SAT-150 Forkhead Box Protein O1 (foxo1) Regulates Hepatic Serine Protease Inhibitor B1 (serpinb1) Expression In A Cell Non-autonomous Fashion

Forkhead Box Protein O3 Transcription Factor Negatively Regulates Autophagy in Human Cancer Cells by Inhibiting Forkhead Box Protein O1 Expression and Cytosolic Accumulation

FoxO proteins are important regulators in cellular metabolism and are recognized to be nodes in multiple signaling pathways, most notably those involving PI3K/AKT and mTOR. FoxO proteins primarily function as transcription factors, but recent study suggests that cytosolic FoxO1 participates in the regulation of autophagy. In the current study, we find that cytosolic FoxO1 indeed stimulates cell...

Cloning and Expression of Forkhead Box O1 (Foxo1): Wildtype and Site Directed Mutagenesis at T24A, S256A, S319A

Associations between Forkhead Box O1 (FoxO1) Expression and Indicators of Hepatic Glucose Production in Transition Dairy Cows Supplemented with Dietary Nicotinic Acid

Forkhead box protein O1 (FoxO1) is a transcription factor which promotes hepatic glucose production (HGP) by up-regulating the transcription of gluconeogenic enzymes in monogastric species. The activity of FoxO1 is inhibited by insulin-induced phosphorylation. The aims of the present study were to find associations between FoxO1 expression and variables associated with HGP as affected by feedin...

Forkhead box O1 promotes INS-1 cell apoptosis by reducing the expression of CD24

Type 2 diabetes seriously affects human health and burdens public health systems. Pancreatic β‑cell apoptosis contributes to a reduction in β‑cell mass, which is responsible for the occurrence of type 2 diabetes. However, the mechanism that underlies this effect remains unclear. In the present study, the role of forkhead box O1 (Foxo1) was investigated (which is a key regulatory factor in β‑cel...

The neutrophil serine protease inhibitor serpinb1 preserves lung defense functions in Pseudomonas aeruginosa infection

Neutrophil serine proteases (NSPs; elastase, cathepsin G, and proteinase-3) directly kill invading microbes. However, excess NSPs in the lungs play a central role in the pathology of inflammatory pulmonary disease. We show that serpinb1, an efficient inhibitor of the three NSPs, preserves cell and molecular components responsible for host defense against Pseudomonas aeruginosa. On infection, wi...