Protein LSM12 homolog (LSM12)

Protein LSM12 homolog (LSM12) is an RNA-binding protein belonging to the like-Sm family, implicated in a variety of RNA processing events including pre-mRNA splicing and mRNA degradation[5][1]. It plays a key role in the regulation of alternative splicing and can modulate gene expression profiles important for cell proliferation, migration, cycle progression, and tumorigenesis, particularly in oral squamous cell carcinoma (OSCC)[2][1]. LSM12 is mostly localized to the cytoplasm and cytoplasmic stress granules, where it associates with other proteins to process RNA[1]. In humans, it also binds nicotinic acid adenine dinucleotide phosphate (NAADP) and acts as an accessory protein for two-pore channel complexes (TPCs), conferring NAADP sensitivity required for calcium release from cellular stores[3]. Overexpression of LSM12 enhances cell growth, migration, and invasion, while knockdown impairs these processes and can result in cell death, highlighting both its functional importance and potential therapeutic relevance[2]. LSM12 is upregulated in several human cancers and has been associated with other diseases such as late-onset Parkinson disease[3]. There are currently no approved or investigational drugs targeting LSM12, and its safety profile as a therapeutic target is unknown.

Other names

LSM12FLJ30656PNAS-135protein LSM12LSM12 homolog

Not applicable (no approved drugs currently targeting LSM12). For experimental modulation: RNA splicing alteration, functional inhibition/overexpression affecting cell survival and proliferation[2].