Hnrnph1, encoding heterogeneous nuclear ribonucleoprotein H1, is an RNA-binding protein involved in multiple RNA metabolic processes. It participates in alternative splicing, a crucial process for gene expression regulation, and is associated with pathways related to germ cell development, mitochondrial homeostasis, and stress responses. Its study through genetic models like knockout mouse models can help reveal its in-vivo functions [1,2].

Conditional knockout of Hnrnph1 in spermatogenic cells leads to abnormal splicing events, affecting meiosis-related genes and germ-Sertoli cell communication, ultimately causing male sterility. Hnrnph1-deficient oocytes also show defective synapsis and cell-cell junctions, leading to female infertility [1]. In mice, conditional knockout of Hnrnph1 in Sertoli cells compromises blood-testis barrier function, delays meiotic progression, increases germ cell apoptosis, and causes infertility [4]. Additionally, in 293T cells, knockdown and over-expression of hnRNPH1 proteins show that hnRNPH1 inhibits the replication of H1N1 and H9N2 influenza viruses by restraining viral polymerase activity [3].

In conclusion, Hnrnph1 is essential for germ cell development and male fertility as demonstrated by KO/CKO mouse models. It also plays a role in inhibiting influenza virus replication. These findings contribute to understanding the biological functions of Hnrnph1 in reproductive processes and antiviral defense mechanisms.