|
Cognition Disorders
|
0.010 |
AlteredExpression
|
group |
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 |
|
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 |
|
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 |
|
Bone Diseases
|
0.010 |
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 |
|
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 |
|
Colonic Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
The mRNA levels of cyclin B1 and Hes5 were downregulated, but p27, ATOH1 and MUC2 were upregulated in the colon tumors from AIB1-deficient mice compared with those from wild-type mice.
|
25263446 |
2015 |
|
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 |
|
Neoplasm Metastasis
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
The data showed that high expression of HES5 was tightly associated with histological grade (P<0.01) and metastasis (P<0.01), and positively correlated with proliferation marker Ki-67 (P<0.01).
|
26342546 |
2015 |
|
Malignant neoplasm of prostate
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Treatment of prostate cancer cells with the demethylating agent 5-aza-2'-deoxycytidine increased HES5 expression and downregulated its transcriptional target HES6, consistent with functional silencing of the HES5 gene in prostate cancer.
|
25560400 |
2015 |
|
Prostate carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Treatment of prostate cancer cells with the demethylating agent 5-aza-2'-deoxycytidine increased HES5 expression and downregulated its transcriptional target HES6, consistent with functional silencing of the HES5 gene in prostate cancer.
|
25560400 |
2015 |
|
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 |
|
Hepatocarcinogenesis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Therefore, we have characterized HES5 and investigated its role during hepatocarcinogenesis.
|
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 |
|
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 |
|
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 |
|
Carcinogenesis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Either Hes1 or Hes5 overactivation is likely to affect cell differentiation, thereby resulting in carcinogenesis.
|
21495212 |
2010 |
|
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 |
|
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 |
|
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 |
|
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 |