Precursor B-cell lymphoblastic leukemia
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
5-aza-2'-deoxycytidine treatment restored Hes5 expression and decreased promoter hypermethylation in most leukemia cell lines and primary B-ALL samples.
|
23637910 |
2013 |
Tumor Cell Invasion
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
HES5 promotes cell proliferation and invasion through activation of STAT3 and predicts poor survival in hepatocellular carcinoma.
|
26342546 |
2015 |
Liver carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
HES5 promotes cell proliferation and invasion through activation of STAT3 and predicts poor survival in hepatocellular carcinoma.
|
26342546 |
2015 |
nervous system disorder
|
0.300 |
Biomarker
|
group |
CTD_human |
A 3-dimensional human embryonic stem cell (hESC)-derived model to detect developmental neurotoxicity of nanoparticles.
|
23203475 |
2013 |
Mucoepidermoid Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Analyses of potential downstream targets of the fusion revealed differential expression of the cAMP/CREB (FLT1 and NR4A2) and Notch (HES1 and HES5) target genes in fusion-positive and fusion-negative MECs.
|
16444749 |
2006 |
Mucoepidermoid Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Analyses of the Notch target genes HES5 and MASH1 in MEC tumors with and without the WAMTP1-MAML2 fusion revealed upregulation of HES5 and downregulation of MASH1 in fusion positive MECs compared to normal salivary gland tissue and MECs lacking the fusion.
|
14720503 |
2004 |
Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Analyses of the Notch target genes HES5 and MASH1 in MEC tumors with and without the WAMTP1-MAML2 fusion revealed upregulation of HES5 and downregulation of MASH1 in fusion positive MECs compared to normal salivary gland tissue and MECs lacking the fusion.
|
14720503 |
2004 |
Carcinogenesis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Either Hes1 or Hes5 overactivation is likely to affect cell differentiation, thereby resulting in carcinogenesis.
|
21495212 |
2010 |
Marijuana Abuse
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Hairy and enhancer of split 1 (Hes1) and Hes5 are target genes for the mammalian Notch pathway, which are highly expressed in epithelia in the process of embryogenesis or in neural stem cells, inhibit cell differentiation via the Notch-Hes-Hash signaling, and promote the survival of stem cells.
|
21495212 |
2010 |
Neuroblastoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
However, in nonserotonergic cells that express 5-HT1A receptors (septal SN48, neuroblastoma SKN-SH, and neuroblastoma/glioma NG108-15 cells), Deaf-1 enhanced 5-HT1A promoter activity at the C(-1019)-allele but not the G-allele, whereas Hes5 repressed in all cell types.
|
16467535 |
2006 |
Central neuroblastoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
However, in nonserotonergic cells that express 5-HT1A receptors (septal SN48, neuroblastoma SKN-SH, and neuroblastoma/glioma NG108-15 cells), Deaf-1 enhanced 5-HT1A promoter activity at the C(-1019)-allele but not the G-allele, whereas Hes5 repressed in all cell types.
|
16467535 |
2006 |
Childhood Neuroblastoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
However, in nonserotonergic cells that express 5-HT1A receptors (septal SN48, neuroblastoma SKN-SH, and neuroblastoma/glioma NG108-15 cells), Deaf-1 enhanced 5-HT1A promoter activity at the C(-1019)-allele but not the G-allele, whereas Hes5 repressed in all cell types.
|
16467535 |
2006 |
Glioma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
However, in nonserotonergic cells that express 5-HT1A receptors (septal SN48, neuroblastoma SKN-SH, and neuroblastoma/glioma NG108-15 cells), Deaf-1 enhanced 5-HT1A promoter activity at the C(-1019)-allele but not the G-allele, whereas Hes5 repressed in all cell types.
|
16467535 |
2006 |
Cone-Rod Dystrophy 2
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In this study, we have demonstrated that spinal cord injury enhanced oligodendrocyte precursor cell number and decreased mRNA expression of transcriptional inhibitors (Id2, Id4, hes5).
|
30527678 |
2019 |
Lung Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
In this study, we show that NOTCH signaling, as measured by the gamma-secretase cleavage product N(IC)-1, is active in both normal human and lung tumor samples; however, downstream NOTCH readouts (i.e., HES-1 and HES-5) are elevated in lung tumors.
|
17804701 |
2007 |
Brain Neoplasms
|
0.300 |
Biomarker
|
group |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Malignant neoplasm of brain
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Benign neoplasm of brain, unspecified
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Brain Tumor, Primary
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Recurrent Brain Neoplasm
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Primary malignant neoplasm of brain
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Neoplasms, Intracranial
|
0.300 |
Biomarker
|
group |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Diabetic Retinopathy
|
0.010 |
Biomarker
|
disease |
BEFREE |
Main conclusions allow certifying that crucial pathways related to Wnt-MAPK signaling pathways or neuroinflammation are epigenetically controlled in the fibrotic disorders involved in retinal detachment, but results also reinforced the contribution of neurovascularization (ETS1, HES5, PRDM16) in diabetic retinopathy.
|
28924151 |
2017 |
Bulbo-Spinal Atrophy, X-Linked
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Moreover, Hes5 over-expression rescued the SBMA cells possibly by inducing Smad2 phosphorylation.
|
30940675 |
2019 |
Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Multiple myeloma cell growth relies on intrinsic aggressiveness, due to a high karyotypic instability, or on the support from bone marrow (BM) niche.We and other groups have provided evidences that Notch signaling is related to tumor cell growth, pharmacological resistance, localization/recirculation in the BM and bone disease.This study indicates that high gene expression levels of Notch signaling members (JAG1, NOTCH2, HES5 and HES6) correlate with malignant progression or high-risk disease, and Notch signaling may participate in myeloma progression by increasing the BM levels of interleukin-6 (IL-6), a major player in myeloma cell growth and survival.
|
27463014 |
2016 |