抗Human HEY2 抗体:
抗Mouse (Murine) HEY2 抗体:
抗Rat (Rattus) HEY2 抗体:
Cow (Bovine) Polyclonal HEY2 Primary Antibody for ELISA - ABIN4317227
Tang, Urs, Liaw: Hairy-related transcription factors inhibit Notch-induced smooth muscle alpha-actin expression by interfering with Notch intracellular domain/CBF-1 complex interaction with the CBF-1-binding site. in Circulation research 2008
we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in non-small cell lung cancer by competitively binding miR-448.
We also highlighted that Hey2 is involved in radiation-induced EndoMT and that Hey2 invalidation reduces EndoMT and tissue damage.
The findings identify HEY2 as a novel component of the NKX2-5 cardiac transcriptional network.
HEY2 as a promising biomarker for unfavorable outcomes and a novel therapeutic target for the clinical management of HCC
Genetic variation of HEY2 is associated with Brugada syndrome through alteration of ion channel expression in the cardiac ventricular wall.
Individuals with HEY2 duplications should be screened for congenital heart defects.
HEY2 CC genotype may be a favorable prognostic marker for BrS, protectively acting to prevent ventricular fibrillation presumably by regulating the repolarization current.
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
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.
Data indicate that culture abrogated differential gene expression in part due to gradual loss of canonical Notch activity and HEY2 expression.
Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death
Hey2 and COUP-TFII have an important role in arteriovenous differentiation of human endothelial cells.
Report down-regulation of Notch signaling components NOTCH3 and HEY2 in abdominal aortic aneurysms.
Through activating the Dll4-Notch-Hey2 signaling pathway, HGF indirectly promotes the proliferation and migration ability of cells, so that offspring artery branches are formed.
In this study, we analyzed the effects of HESR1, -2, and -3 on DAT1 expression in human neuroblastoma SH-SY5Y cells
These results indicate that the molecular association between HES1-, HEY2- and SIRT1-related proteins is conserved among metazoans, from Drosophila to human, and suggest that the Sir2-bHLH interaction also plays important roles in human cells.
To clarify the role of HEY2 in human CHD and AGS, we screened by direct sequencing 23 children with CHD and 38 patients diagnosed with AGS. Mutation of HEY2 is not a major contributing factor.
HERP1 may play a role in promoting the phenotypic modulation of vascular smooth muscle cells during vascular injury and atherosclerotic process by interfering with SRF binding to CArG-box
CHF1/Hey2 may affect smooth-muscle cell phenotype through an important transcriptional mechanism
Authors found that Hey2 is expressed in the endocardial cells of the atrioventricular canal and the outflow tract, as well as at the base of trabeculae, in addition to the reported expression in the ventricular compact myocardium.
miR98 reduced the production of Abeta and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in Alzheimer's disease mice.
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.
Hey proteins mechanistically repress target genes via histone deacetylase recruitment and histone deacetylation.
Results suggest that bone morphogenetic protein signaling plays pivotal roles in retinal progenitor cell differentiation into late differentiating retinal cell types and in Muller glia maturation; these effects were mediated, at least in part, by Hey2
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.
CHF1/Hey2 may contribute to Brugada syndrome.
Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death.
Data indicate that Hairy and Enhancer of Split-related with YRPW motif (HEY)2 decreases skeletal mass and regulates bone remodeling in male mice.
Data indicate that Notch1 and Notch2 are expressed and localized in the nuclei of the label-retaining cells (LRCs), and the expression of Notch-inducible genes, Hes1 and Hey2, was elevated in LRCs.
Survivor mice lacking the Hesr2 gene exhibit fibrosis in the aortic valve and ventricle in adulthood, thus suggesting that Hesr2 plays an important role in maintaining the homeostasis of the aortic valve and ventricle.
Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6.
These findings support the hypothesis that CHF1/Hey2 is an important regulator of MMP10 expression.
Hey2 regulates the later steps of coronary vascular development in both a myocardial-dependent, non-cell autonomous fashion and likely a vascular cell-specific effect as well.
CHF1/Hey2 expression levels influence hypertrophy and the progression to heart failure in response to pressure overload through modulation of apoptosis and GATA4 activity.
Data demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy through suppression of apoptosis and regulation of multiple transcriptional pathways.
Hey2 loss does not affect aortic development, but it instead leads to a massive postnatal cardiac hypertrophy with high lethality during the first 10 days of life.
Homozygotes for the Hey2 mutant allele display a spectrum of cardiac malformations including ventricular septal defects, tetralogy of Fallot, and tricuspid atresia.
These data suggest a previously unappreciated role for Hey2 in controlling the proliferative capacity of cardiac progenitors.
essential role for Hey2 upstream of Notch in hematopoietic stem cell formation
Forms a complex with Gata5 through the carboxyl region and can repress Gata5-mediated transcription.
The snrk-1 gene acts downstream or parallel to notch and upstream of gridlock during artery-vein specification
This gene encodes a member of the hairy and enhancer of split-related (HESR) family of basic helix-loop-helix (bHLH)-type transcription factors. The encoded protein forms homo- or hetero-dimers that localize to the nucleus and interact with a histone deacetylase complex to repress transcription. Expression of this gene is induced by the Notch signal transduction pathway. Two similar and redundant genes in mouse are required for embryonic cardiovascular development, and are also implicated in neurogenesis and somitogenesis. Alternatively spliced transcript variants have been found, but their biological validity has not been determined.
hairy/enhancer-of-split related with YRPW motif protein 2
, HES-related repressor protein 1
, HES-related repressor protein 2
, cardiovascular basic helix-loop-helix factor 1
, cardiovascular helix-loop-helix factor 1
, class B basic helix-loop-helix protein 32
, hairy and enhancer of split-related protein 2
, hairy-related transcription factor 2
, protein gridlock homolog
, Hairy-E(spl)-related with YRPW motif 2
, hairy and enhancer of split related 2
, protein gridlock