Hnrnpab, also known as heterogeneous nuclear ribonucleoprotein A/B, is an RNA-binding protein closely associated with the biological function and metabolism of RNA. It participates in processes such as RNA splicing, nuclear export, and sensing, which are crucial for normal cellular function [4,5].

In pancreatic ductal adenocarcinoma (PDAC), hnRNPAB promotes cell migration, invasion, and liver metastasis. Deprivation of hnRNPAB in xenograft tumor mouse models significantly attenuated liver metastasis. It binds to MYC mRNA, prolonging its half-life, and induces PDAC cells to secrete CXCL8 via MYC, promoting neutrophil recruitment and tumor cell entry into the hepatic parenchyma [1].

In the context of Influenza A virus infection, hnRNPAB-deficient mice display higher viral burdens, enhanced cytokine production, and increased mortality. hnRNPAB interacts with NP of IAV to inhibit the interaction between PB1 and NP, disturbing polymerase activity and thus inhibiting viral infection [2].

In neural cell development, migration of cells from the SVZ of developing Hnrnpab-/-mouse brains is impaired. Hnrnpab regulates neural cell motility by co-regulating Eps8 transcription in the mouse SVZ [3].

In summary, hnRNPAB plays diverse and significant roles in various biological processes and disease conditions. Gene knockout models, especially in mice, have been instrumental in revealing its functions in cancer metastasis, viral infection, and neural cell migration, providing valuable insights into potential therapeutic targets and disease mechanisms.