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HEY1 is negatively regulated by NFI family proteins and is associated with increased proliferation, decreased migration, and increased stem cell properties in glioblastoma cells.
Simulation of HEY1 Ser-68 phosphorylation prevents its interaction with p53, RPL11 and MDM2 and abolishes HEY1 migration to nucleolar caps upon ribosomal stress. Our findings uncover a novel mechanism for cross-talk between Notch signalling and nucleolar stress
Pancreatic involvement occurs in mesenchymal chondrosarcoma harboring the HEY1-NCOA2 gene fusion.
HGF-induced FRA1 activation is associated with the fibrosis-dependent development of Hepatocellular Carcinoma.
Expression of Hey1 induces translocation of FBXO45 into the nucleus.
Overexpression of HEY1 and HEY2 in esophageal squamous cell carcinoma (ESCC) is correlated to different indices of poor prognosis, and it is extrapolated that such overexpression is important in progression and development of ESCC tumorigenesis.
bone morphogenic proteins within the serum of cell culture medium are potent inducers of endothelial Hey1 and Hey2 gene expression within the first few hours after medium change
PML degradation mechanism through Notch/Hey1-induced repression of the PML deubiquitinase USP11 involved in brain tumour pathogenesis
MMP9 was a downstream effector of HEY1 that promotes the invasion of osteosarcoma cells. Knockdown of HEY1 decreased the expression of MMP9.
In prostate tumors, the overexpression of PTOV1 was associated with decreased expression of HEY1 and HES1, and this correlation was significant in metastatic lesions.
a new HRD1-associated membrane protein named HERP2, which is homologous to the previously identified HRD1 partner HERP1. Despite sequence homology, HERP2 is constitutively expressed in cells, whereas HERP1 is highly induced by ER stress.
The identification of HEY1-NCOA2 can be used as an auxiliary diagnostic tool to differentiate meningeal hemangiopericytoma from mesenchymal chondrosarcoma.
HEY1 was overexpressed in colorectal cancer, and correlated with perineural and vascular invasion and lymph node metastasis as well as poorer prognosis.
Data show that the periodontal ligament-derived mesenchymal stem cells (hPDLSCs) on a Jagged-1-modified surface had increased expression of Notch signaling target genes, Hes-1 and Hey-1, suggesting the involvement of Notch signaling in hPDLSCs.
The current study adds further support for the use of HEY1-NCOA2 fusion as a valid diagnostic marker for Mesenchymal chondrosarcoma
These data further support a central role for Notch signalling in pancreatic cancer and suggest that nuclear expression of Notch3 and its target gene, HEY-1, merit validation in biomarker panels for diagnosis, prognosis and treatment efficacy.
Data suggest that HEs-1/Hey-1 transcriptional modulation of insulin degrading enzyme may impact amyloid beta metabolism by providing a functional link between Notch signaling and the amyloidogenic pathway.
The novel HEY1-NCOA2 fusion appears to be the defining and diagnostic gene fusion in mesenchymal chondrosarcomas
In this study, we analyzed the effects of HESR1, -2, and -3 on DAT1 expression in human neuroblastoma SH-SY5Y cells
In transgenic mice Hey1 overexpression results in distinct progressive osteopenia and inhibition of osteoblasts ex vivo, an effect apparently dominant to a mild inhibition of osteoclasts.
Data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation.
stable Hey1overexpressing cells expressed higher levels of dentin sialophosphoprotein (DSPP) and exhibited higher mineralization capabilities following stimulation by differentiation medium. Furthermore, RNA interferencemediated knockdown of Hey1 downregulated the expression levels of DSPP in OLCs stimulated by differentiation medium.
A Jagged1-Hey1 signal might mediate the impairment of angiogenesis induced by Ang II during cardiac hypertrophy.
Cyclic stretch enhanced the BMP-2induced osteoblastic differentiation through the inhibition of Hey1.
Hes/Hey signaling at the Atoh1 promoter has a role in selection of cell fate in the organ of Corti
These in vitro and in vivo data support an anti-adipogenic role of COUP-TFII via downregulating the Notch signaling target gene Hey1.
