AKT-interacting protein is a protein that in humans is encoded by the AKTIPgene.[1][2][3]
The mouse homolog of this gene produces fused toes and thymic hyperplasia in heterozygous mutant animals while homozygous mutants die in early development. This gene may play a role in apoptosis as these morphological abnormalities are caused by altered patterns of programmed cell death. The protein encoded by this gene is similar to the ubiquitin ligase domain of other ubiquitin-conjugating enzymes but lacks the conserved cysteine residue that enables those enzymes to conjugate ubiquitin to the target protein. This protein interacts directly with serine/threonine kinase protein kinase B (PKB)/Akt and modulates PKB activity by enhancing the phosphorylation of PKB's regulatory sites. Alternative splicing results in two transcript variants encoding the same protein.[3]
The association between the AKTIP gene variants in a sample of 273 bipolar patients using 3 single-nucleotide polymorphisms has been investigated. No association between suicidal behavior and AKTIP variants nor any interaction between AKTIP and AKT1 polymorphisms was observed.[5]
References
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↑Aiyar N, Rand K, Elshourbagy NA, Zeng Z, Adamou JE, Bergsma DJ, Li Y (Jun 1996). "A cDNA encoding the calcitonin gene-related peptide type 1 receptor". J Biol Chem. 271 (19): 11325–9. doi:10.1074/jbc.271.19.11325. PMID8626685.
↑Magno LA, Miranda DM, Neves FS, Pimenta GJ, Mello MP, De Marco LA, Correa H, Romano-Silva MA (January 2010). "Association between AKT1 but not AKTIP genetic variants and increased risk for suicidal behavior in bipolar patients". Genes Brain Behav. 9 (4): 411–8. doi:10.1111/j.1601-183X.2010.00571.x. PMID20132317.
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