AKT-interacting protein (AKTIP)

AKT-interacting protein (AKTIP) is a ubiquitin E2 variant (UEV) domain-containing protein that lacks catalytic residual activity but shares structural features with E2 ubiquitin-conjugating enzymes[1][3][4]. AKTIP is essential for telomere maintenance in mammals as it binds directly to shelterin components (TRF1, TRF2), interacts with telomeric DNA, and is required for proper telomere replication[1][4]. Depletion of AKTIP leads to hallmarks of telomere dysfunction (fragile telomeres, defective S-phase progression, increased DNA damage signals) and induces activation of DNA damage responses[1][4]. In mice, loss of AKTIP's orthologue Ft1 produces progeroid (premature aging) traits via a p53-dependent mechanism[2], implicating AKTIP as a novel player in aging. AKTIP also interacts with PCNA and RPA70, supporting its role in DNA replication. Additionally, AKTIP can modulate PKB/AKT signaling activity by enhancing AKT/PKB phosphorylation[3][5]. While it is primarily classified as a DNA maintenance and shelterin-interacting factor, its diverse molecular interactions extend to apoptosis regulation and possibly vesicle trafficking[1][3][4][5]. There is no evidence supporting its use as a direct therapeutic target, nor are there known drugs or clinical biomarkers that interact with or are based on AKTIP[1][2][3][4][5].

Other names

AKTIPFT1FTSFused toes protein homologfused toes homologFLJ13258Ft1