Adenylate kinase 5 (AK5)

Adenylate kinase 5 (AK5) is an atypical, cytosolic member of the adenylate kinase family that catalyzes reversible phosphoryl transfer reactions between adenine nucleotides, thereby regulating cellular nucleotide and energy homeostasis[1][2][4]. AK5 is structurally characterized by two independent catalytic domains and is predominantly expressed in the brain (notably in neurons), but is also present in the pancreas and other tissues[1][3]. It contributes to neuronal energy metabolism, is involved in the regulation of K-ATP channels in pancreatic beta cells, and participates in various cell signaling processes—including the AMPK/mTOR axis[1][2][3]. Abnormal AK5 expression is implicated in cancers (where it acts variously as a prognostic marker and regulator of cell proliferation or autophagy), neurodegenerative diseases, metabolic disorders such as diabetes, and as an autoantigen in limbic encephalitis. DNA methylation of the AK5 promoter is an important regulatory mechanism modulating its expression, especially in cancer[2][3]. There are no approved therapeutics directly targeting AK5, though it has been experimentally modulated via epigenetic drugs and is of emerging interest for diagnostic and prognostic applications[1][2][3][4].

Other names

Adenylate kinase isoenzyme 5AK 5ATP-AMP transphosphorylase 5AK6adenylate kinase 6

Modulation of DNA methylation to regulate AK5 expression (as with 5-aza in preclinical cancer models)[2] Regulation of cellular signaling pathways affecting proliferation, apoptosis, and autophagy, especially through AMPK and mTOR