KHSRP, the KH-type splicing regulatory protein, is a multifunctional RNA-binding protein. It is involved in various biological processes such as mRNA decay, alternative splicing, and miRNA biogenesis. It also participates in key pathways like the FAK signaling pathway [1]. KHSRP's functions are of great biological importance, influencing processes from cell differentiation to tumor progression, and genetic models are crucial for studying its effects.

In pancreatic ductal adenocarcinoma (PDAC), KHSRP acts as an m6A-binding protein. High levels of KHSRP predict poor patient survival, and KHSRP deficiency suppresses PDAC growth and metastasis in vivo. It stabilizes FAK pathway mRNAs in an m6A-dependent manner, activating downstream FAK signaling to promote PDAC progression [1].

In mice lacking KHSRP (Khsrp-/ -), there are upregulated mRNAs involved in neuronal morphology, axon guidance, etc. These mice show increased axon growth, dendritic spine density, and synaptic transmission, along with memory consolidation deficits, indicating KHSRP's role in neuronal development [2].

In acute liver failure murine models, knockdown of KHSRP leads to splicing defects and exacerbation of liver injury, while KHSRP protects against ALF by regulating pre-mRNA splicing in vivo [3].

In conclusion, KHSRP plays essential roles in multiple biological processes. Gene knockout mouse models, like Khsrp-/-mice, have revealed its significance in diseases such as PDAC, liver failure, and in neuronal development. Understanding KHSRP's functions provides potential therapeutic targets for relevant diseases.