|
Neuronal Ceroid-Lipofuscinoses
|
0.210 |
Biomarker
|
disease |
MGD |
ClC-3 chloride channels facilitate endosomal acidification and chloride accumulation.
|
15504734 |
2005 |
|
Neuronal Ceroid-Lipofuscinoses
|
0.210 |
Biomarker
|
disease |
MGD |
These results indicated that the neurodegeneration observed in the Clcn3-/- mice was caused by an abnormality in the machinery which degrades the cellular protein and was associated with the phenotype of neuronal ceroid lipofuscinosis (NCL).
|
12059962 |
2002 |
|
Neuronal Ceroid-Lipofuscinoses
|
0.210 |
Biomarker
|
disease |
BEFREE |
These results indicated that the neurodegeneration observed in the Clcn3-/- mice was caused by an abnormality in the machinery which degrades the cellular protein and was associated with the phenotype of neuronal ceroid lipofuscinosis (NCL).
|
12059962 |
2002 |
|
Late-Infantile Neuronal Ceroid Lipfuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
ClC-3 chloride channels facilitate endosomal acidification and chloride accumulation.
|
15504734 |
2005 |
|
Adult Neuronal Ceroid Lipofuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
ClC-3 chloride channels facilitate endosomal acidification and chloride accumulation.
|
15504734 |
2005 |
|
Juvenile Neuronal Ceroid Lipofuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
ClC-3 chloride channels facilitate endosomal acidification and chloride accumulation.
|
15504734 |
2005 |
|
Late-Infantile Neuronal Ceroid Lipfuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.
|
12059962 |
2002 |
|
Adult Neuronal Ceroid Lipofuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.
|
12059962 |
2002 |
|
Juvenile Neuronal Ceroid Lipofuscinosis
|
0.200 |
Biomarker
|
disease |
MGD |
CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.
|
12059962 |
2002 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Genome-Wide Association Study Detected Novel Susceptibility Genes for Schizophrenia and Shared Trans-Populations/Diseases Genetic Effect.
|
30285260 |
2019 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
BEFREE |
By integrating CRISPR-mediated gene editing, activation and repression technologies to study one putative SZ eQTL (FURIN rs4702) and four top-ranked SZ eQTL genes (FURIN, SNAP91, TSNARE1 and CLCN3), our platform resolves pre- and postsynaptic neuronal deficits, recapitulates genotype-dependent gene expression differences and identifies convergence downstream of SZ eQTL gene perturbations.
|
31548722 |
2019 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection.
|
29483656 |
2018 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Meta-analysis of GWAS of over 16,000 individuals with autism spectrum disorder highlights a novel locus at 10q24.32 and a significant overlap with schizophrenia.
|
28540026 |
2017 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association analysis identifies 30 new susceptibility loci for schizophrenia.
|
28991256 |
2017 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association study of schizophrenia in Ashkenazi Jews.
|
26198764 |
2015 |
|
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
GWASCAT |
Biological insights from 108 schizophrenia-associated genetic loci.
|
25056061 |
2014 |
|
Child Development Disorders, Pervasive
|
0.100 |
GeneticVariation
|
group |
GWASCAT |
Meta-analysis of GWAS of over 16,000 individuals with autism spectrum disorder highlights a novel locus at 10q24.32 and a significant overlap with schizophrenia.
|
28540026 |
2017 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
The expression level of ClC-3 was closely-related to the histological differentiation (p = 0.029), tumour staging (<i>p </i>= 0.016), tumour size (<i>p </i>= 0.039), vascular invasion (<i>p </i>= 0.045), interstitial infiltration depth (<i>p </i>= 0.012), lymphatic metastasis (<i>p </i>= 0.036), and HPV infection (<i>p </i>= 0.022).
|
30636929 |
2019 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
BACKGROUND Recently, ClC-3 chloride channel expression has been noted to be high in some tumors.
|
31281178 |
2019 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
Moreover, up-regulation of CIC-3 markedly correlated with tumor size and overall prognosis, suggesting that CIC-3 expression could predict both tumor size and overall prognosis in hepatocarcinoma.
|
30678806 |
2019 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
Chloride channel-3 (ClC-3) is over-expressed in a variety of cancers and involves multiple tumor biological events.
|
31606620 |
2019 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Chloride channel-3 (CLC-3) has been reported to promote the proliferation and invasion in various tumors, yet little is known about its role in gastric cancer.
|
29795988 |
2018 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
ClC-3 is a type of chloride channel that has multiple functions in tumorigenesis and tumor growth, and can be blocked by DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid).
|
29749557 |
2018 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Together, our data suggest that upregulation of ClC-3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.
|
29963105 |
2018 |
|
Tumor Cell Invasion
|
0.060 |
AlteredExpression
|
phenotype |
BEFREE |
The expression level of ClC-3 was closely-related to the histological differentiation (p = 0.029), tumour staging (<i>p </i>= 0.016), tumour size (<i>p </i>= 0.039), vascular invasion (<i>p </i>= 0.045), interstitial infiltration depth (<i>p </i>= 0.012), lymphatic metastasis (<i>p </i>= 0.036), and HPV infection (<i>p </i>= 0.022).
|
30636929 |
2019 |