancing our understanding of uterine function and pregnancy establishment. - Source: PubMed
Nguyen Loan Thi KimTran Dinh NamNahar ShamsunKim Tae HoonJeong Jae-WookYoo Jung-Yoon