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抗Human HES5 抗体:
抗Mouse (Murine) HES5 抗体:
抗Rat (Rattus) HES5 抗体:
Over-expression of her12, her15 or her7 disrupts cyclic gene expression and somite border formation, and structure function analysis of Her7 indicates that DNA binding, but not Groucho-recruitment seems to be important in this process.
HES5 might contribute to the proliferation of non-small cell lung cancer by STAT3 signaling.
that suppression of the HES5 leading to inhibition of proliferation may be one of the mechanisms against Hepatocellular carcinoma
HES5 silencing is an early and recurrent change in prostate tumourigenesis
these data identify HES5 as a key mediator of the Wnt-3a proneurogenic effect occurring independently of the classical Wnt/beta-catenin signaling cascade thus further deciphering crosstalk mechanisms of Wnt and Notch signaling pathways regulating cell fate
the downstream Notch signalling effector HES5 directly represses transcription of the E3 ligase Fbw7beta.
Notch3 and Hes5 are hypermethylated in human B cell acute lymphoblastic leukemia (ALL).
Hes5 overactivation is associated with cell differentiation, thereby resulting in uterine carcinogenesis.
In this study, HES 5 transcription factor was detected in the lining epithelium of human periapical cysts with limited inflammation, showing Notch pathway activation in those cells.
The expression of HES5 in adenocarcinoma was significantly higher than those in adenoma and normal control
For marking and purifying neural stem cells to ascertain whether differences exist, we generated transgenic mice using promoters from Hes genes (pHes1 or pHes5) to drive expression of destabilized enhanced green fluorescent protein.
Notch protein binding to Hes5-GFP is extinguished fast and recovered slowly, whereas Hes1-GFP is inhibited late and recovered quickly
The HLH gene HES5 on the other hand was only detected in chondrocytes.
Human HES5 gene is coupled to the Notch receptor family and expression of Notch markers (including HES5) decreases during cartilage differentiation.
expression significantly higher in squamous cervical carcinoma than in CIN as well as higher in CIN than normal cervical epithelia
Data show that HES5 are abundantly expressed in osteoarthritis.
regulates brain development process.[review]
These results suggest that hyperhomocysteinemia-enhanced brain damage is associated with increased autophagy and neuronal apoptosis in Apo E(-/-) mice, in which downregulation of hes1 and hes5 is involved.
Although Hes5-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-GFP expression pattern, coupled with its derepressed expression in Hes1 mutants, suggests that this transgene contains the relevant cis-regulatory elements that regulate endogenous Hes5 in the mouse lens and retina.
Hes5 is expressed in the nascent mesoderm of gastrulating mouse embryos. Hes5 knockdown enhances primitive erythropoiesis in mouse embryonic stem cells. A stage-specific pulse of Hes5 instructs preferential cardiac fate in mouse embryonic stem cells.
Sox2 activity is crucial for the induction of the neural progenitor gene Hes5 and for subsequent differentiation of the neuronal lineage.
Hes5 regulates the transition timing between phases for specification of neocortical neurons and between neurogenesis and gliogenesis.
the RBPjkappa-dependent Notch targets HES1 and HES5 suppress chondrogenesis and promote the onset of chondrocyte hypertrophy.
This study demonstrated that Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development.
delivery of siRNA to Hes1 and Hes5 using a transfection reagent or siRNA to Hes1 encapsulated within nanoparticles increased hair cell numbers in non-toxin treated organotypic cultures of cochleae and maculae
The transcription and expression patterns of Notch pathway components (Notch 1-3, Delta1 and 4, Jagged1) and effectors (Hes1, Hes2, Hes5 and Nrarp) were evaluated in the mouse testis
Hes1 and Hes5 regulate vascular remodeling and arterial fate specification of endothelial cells in the development of the brain; they are critical transducers of Notch signals in brain vascular development.
Data demonstrate that Hes5 levels in the utricle decreased after the application of siRNA and that the number of hair cells in these utricles was significantly larger than following control treatment.
Epigenetic silencing of Hes5 leads to neuronal differentiation despite active Notch signaling.
Simultaneous overexpression of Hes5 and Sox21 reveals Hes5 as a downstream effector of Sox21 in adult hippocampus neurogenesis.
This study suggested that Hes5 expression is serially activated first by Gcms and later by the canonical Notch pathway
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.
ZFP423 coordinates Notch1 and bone morphogenetic protein signaling, selectively up-regulating Hes5 gene expression.
Atoh1 up-regulation may either be a result of Hes5 down-regulation or mediated by another signaling pathway during hair cell regeneration in the mouse utricle.
Lack of altered phenotype in the conditional HES1;HES5 double mutant mice can be explained by the HES1 and HES5 genes not being involved in cartilage and endochondral bone development or by redundancy between the genes of the family of HES genes.
Fezf1 and Fezf2 control differentiation of neural stem cells by repressing Hes5 and, in turn, by derepressing neurogenin 2 in the forebrain.
This gene encodes a member of a family of basic helix-loop-helix transcriptional repressors. The protein product of this gene, which is activated downstream of the Notch pathway, regulates cell differentiation in multiple tissues. Disruptions in the normal expression of this gene have been associated with developmental diseases and cancer.
hairy and enhancer of split 5
, transcription factor HES-5
, Transcription factor HES-5
, class B basic helix-loop-helix protein 38