Pik3ap1, also known as B-cell adapter for PI3K (BCAP), plays a crucial role in the PI3K/AKT signaling pathway [1,2,3,4,5,6]. This gene is important for various biological processes such as the regulation of immune responses and cell proliferation [2,3,4,5]. Genetic models, like gene knockout mouse models, can be used to study its functions in vivo.

In macrophage-specific BCAP-deficient mice, they fail to recover from dextran sulfate sodium-induced colitis due to prolonged intestinal inflammation and impaired tissue repair, indicating that Pik3ap1 is essential for the transition of macrophages from an inflammatory to a reparative state [1]. In gastric epithelial cells (GES-1) stimulated by Helicobacter pylori, hypermethylation of the Pik3ap1 promoter leads to down-regulation of Pik3ap1, which in turn affects the expression of downstream genes like AKT and the immunoinflammatory gene IL-6, and also impacts cell proliferation [2]. In cervical cancer, increased expression of Pik3ap1 is observed, and silencing it inhibits cervical cancer progression [5].

In conclusion, Pik3ap1 is a key regulator in the PI3K/AKT signaling pathway and is involved in important biological processes such as macrophage state transition, immune response regulation, and cell proliferation. Its dysregulation is associated with diseases like colitis, gastric inflammation, and cervical cancer. The study of Pik3ap1 using gene knockout models has provided valuable insights into its functions in these disease-related biological processes.