ArticleCell cycle (Georgetown, Tex.)2016
FANCI is a negative regulator of Akt activation.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- FANCI: from genome guardian to translational therapeutic target.Frontiers in oncology · 2026Review
- FANCI is involved in the malignant progression of glioma cells by regulating the Akt/Bcl-2 signaling pathway.Discover oncology · 2025Article
- An Analysis of Genetic Polymorphisms in 76 Genes Related to the Development of Ovarian Tumors of Different Aggressiveness.International journal of molecular sciences · 2024Article
- Molecular Genetic Characteristics ofGenes · 2023Article
- FANCI serve as a prognostic biomarker correlated with immune infiltrates in skin cutaneous melanoma.Frontiers in immunology · 2023Article
- RosettaDDGPrediction for high-throughput mutational scans: From stability to binding.Protein science : a publication of the Protein Society · 2023Article
- Up-regulation of the PI3K/AKT and RHO/RAC/PAK signalling pathways in CHK1 inhibitor resistant Eµ-Myc lymphoma cells.The Biochemical journal · 2022Article
- Novel neoplasms associated with syndromic pediatric medulloblastoma: integrated pathway delineation for personalized therapy.Cell communication and signaling : CCS · 2022Article
- UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT.Oncology reports · 2022Article
- Global miRNA expression of bone marrow mesenchymal stem/stromal cells derived from Fanconi anemia patients.Human cell · 2022Article
- A functionally impaired missense variant identified in French Canadian families implicates FANCI as a candidate ovarian cancer-predisposing gene.Genome medicine · 2021Article
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- On the PHLPPside: Emerging roles of PHLPP phosphatases in the heart.Cellular signalling · 2021Review
- System-wide identification and prioritization of enzyme substrates by thermal analysis.Nature communications · 2021Article
- PHLPPing the Script: Emerging Roles of PHLPP Phosphatases in Cell Signaling.Annual review of pharmacology and toxicology · 2021Review
- Identification of novel biomarkers and candidate small-molecule drugs in cutaneous melanoma by comprehensive gene microarrays analysis.Journal of Cancer · 2021Article
- PARP Inhibition Increases the Reliance on ATR/CHK1 Checkpoint Signaling Leading to Synthetic Lethality-An Alternative Treatment Strategy for Epithelial Ovarian Cancer Cells Independent from HR Effectiveness.International journal of molecular sciences · 2020Article
- Participation of the ATR/CHK1 pathway in replicative stress targeted therapy of high-grade ovarian cancer.Journal of hematology & oncology · 2020Review
- Genetic and histologic spatiotemporal evolution of recurrent, multifocal, multicentric and metastatic glioblastoma.Acta neuropathologica communications · 2020Article
- Bioinformatics Analysis of Prognostic miRNA Signature and Potential Critical Genes in Colon Cancer.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Akt is a critical mediator of the oncogenic PI3K pathway, and its activation is regulated by kinases and phosphatases acting in opposition. We report here the existence of a novel protein complex that is composed minimally of Akt, PHLPP1, PHLPP2, FANCI, FANCD2, USP1 and UAF1. Our studies show that depletion of FANCI, but not FANCD2 or USP1, results in increased phosphorylation and activation of Akt. This activation is due to a reduction in the interaction between PHLPP1 and Akt in the absence of FANCI. In response to DNA damage or growth factor treatment, the interactions between Akt, PHLPP1 and FANCI are reduced consistent with the known phosphorylation of Akt in response to these stimuli. Furthermore, depletion of FANCI results in reduced apoptosis after DNA damage in accord with its role as a negative regular of Akt. Our findings describe an unexpected function for FANCI in the regulation of Akt and define a previously unrecognized intersection between the PI3K-Akt and FA pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.