Palmdelphin (PALMD)

Palmdelphin (PALMD) is a cytosolic protein belonging to the paralemmin protein family, structurally related to paralemmin-1, paralemmin-2, and paralemmin-3[2][4]. PALMD plays critical roles in skeletal muscle biology, where it promotes myoblast differentiation and is required for efficient muscle regeneration after injury; loss of PALMD function impairs muscle fiber formation and differentiation[1]. It also participates in cytoskeletal regulation and nuclear integrity, especially in endothelial cells, where its deficiency leads to defective nuclear-cytoskeletal coupling and impaired resilience of the nucleus to mechanical stress[4]. At the molecular level, PALMD interacts with factors such as RANGAP1 and influences the localization of key regulators of gene transcription, including p53 and p21, thereby affecting nucleocytoplasmic transport[4]. Genetically, decreased PALMD expression (driven by risk alleles or polymorphisms) is a strong risk factor for calcific aortic valve stenosis and is linked to adverse cardiovascular outcomes[3][4]. In response to DNA damage, PALMD can be transcriptionally induced by p53 (phosphorylated at serine-46) to trigger apoptotic cell death, while suppression of PALMD may favor necroptosis-like cell death[3]. PALMD is not a classical therapeutic target (such as a receptor or enzyme), and no direct interacting drugs or clinical mechanisms of action have been established. However, its roles in muscle and cardiovascular health suggest it is a biologically relevant disease-associated gene and a potential biomarker for certain conditions[1][3][4].

Other names

C1orf11PALMLFLJ20271Paralemmin-like proteinparalemmin-like proteinparalemnin-like protein