Hey proteins mechanistically repress target genes via histone deacetylase recruitment and histone deacetylation.
Hey1 and Hey2 in endothelial cells play important roles in vascular development.
findings indicate that Hey1 and Hey2 control the spatial and temporal pattern of auditory HC differentiation.
This study demonistrated that demonstrates that the lack of Hesr1 leads to an alteration in sensitivity to dopamine accompanied by enhanced prepulse inhibition.
A muscle-specific regulatory element of p57(kip2) directly activated by muscle regulatory factors in myoblasts but repressed by the Notch targets Hes1/Hey1 in progenitor cells, is identified.
Notch-RBPjk signaling functions in part through Hey1-mediated inhibition of NFATc1 to suppress osteoblastogenesis, contributing to bone homeostasis in vivo
These results indicate that Hesr1 and Hesr3 are essential for the generation of adult satellite cells and for the maintenance of skeletal muscle homeostasis.
Hes1, Hes5 and Hey1 cooperatively inhibit hair cell formation, and one allele of Hes1, Hes5 or Hey1 is sufficient for supporting cell production probably by lateral inhibition in the sensory epithelium.
Hey1 inhibits myogenesis by associating with and repressing expression of key myogenic targets.
results indicate that hairy enhancer of split related with YRPW motif 1 and 2 negatively regulate neuronal basic helix- loop-helix genes, promote maintenance of neural precursor cells, and increase late-born cell types in the developing brain
Loss of Hey1/2 leads to elevated GATA4/6 and ANF mRNA levels in embryoid bodies, while forced expression of Hey factors strongly represses expression of the GATA4 and GATA6 promoter.
Hesr1 and Hesr2 may prevent cells from expressing the AV canal-specific genes that lead to the precise formation of the AV boundary
We report that combined inactivation of Hey1 and HeyL, two primary target genes of Notch, causes severe heart malformations, including membranous ventricular septal defects and dysplastic atrioventricular and pulmonary valves.
Hesr1 and Hesr2 are the downstream mediators of the prosensory function of Notch in early cochlear development.
abrogation of Hey1 function in adult pallial Neural stem cells in vivo, including quiescent Neural stem cells, leads to their differentiation without affecting their proliferation state.
Expression of seven hairy/E(spl) (her) genes is reported in three neurogenic areas of the adult zebrafish brain (telencephalon, hypothalamus, and midbrain) in relation to radial glia, proliferation, and neurogenesis.
hey1 represents a target of Delta-Notch signaling dynamically expressed during somite formation in zebrafish
Results suggest that the negative regulatory loops between BMP/Tbx2 and Gremlin or Hey1 are responsible for defining the territory of the pronephric nephron.
HRT1 encodes a bhlh domain motif, a transcription repressor, which acts as an extended dimerization domain that contributes to the selection of partners.
XHRT1 plays an important role in glomerular development and early proximodistal patterning. [Xenopus HRT1]
This gene encodes a nuclear protein belonging to the hairy and enhancer of split-related (HESR) family of basic helix-loop-helix (bHLH)-type transcriptional repressors. Expression of this gene is induced by the Notch and c-Jun signal transduction pathways. Two similar and redundant genes in mouse are required for embryonic cardiovascular development, and are also implicated in neurogenesis and somitogenesis. Alternative splicing results in multiple transcript variants.
HES-related repressor protein 1
, HES-related repressor protein 2
, basic helix-loop-helix protein OAF1
, cardiovascular helix-loop-helix factor 2
, class B basic helix-loop-helix protein 31
, hairy and enhancer of split-related protein 1
, hairy-related transcription factor 1
, hairy/enhancer-of-split related with YRPW motif protein 1
, bHLH protein Hesr-1/Hey1
, cardiovascular basic helix-loop-helix factor 2
, Hairy/E(spl)-related with YRPW motif 1
, basic helix-loop-helix transcription factor
, protein xbc8