Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
---|---|---|---|---|---|---|---|---|---|---|---|
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0.080 | AlteredExpression | disease | BEFREE | Furthermore, RIPC substantially reversed the downregulation of miR-144 and upregulation of PTEN in renal tissues of Cis-induced AKI mice and alleviated tubular cell apoptosis via activating PTEN/AKT signaling. | 31781349 | 2019 | ||||
|
0.080 | Biomarker | disease | BEFREE | Phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and E3 ubiquitin-protein ligase Parkin are involved in mitophagy regulation; however, little is known about the role of PINK1-Parkin mitophagy in septic AKI. | 31567378 | 2019 | ||||
|
0.080 | AlteredExpression | disease | BEFREE | We examined the effect on post kidney fibrosis of inhibiting PTEN activity in mice in an IR induced AKI experimental model. | 29049990 | 2017 | ||||
|
0.080 | Biomarker | disease | BEFREE | These results have demonstrated that PTEN plays a crucial role in the pathogenesis of ischemic acute kidney injury through regulating tubular cell apoptosis and inflammation suggesting PTEN could be a potential therapeutic target for acute kidney injury. | 28842716 | 2017 | ||||
|
0.080 | AlteredExpression | disease | BEFREE | Determinants of hepcidin levels in sepsis-associated acute kidney injury: Impact on pAKT/PTEN pathways? | 27266727 | 2016 | ||||
|
0.080 | Biomarker | disease | BEFREE | The PTEN and INK4A/ARF tumor suppressors maintain myelolymphoid homeostasis and cooperate to constrain histiocytic sarcoma development in humans. | 16697958 | 2006 | ||||
|
0.080 | AlteredExpression | disease | BEFREE | Dual inactivation of PTEN and INK4a/ARF tumor suppressor genes is a common feature observed in a broad spectrum of human cancer types. | 11818530 | 2002 | ||||
|
0.080 | GeneticVariation | disease | BEFREE | Thus, whereas germ-line mutations of PTEN, p53, p16(INK4A)/p14(ARF), and CDK4 are not common events in familial glioma, outside of familial cancer syndromes, point mutations of p53 and hemizygous deletions and other rearrangements of the p16(INK4A)/p14(ARF) tumor suppressor region may account for a subset of familial glioma cases. | 10797439 | 2000 |