Hnrnpf-flox Mouse

Hnrnpf, a member of the HNRNPF/H family of heterogeneous nuclear RNA proteins, is a critical regulator of RNA maturation. It is involved in regulating splicing, especially alternative splicing, 5' capping, 3' polyadenylation of RNAs, and RNA export. Hnrnpf typically binds RNA sequences rich in guanine (G) residues, which can potentially form G-quadruplex structures [1].

In gastric cancer, the VAX2-LINC01189-hnRNPF signaling axis regulates cell invasion and migration. VAX2, as an oncogene, represses LINC01189 transcription. LINC01189 binds to hnRNPF to enhance its degradation through ubiquitination, thus influencing GC cell invasion and migration [2].

In male infertility, overexpressing the hnrnpH/F-orthologue Glorund in Drosophila led to low-quality semen production, suggesting that dysregulation of hnrnpH/F may cause subfertility or infertility in men [3].

In myocardial infarction, circCacna1c can inhibit the Hnrnpf/RIPK1-mediated cardiomyocyte necroptosis, improving cardiac function. CircCacna1c interacts with Hnrnpf in the cytoplasm, preventing its nuclear translocation and reducing Hnrnpf-dependent RIPK1 expression [4].

In conclusion, Hnrnpf is essential for RNA maturation processes. Model-based research, such as Drosophila overexpression and in-vivo studies in mouse models for diseases like gastric cancer, male infertility, and myocardial infarction, has revealed its role in various biological processes and disease conditions. These findings provide insights into potential therapeutic targets for related diseases.