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This protein belongs to the basic helix-loop-helix family of transcription factors. De plus, nous expédions HES1 Anticorps (165) et HES1 Kits (16) et beaucoup plus de produits pour cette protéine.
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HES1 is mono-ubiquitinated in a Fanconi anemia (Montrer PALB2 Protéines) core complex-dependent manner.
Hes-1 knockdown promotes osteopontin (Montrer SPP1 Protéines) expression in HUVECs and enhances OPN (Montrer SPP1 Protéines)-induced angiogenesis.
Our results suggest that KN promotes goblet cell differentiation by regulating Wnt (Montrer WNT2 Protéines), Notch (Montrer NOTCH1 Protéines), and AhR (Montrer AHR Protéines) signals and expression of Hes1 and Hath1 (Montrer ATOH1 Protéines).
In the present study, the authors reported the first observation of Hes1 oscillatory expression in human neural progenitor /stem cells, with an approximately 1.5 hour periodicity and a Hes1 protein half-life of about 17 (17.6 +/- 0.2) minutes. Human cytomegalovirus infection disrupts the Hes1 rhythm and down-regulates its expression.
A three-molecule score based on the expression of Notch (Montrer NOTCH1 Protéines) pathway molecules: Jagged1 (Montrer JAG1 Protéines), intracellular Notch1 (Montrer NOTCH1 Protéines) (ICN1) and Hes1 (JIH score) to assess prognostic value in non-metastasis clear cell renal cell carcinoma (Montrer MOK Protéines) (ccRCC).
we demonstrate for the first time an essential role of HPV oncoprotein E6 that selectively overexpresses in CaCxSLCs and participates in maintenance of stem cell phenotype and stemness through upregulation of Hes1 while preponderance of E7 leads to differentiation.
IE1 is involved in Hes1 degradation by assembling a ubiquitination complex and promoting Hes1 ubiquitination as a potential E3 ubiquitin ligase (Montrer MUL1 Protéines), followed by proteasomal degradation of Hes1.
Notch (Montrer NOTCH1 Protéines) signaling and Id2/3 regulate neurogenesis in a complementary manner and ID factors can induce neural stem cell maintenance and quiescence in the absence of Notch (Montrer NOTCH1 Protéines).
The phenotype was rescued by ectopic expression of miRNA182-5p in Delta182 cells. A bioinformatic analysis and Hes1 modulation data suggested that Hes1 could be a putative target of miRNA182-5p. A reciprocal relationship between miRNA182-5p and Hes1 was seen in the context of TK inhibition
These results suggest that HES1 promotes extracellular matrix protein expression and inhibits proliferative and migratory functions in the trabecular meshwork cells under oxidative stress, thereby providing a novel pathogenic mechanism underlying and a potential therapeutic target to primary open-angle glaucoma
the results raise the possibility that HES1 or other genes that affect HES1 expression could be involved in the etiology of Ectopic pancreas .
These results suggest that hyperhomocysteinemia-enhanced brain damage is associated with increased autophagy and neuronal apoptosis in Apo E (Montrer APOE Protéines)(-/-) mice, in which downregulation of hes1 and hes5 (Montrer HES5 Protéines) is involved.
Although Hes5 (Montrer HES5 Protéines)-GFP and Hes1 are coexpressed in particular developmental contexts, we also noted cohorts of lens or retinal cells expressing just one factor. The dynamic Hes5 (Montrer HES5 Protéines)-GFP expression pattern, coupled with its derepressed expression in Hes1 mutants, suggests that this transgene contains the relevant cis (Montrer CISH Protéines)-regulatory elements that regulate endogenous Hes5 (Montrer HES5 Protéines) in the mouse lens and retina.
there is a link between Dmrta2 (Montrer DMRTA2 Protéines) modulation of Hes1 expression and the maintenance of neural progenitor cells during cortical development
Hes-1 expression is maintained in neural progenitor territory throughout mouse neocortical development, a simple shift from Notch (Montrer NOTCH1 Protéines)-independent to -dependent state makes it pleiotropic as the former maintains the neural stem cells in a non-dividing/slow-dividing state, whereas the latter is very much required for maintenance and proliferation of radial glial cells.
inhibition of PTEN by Notch1 (Montrer NOTCH1 Protéines)/Hes1 in response to high glucose concentration inhibits autophagy, which is associated with the progression of fibrosis in diabetic nephropathy
this paper shows the critical role of the Notch1 (Montrer NOTCH1 Protéines)-Hes1 signaling cascade in the regulation of innate immunity in acetaminophen-triggered liver inflammation
results suggest that SCF (Montrer KITLG Protéines)(FBXL14 (Montrer FBXL14 Protéines)) promotes neuronal differentiation by targeting HES1 for ubiquitin-dependent proteolysis and that the C-terminal WRPW motif in HES1 is required for this process
that HIF-1alpha (Montrer HIF1A Protéines) but not HIF-2alpha (Montrer EPAS1 Protéines) is able to interact with either GA-binding protein alpha or GA-binding protein beta1
study identified nucleolar complex protein 3 homolog(FAD24 (Montrer NOC3L Protéines)) as a novel downstream target of transcription factor HES1 during adipogenesis
This protein belongs to the basic helix-loop-helix family of transcription factors. It is a transcriptional repressor of genes that require a bHLH protein for their transcription. The protein has a particular type of basic domain that contains a helix interrupting protein that binds to the N-box rather than the canonical E-box.
class B basic helix-loop-helix protein 39
, hairy homolog
, hairy-like protein
, transcription factor HES-1
, Hairy and enhancer of split 1-A
, Protein hairy-1
, transcription factor HES-1-A
, hairy and enhancer of split 1
, LOW QUALITY PROTEIN: transcription factor HES-1