Arhgap11a, a Ras homology GTPase-activating protein, is involved in multiple biological processes. It plays a role in regulating cell motility, and is associated with pathways such as RhoA/ROCK/Erk signaling. Its function is crucial in the development and disease-related processes in various tissues, and genetic models like KO/CKO mouse models are valuable for studying its effects [1-10].

In Alzheimer's disease (AD)-like mouse models, reducing Arhgap11a level in neurons inhibits Aβ generation by decreasing the expression of APP, PS1, and BACE1 via the RhoA/ROCK/Erk signaling pathway. It also reduces Aβo neurotoxicity by decreasing apoptosis-related p53 target gene expressions. Specific reduction of Arhgap11a level in neurons of APP/PS1 mice significantly reduces Aβ production, plaque deposition, and ameliorates neuronal damage, neuroinflammation, and cognitive deficits [1].

In radial glial progenitors, mRNA localization and local translation of Arhgap11a in the basal endfeet control their morphology and mediate neuronal positioning. Proper RGC morphology relies on active Arhgap11a mRNA transport and localization, where the protein is locally synthesized, which is essential for interneuron positioning at the basement membrane [2].

In gastric cancer, Arhgap11a knockout significantly inhibits cell proliferation, migration, and invasion in vitro and tumorigenic ability in nude mice in vivo [4]. In clear cell renal cell carcinoma (ccRCC), knockdown of Arhgap11A suppresses cell proliferation, colony formation, and migration [3].

In conclusion, Arhgap11a is essential in regulating cell-related functions such as cell motility, neuronal positioning, and amyloid-β generation. Gene-knockout studies in mouse models have revealed its significance in diseases like Alzheimer's disease, gastric cancer, and ccRCC, providing insights into potential therapeutic strategies for these conditions.