HEY1
- Known as:
- HEY1
- Catalog number:
- NB100-75431
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- HEY1
Related genes to: HEY1
- 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
Related articles to: HEY1
- 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 - Hepatocellular carcinoma (LIHC) is the most common primary liver cancer, with high recurrence and metastasis rates, and its molecular mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/04/02
Hong LingjuKe ShaoyingLin ShaozeWu GongleWang Congren - A 50-year-old man presented with lower abdominal pain. Imaging revealed a pelvic mass extending from the right internal iliac vein into the inferior vena cava. Fluorodeoxyglucose-positron emission tomography revealed intense uptake (SUVmax 13.97) without metastasis. Biopsy revealed a biphasic tumor with cartilaginous matrix and staghorn vasculature. Immunohistochemistry indicated positive for SMA, desmin, MyoD1, and NKX3.1. Moreover, genomic analysis identified a HEY1::NCOA2 fusion, confirming mesenchymal chondrosarcoma (MCS). Given the extent of the tumor, chemoradiotherapy was initiated. MCS is a rare, high-grade sarcoma with limited treatment options. Targeted therapies against HEY1::NCOA2-associated pathways are promising and are currently under investigation. - Source: PubMed
Publication date: 2026/03/24
Ichikawa JiroOnohara KojiroInoue TomohiroWako MasanoriKawasaki Tomonori - Notch receptor activation requires γ-secretase-mediated release of Notch intracellular domain 1 (NICD1) to regulate gene transcription. Here, we identify the proton-driven solute carrier 11a2 (Slc11a2) or divalent metal transport protein Dmt1 as an inhibitor of Notch signaling via regulating iron homeostasis and lysosomal integrity. Dmt1 loss reduces ferritin levels and increases labile Fe, causing elevated reactive oxygen species (ROS) and lipid peroxidation. These changes compromise lysosomal function and impair degradation of S3-Val1744 cleaved NICD1, resulting in its accumulation. Dmt1 has isoforms with or without an iron-responsive element (IRE): Re-expressing Dmt1 + IRE robustly increases ferritin heavy-chain (FTH), whereas Dmt1-IRE moderately elevates FTH and ferritin light-chain (FTL), with co-expression further enhancing FTL levels. Restoration of Dmt1 expression rescues ferritin levels, lysosomal activity, and NICD1 degradation while reducing oxidative stress and lipid peroxidation. Notably, Dmt1 deficiency decreases NICD1 binding to RBP-Jκ/CSL and its recruitment to Notch target gene promoters Hes1 and Hey1. Collectively, our findings demonstrate that Dmt1 regulates lysosomal function through iron homeostasis and that lysosomal dysfunction from Dmt1 loss impairs NICD1 degradation and disrupts Notch signaling, linking cellular iron metabolism and Notch pathway activity. - Source: PubMed
Publication date: 2026/03/30
Zhang RuiAhmadian SomaiehPiepers JolandaBock FlorianKeulers TomVooijs Marc A