Rplp1, also known as ribosomal protein lateral stalk subunit P1, is a ribosomal protein. It is involved in ribosome and translation pathways and is crucial for the biogenesis of multi-pass transmembrane proteins. It helps relieve ribosome pausing during translation, and is part of the ribosomal stalk structure, which is important for the elongation phase of translation [5,6].

Disrupting Rplp1 in mouse germline and central nervous system (Rplp1CNSΔ) led to body size reductions, male infertility, systemic abnormalities, high-frequency early postnatal death, perinatal lethality, and brain atrophy in newborn mice. In the neocortex, it caused progenitor cell proliferation arrest and apoptosis due to dysregulation of key cell cycle and apoptosis regulators. Deletion in primary mouse embryonic fibroblasts did not change global protein synthesis but altered the expression patterns of specific protein subsets [4]. Knocking down Rplp1 in various cell lines and organisms also demonstrated its role in different biological processes. In Hep3b cells, downregulation of RPLP1 suppressed proliferation, migration, and invasion. In endometrial adenocarcinoma cell lines, knockdown was associated with reduced cell survival and migration. Lentivirus-mediated shRNA knockdown of RPLP1 attenuated CSFV growth [1,2,3].

In conclusion, Rplp1 is essential for embryonic and brain development, proper cell proliferation, and plays important roles in various disease-related processes such as viral infections, cancer progression, and metabolic-associated diseases. Studies using gene knockout mouse models like Rplp1CNSΔ have been instrumental in revealing these functions, providing insights into the underlying mechanisms of these biological processes and diseases [4].