Ncoa7, or nuclear receptor coactivator 7, is a protein associated with multiple biological functions. It is a member of the Tre2/Bub2/Cdc16 (TBC), lysin motif (LysM), domain catalytic (TLDc) protein family. Ncoa7 is crucial for the normal assembly and activity of the vacuolar (V)-ATPase, a critical proton pump, and is involved in processes like endolysosomal homeostasis, which is essential for neurodevelopment [2]. It also plays a role in the MAPK/ERK signaling pathway, and is associated with the regulation of cell proliferation, invasion, and metastasis in certain cancers [1].

Gene knockout studies in mice have provided valuable insights. Targeted deletion of the Ncoa7 gene in mice led to incomplete distal renal tubular acidosis, indicating its importance in maintaining the function of collecting duct intercalated cells and urine acidification, likely through modulating the abundance of V-ATPase and other key acid-base regulators in the renal medulla [3]. In the nervous system, Ncoa7-deficient mice exhibited anxiety and social defects, along with abnormal neuronal patterning and reduced lysosomal markers, suggesting its role in modulating lysosomal function, neuronal connectivity, and behavior [2].

In summary, Ncoa7 is an important regulatory protein involved in multiple biological processes. Mouse models with Ncoa7 gene knockout have been instrumental in revealing its role in diseases such as incomplete distal renal tubular acidosis and neurodevelopmental disorders, highlighting its potential as a therapeutic target and prognostic marker in these areas.