Arhgap11a, a member of the RhoGAPs family, is a Ras homology GTPase-activating protein. It is vital for cell motility and is involved in regulating multiple cellular processes, such as Rho-ROCK signaling pathway which impacts actin cytoskeleton dynamics and cell morphology [3,6,7].

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

In radial glial progenitors, subcellular mRNA localization and local translation of Arhgap11a control their morphology and mediate neuronal positioning [2].

In gastric cancer, Arhgap11a knockout significantly inhibits cell proliferation, cell migration, and invasion in vitro and tumorigenic ability in nude mice in vivo, and it promotes cancer progression by regulating actin filament stability through TPM1 [5].

In clear cell renal cell carcinoma, knockdown of Arhgap11a suppresses cell proliferation, colony formation, and migration [4].

In conclusion, Arhgap11a plays crucial roles in various biological processes and disease conditions. Gene-knockout and conditional-knockout mouse models have revealed its significance in AD-related neuropathology, cortical development, and cancer progression, providing valuable insights into disease mechanisms and potential therapeutic targets for these diseases.