FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis.

By J. Paik, R. Kollipara, Gerald C. Chu, Hongkai Ji, Yonghong Xiao, Z. Ding, L. Miao, Z. Tothova, J. Horner, D. Carrasco and 6 more. Cell, 2007

1,101 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/985f46f661b317ac1e080a24833d3b2c737e1cb0

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Citations in the corpus

From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “This fact has been convincingly demonstrated by the striking overproduction of new blood vessels in mice with conditional deletion of the three major FoxO genes (80).”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…recent finding that Sprouty2, a gene involved in suppression of Ras signaling during oncogene-induced senescence, is also a direct transcriptional target of FoxO emphasizes the complexity of cross-talk that exists between the Ras/MAPK and PI3K pathways (Courtois-Cox et al. 2006; Paik et al. 2007).”
Regulation of autophagy and the ubiquitin–proteasome system by the FoxO transcriptional network during muscle atrophy (2015, positive): “Mice bearing FoxO1,3,4 -ﬂoxed alleles ( FoxO1,3,4 f/f ) 25 were crossed with transgenic mice expressing Cre either under the control of a Myosin Light Chain 1 fast promoter ( MLC1f-Cre ) 2,26 or with transgenic expressing a Cre-ER driven by human skeletal actin promoter 27 .”
Pancreatic β-Cell Dedifferentiation As Mechanism Of Diabetic β-Cell Failure (2012, neutral): “, 1996), and Foxo1 mice have been described (Paik et al., 2007).”
Impaired regulation of hepatic glucose production in mice lacking the forkhead transcription factor Foxo1 in liver. (2007, methodology): “Foxo1 Knockouts To ablate Foxo1 in hepatocytes, we intercrossed mice homozygous for a floxed Foxo1 allele (Paik et al., 2007) with a1 antitrypsin-cre mice (henceforth, l-Foxo1 mice).”
Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging (2017, background): “FOXO1 and FOXO3 are essential to numerous endogenous processes as development, differentiation, and tumor suppression, roles not prominently attributed to FOXO4 (Hosaka et al., 2004; Nakae et al., 2003; Paik et al., 2007; Renault et al., 2009).”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Paik et al. (2007) showed that triple knockout mice prompted a progressive cancer-prone condition characterized by thymic lymphomas and hemangiomas which lead to early death.”
FoxO3 regulates neural stem cell homeostasis (2009, positive): “Because FoxO3 has been shown to play an important role in specific endothelial cells (Paik et al., 2007), a portion of the defect observed in the brain of FoxO3 / mice might come from FoxO3 loss in blood vessels.”
Redox regulation of FoxO transcription factors (2015, background): “Single and double FoxO knockout mice did not show increased rates of tumorigenesis, but the triple deletion of Foxo1a, Foxo3a and Foxo4 resulted in accelerated tumor progression in adult mice, together with increased intracellular ROS levels [250].”
Cellular and molecular mechanisms of muscle atrophy (2013, neutral): “…such as regulating certain cell signaling pathways [e.g. modulating nuclear factor-κB (NFκB) activity] and being involved in autophagydependent cargo recognition via interacting with the scaffold protein p62 (also known as SQSTM1) (Kirkin et al., 2009; Komatsu et al., 2007; Pankiv et al., 2007).”