Xpo7, short for exportin 7, is a bidirectional transporter crucial for regulating the nuclear-cytoplasmic shuttling of a wide range of substrates [4]. It is involved in multiple biological pathways, such as the Hedgehog signaling pathway, where it negatively regulates the pathway by exporting Gli2 from the nucleus [3]. It also plays a role in NF-κB/p65 nuclear translocation, as knockdown of Xpo7 reduces the amount of nuclear p65 following TNF-α stimulation [6]. Xpo7 is of great biological importance, with its functions being studied through various genetic models.

In cancer research, Xpo7 shows a dual role. In some cancers like liver cancer, deletion of Xpo7 correlates with poorer overall survival, and its depletion alleviates oncogene-induced senescence (OIS) and increases tumor formation, suggesting it as a tumor suppressor regulating p21CIP1-dependent senescence [1]. However, in prostate cancer, higher Xpo7 expression is found, and its overexpression promotes cell proliferation, migration, cell cycle progression, and EMT, acting as an oncogenic factor via upregulation of TCF3 [2]. In erythropoiesis, gene-targeted mouse models lacking the erythroid-specific isoform Xpo7B exhibit mild anemia and altered stress erythropoiesis, while complete Xpo7 deficiency leads to partially penetrant embryonic lethality during definitive erythropoiesis in the fetal liver [7]. Also, in schizophrenia-related studies, Xpo7 haploinsufficiency in mice causes cognitive and social behavioral impairments [5].

In conclusion, Xpo7 is a multifunctional protein involved in various biological processes and disease conditions. Gene-targeted mouse models, including KO and CKO models, have been instrumental in revealing its role in cancer, erythropoiesis, and schizophrenia-related pathologies. These studies contribute to a better understanding of Xpo7's biological functions and offer potential therapeutic targets for associated diseases.