Asap1-flox Mouse

ASAP1, an ADP-ribosylation factor GTPase-activating protein, has multiple functions including regulating cytoskeletal dynamics, small GTP-binding protein receptor recycling, and intracellular vesicle trafficking [4,5,6]. It is involved in pathways such as the IQGAP1/CDC42 pathway [1], NRAS/MEK1/ERK1-2 signaling [2], and the Wnt/β-catenin pathway [7]. These functions are crucial for various biological processes, and its dysregulation is associated with cancer and infectious diseases.

In cancer, ASAP1 shows diverse effects. In gastric cancer, its overexpression activates the IQGAP1/CDC42 pathway, promoting tumor progression and chemotherapy resistance [1]. In glioblastoma, circular RNA ASAP1 promotes tumorigenesis and temozolomide resistance via the NRAS/MEK1/ERK1-2 signaling [2]. In hepatocellular carcinoma, high ASAP1 expression is associated with aggressive clinicopathological characteristics and poor outcomes [3]. However, in the MMTV-PyMT model of luminal breast cancer, ablation of ASAP1 accelerates tumorigenesis and promotes metastasis by activating AKT [5]. In zebrafish, knockdown of asap1 homologs increases susceptibility to Mycobacterium marinum infection by reducing macrophage migration [4].

In conclusion, ASAP1 is a key regulator in multiple biological processes. Its role in cancer and infectious diseases has been revealed through various in vivo models. These findings contribute to understanding disease mechanisms, with implications for potential therapeutic strategies targeting ASAP1-related pathways in these disease areas.