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 |
Neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
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 |
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 |
Hyperhomocysteinemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
These results suggest that HHcy-enhanced brain damage is associated with increased autophagy and neuronal apoptosis in Apo E<sup>-/-</sup> mice, in which downregulation of hes1 and hes5 is involved.
|
29171783 |
2017 |
Hyperhomocysteinemia
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
These findings confirm that hyperhomocysteinemia induces injury in olfactory bulb neurons by downregulating Hes1 and Hes5 expression.
|
29557377 |
2018 |
Central neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
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 |
Childhood Neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
Astrocytoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Using RT-PCR, we found that most human astrogliomas of different grades expressed moderate to high level of Notch receptors and ligands. mRNA of Hes5 but not Hes1, both of which are major downstream molecules of the Notch pathway, was also detected.
|
17849174 |
2008 |
Non-Small Cell Lung Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Taken together, out data have delineated that HES5 might contribute to the proliferation of NSCLC by STAT3 signaling.
|
27878283 |
2017 |
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 |
Endometriosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Notch signaling receptors NOTCH1 and NOTCH4, ligands JAGGED2 and DLL4, as well as direct target genes HES5 and HEY1 were decreased in the eutopic endometrium of women and baboons with endometriosis.
|
25546156 |
2015 |
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 |
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 |
Multiple Myeloma
|
0.010 |
Biomarker
|
disease |
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 |
Degenerative polyarthritis
|
0.010 |
AlteredExpression
|
disease |
LHGDN |
Notch1, Jagged1, and HES5 are abundantly expressed in osteoarthritis.
|
18354251 |
2008 |
Degenerative polyarthritis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Notch1, Jagged1, and HES5 are abundantly expressed in osteoarthritis.
|
18354251 |
2008 |
Impaired cognition
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We found that Rip ameliorated cognitive deficits and restored cell proliferation in MK801-treated mice in a manner associated with the up-regulation of Notch signaling molecules, including Notch1, Hes1, and Hes5.
|
29037878 |
2017 |