|
Focal glomerulosclerosis
|
0.310 |
AlteredExpression
|
disease |
BEFREE |
Consistent with a role for Arhgap24 in normal podocyte functioning in vivo, sequencing of the ARHGAP24 gene in patients with FSGS identified a mutation that impaired its Rac1-GAP activity and was associated with disease in a family with FSGS.
|
21911940 |
2011 |
|
Focal glomerulosclerosis
|
0.310 |
Biomarker
|
disease |
GENOMICS_ENGLAND |
Consistent with a role for Arhgap24 in normal podocyte functioning in vivo, sequencing of the ARHGAP24 gene in patients with FSGS identified a mutation that impaired its Rac1-GAP activity and was associated with disease in a family with FSGS.
|
21911940 |
2011 |
|
NEPHROTIC SYNDROME, STEROID-RESISTANT, AUTOSOMAL RECESSIVE
|
0.300 |
GermlineCausalMutation
|
disease |
ORPHANET |
Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
|
21911940 |
2011 |
|
Focal Segmental Glomerulosclerosis, Not Otherwise Specified
|
0.300 |
Biomarker
|
disease |
GENOMICS_ENGLAND |
Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
|
21911940 |
2011 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Taken together, the present study suggests that AGAP1 may regulate subcellular localization of FilGAP and control cell migration and invasion through interaction with FilGAP.
|
31785816 |
2020 |
|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Malignant neoplasm of breast
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
There was no association between G4A p73 polymorphism and the risk of breast cancer in a northeastern Iranian population.
|
31850263 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, p73 participates in the control of angiogenesis in development and cancer.
|
31582429 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family.
|
31090271 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The transcription factor p73 synthesizes a large number of isoforms and presents high structural and functional homology with p53, a well-known tumor suppressor and a famous "Holy Grail" of anticancer targeting. p73 has attracted increasing attention mainly because (a) unlike p53, p73 is rarely mutated in cancer, (b) some p73 isoforms can inhibit all hallmarks of cancer, and (c) it has the ability to mimic oncosuppressive functions of p53, even in p53-mutated cells.
|
30635889 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We demonstrate that melanomas with high levels of DNp73, a cancer-specific variant of the p53 family member p73 and driver of melanoma progression show, in contrast to their less-aggressive low-DNp73 counterparts, hypopigmentation in vivo.
|
30445206 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, we checked the expression levels of this p73 variant in the tumor and normal tissue of 26 patients with colon cancer.
|
31025168 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family.
|
31090271 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The transcription factor p73 synthesizes a large number of isoforms and presents high structural and functional homology with p53, a well-known tumor suppressor and a famous "Holy Grail" of anticancer targeting. p73 has attracted increasing attention mainly because (a) unlike p53, p73 is rarely mutated in cancer, (b) some p73 isoforms can inhibit all hallmarks of cancer, and (c) it has the ability to mimic oncosuppressive functions of p53, even in p53-mutated cells.
|
30635889 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The high expression of p73 in the peripheral blood of children with WT was positively correlated with the clinical stage of the tumor, and was closely related with the low survival rate of patients.
|
31186762 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Ectopic p73 overexpression largely mimics p53 activities as a tumor suppressor and activates the transcription of p53-responsive genes and as a result induce apoptosis.
|
31850263 |
2019 |
|
Malignant neoplasm of lung
|
0.100 |
Biomarker
|
disease |
BEFREE |
CONCLUSIONS Our findings indicate that ARHGAP24 silencing promotes lung cancer cell migration and invasion through activating β-catenin signaling.
|
30599132 |
2019 |
|
Electrocardiogram: P-R interval
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Genetic analyses of diverse populations improves discovery for complex traits.
|
31217584 |
2019 |
|
Electrocardiogram: P-R interval
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Genome-wide association meta-analysis of 30,000 samples identifies seven novel loci for quantitative ECG traits.
|
30679814 |
2019 |
|
Breast Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
There was no association between G4A p73 polymorphism and the risk of breast cancer in a northeastern Iranian population.
|
31850263 |
2019 |
|
Carcinoma of lung
|
0.100 |
Biomarker
|
disease |
BEFREE |
CONCLUSIONS Our findings indicate that ARHGAP24 silencing promotes lung cancer cell migration and invasion through activating β-catenin signaling.
|
30599132 |
2019 |
|
Systolic Pressure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Trans-ethnic association study of blood pressure determinants in over 750,000 individuals.
|
30578418 |
2019 |
|
Systolic Pressure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CONCLUSIONS Our findings indicate that ARHGAP24 silencing promotes lung cancer cell migration and invasion through activating β-catenin signaling.
|
30599132 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family.
|
31090271 |
2019 |