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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 (show STAT3 ELISA Kits) 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 (show WNT3A ELISA Kits) proneurogenic effect occurring independently of the classical Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling cascade thus further deciphering crosstalk mechanisms of Wnt (show WNT2 ELISA Kits) and Notch (show NOTCH1 ELISA Kits) signaling pathways regulating cell fate
the downstream Notch (show NOTCH1 ELISA Kits) signalling effector HES5 directly represses transcription of the E3 ligase Fbw7beta.
Notch3 (show NOTCH3 ELISA Kits) 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 (show NOTCH1 ELISA Kits) 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 (show RRBP1 ELISA Kits) genes (pHes1 or pHes5) to drive expression of destabilized enhanced green fluorescent protein.
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 (show NOTCH1 ELISA Kits) 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 (show NOTCH1 ELISA Kits) signaling.
Simultaneous overexpression of Hes5 and Sox21 (show SOX21 ELISA Kits) reveals Hes5 as a downstream effector of Sox21 (show SOX21 ELISA Kits) in adult hippocampus neurogenesis.
This study suggested that Hes5 expression is serially activated first by Gcms and later by the canonical Notch (show NOTCH1 ELISA Kits) pathway
Hes1, Hes5 and Hey1 (show HEY1 ELISA Kits) cooperatively inhibit hair cell formation, and one allele of Hes1, Hes5 or Hey1 (show HEY1 ELISA Kits) is sufficient for supporting cell (show PTPRJ ELISA Kits) production probably by lateral inhibition in the sensory epithelium.
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