Disruption of forkhead transcription factor (FOXO) family members in mice reveals their functional diversification.

By Taisuke Hosaka, W. Biggs, D. Tieu, Antonia D. Boyer, N. Varki, W. Cavenee, K. Arden. Proceedings of the National Academy of Sciences of the United States of America, 2004

714 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0c70e88909feb8e61f681e78704759b218862a02

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Citations in the corpus

Defining the role of mTOR in cancer. (2007, background): “FOXO transcription factors, which regulate the cell cycle, apoptosis, and metabolism, and appear to function in angiogenesis among other processes, are inhibited by AKT (Furuyama et al., 2004; Greer and Brunet, 2005; Hosaka et al., 2004; Potente et al., 2005).”
The mammalian ovary from genesis to revelation. (2009, neutral): “abundant zona pellucida remnants (172, 173), suggesting”
FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis. (2007, positive): “Yet, mouse FoxO knockouts have revealed unique roles for the FoxOs, such as the requirement for FoxO3 in ovarian primordial follicle activation (Castrillon et al., 2003; Hosaka et al., 2004) and FoxO1 in vasculogenesis (Furuyama et al., 2004; Hosaka et al., 2004).”
FOXO transcription factors at the interface between longevity and tumor suppression (2005, background): “FOXO1-null mice die at embryonic day 10.5, from defects in angiogenesis (Furuyama et al., 2004; Hosaka et al., 2004).”
Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “FoxO3 null Viable but female sterility Normal growth [ 133 ,36]”
FoxOs at the crossroads of cellular metabolism, differentiation, and transformation. (2004, positive): “…mammalian metabolism and life span. three main FoxO isoforms display remarkably different Three of the four FoxOs (1, -3a, and –4) are substrates phenotypes (Hosaka et al., 2004): FoxO1 ablation is emof the serine/threonine kinase Akt, while FoxO6 lacks bryonic lethal due to defective angiogenesis.”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Female Foxo3 knockout mice were found to be sterile due to global primordial follicle activation with subsequent oocyte exhaustion (Castrillon et al., 2003; Hosaka et al., 2004).”
FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis (2009, methodology): “Ce To circumvent embryonic lethality associated with impaired vascular development because of broad FoxO1 deficiency (Hosaka et al., 2004), we utilized conditional knockout alleles of FoxO1, 3, and 4 (FoxO1/3/4) to achieve somatic inactivation of FoxO in the mouse brain.”
SIRT1 controls endothelial angiogenic functions during vascular growth. (2007, background): “Foxo1 is highly expressed in the vascular endothelium and has been shown to be an essential negative transcriptional regulator of embryonic and postnatal vessel formation (Daly et al. 2004; Furuyama et al. 2004; Hosaka et al. 2004; Potente et al. 2005; Paik et al. 2007).”
FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “…due to global primordial follicle activation with subsequent oocyte exhaustion (Castrillon et al., 2003), as well as develop lymphoproliferation and inflammation in a FoxO3 gene-trap model (Lin et al., 2004); and FoxO4-deficient animals are viable and have no overt phenotype (Hosaka et al., 2004).”
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).”