Rnps1, the RNA-binding protein with serine-rich domain 1, is an essential regulator in mRNA metabolism. It is involved in constitutive and alternative splicing, transcriptional regulation, and nonsense-mediated mRNA decay. It also associates with the exon junction complex (EJC) during splicing and plays a role in maintaining transcriptome integrity by suppressing the use of cryptic splice sites [3,5]. Rnps1 is involved in many biological processes, and its dysregulation is related to various diseases [2-3, 7].

In cervical cancer cells, RNPS1 promotes cell proliferation, colony-forming ability, migration-invasion, and regulates the splicing of key genes like Rac1 and RhoA, favoring an active Rac1b/RhoA signaling axis for cancer cell invasion and metastasis [1]. In ischemic stroke, knockdown of RNPS1 in mice aggravates ischemic brain injury, promotes neuronal death, and exacerbates apoptosis while downregulating anti-apoptotic proteins [2]. In hematopoiesis, homozygous Rnps1 missense allele (F181I) mice show a stem cell-intrinsic defect due to excessive apoptosis from TNF-dependent death signaling, and Tnf knockout can rescue hematopoietic cells in these mice [4].

In conclusion, Rnps1 is crucial for mRNA metabolism, playing significant roles in multiple biological processes. Gene-knockout or conditional-knockout mouse models, like those in ischemic stroke and hematopoiesis studies, have revealed its importance in specific disease-related biological processes. Understanding Rnps1 functions through these models helps in exploring potential therapeutic strategies for related diseases such as cervical cancer, ischemic stroke, and hematopoietic disorders.