Arkadia N-terminal like PKA signaling regulator 2N (ARK2N)

Arkadia N-terminal like PKA signaling regulator 2N (ARK2N) is a highly conserved vertebrate protein with major roles as a molecular adaptor or scaffold without E3 ligase activity[2][3]. ARK2N directly interacts with casein kinase 2 beta (CK2β) and is critical for recruiting CK2 and the DNA repair protein Cockayne syndrome B (CSB) to sites of RNA polymerase II (RNAPII) stalling following DNA damage. The ARK2N–CK2 complex facilitates CSB phosphorylation, enhancing CSB's binding to stalled RNAPII and triggering transcription-coupled nucleotide excision repair (TC-NER), a process vital for resolving transcription-blocking DNA lesions[2][3]. Loss of ARK2N in mice leads to features resembling Cockayne syndrome, underscoring its importance in genome stability and transcriptional integrity. Separately, ARK2N is phosphorylated by AMP-activated protein kinase (AMPK) in skeletal muscle, modulating contractile force and calcium handling in fast-twitch muscle fibers. Knockout models show impaired muscle strength and endurance, positioning ARK2N as critical for both DNA repair in the nucleus and specialized contractility function in muscle tissue, though it is not currently considered a direct therapeutic drug target or receptor[1][2][3].

Other names

Protein ARK2NARKL1C18orf25MGC12909RNF111L1Arkadia-like protein 1Arkadia (RNF111) N-terminal like PKA signaling regulator protein 2NArkadia-like 1ARKadia-like protein 1protein C18orf25uncharacterized protein C18orf25