FOXO1

FOXO1

The gene on chromosome 13q14.1 which encodes a forkhead family transcription factor that regulates cell responses to oxidative stress. In the presence of KIRT1, it downregulates cyclin D1 and upregulates CDKN1B as required for cell transition from proliferation to quiescence. It may play a role in myogenic growth and differentiation.

Molecular pathology
FOXO1 translocation with PAX3 has been associated with alveolar rhabdomyosarcoma.
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Meanwhile, ROS promoted nuclear the translocation/activation of FoxO1, which in turn prevents [beta] cell replication through the inhibition of Pdx-1 and possibly other [beta] cell-related gene transcriptions.
On the other hand, FoxO1 activities are also regulated by the InsR/PI3K/Akt signaling pathway, in which insulin induces Akt phosphorylation, followed by inactivation of FoxO1 due to its phosphorylation by p-Akt [17].
Several transcription factors such as peroxisome proliferator-activated receptor alpha (PPARa), sterol regulatory element-binding protein 1/2 (SREBP1/2), carbohydrate response element-binding protein (ChREBP), and forkhead box O transcription factor 1 (FoxO1) are considered to account for fish oil regulation of hepatic gene transcription modification [21, 22].
Meanwhile, activation of PI3K pathway was reported to reduce the nuclear content of the transcription factor FoxO1 deficiency, the key nutrigenomic regulator of acne target genes.
On the other hand, scopoletin increased activation FoxO1 in this study.
According to the foxO1 expression profile of human and mouse indicating that miR-133b may be involved in the regulation of foxO1 in B cell development (Liang et al.
The scientists were able to teach human gut cells to make insulin in response to physiological circumstances by deactivating the cells' FOXO1 gene.
The ability of the Akt-mediated signaling to dictate changes in muscle size appears to be due, in part, through its influence on the transcription factor FoxO1. Specifically, FoxO1, a known target of Akt kinase activity (28), is phosphorylated and subsequently sequestered in the cytoplasm and kept removed from its nuclear target genes upon Akt activation (6,28,35).
One of SIRTl's functions is to deacetylate and activate two proteins called forkhead box protein Ol (FOXO1) and peroxisome proliferator-activated receptor-[gamma] coactivator 1a (PGC-1[alpha]), a key regulator of energy metabolism.
Active Akt signaling functions to inhibit apoptosis through phosphorylation of proapoptotic factors such as BAD [encoded by BCL2-associated agonist of cell death (BAD)], CASP9 [encoded by caspase 9, apoptosis-related cysteine peptidase (CASP9)], and FOXO1 [encoded by forkhead box O1 (FOXO1)].
Foxo1 was also found to be important in regulating the generation of activated Treg cells in the TME.