TY - JOUR T1 - Menin molecular interactions: insights into normal functions and tumorigenesis. AU - Agarwal,S K, AU - Kennedy,P A, AU - Scacheri,P C, AU - Novotny,E A, AU - Hickman,A B, AU - Cerrato,A, AU - Rice,T S, AU - Moore,J B, AU - Rao,S, AU - Ji,Y, AU - Mateo,C, AU - Libutti,S K, AU - Oliver,B, AU - Chandrasekharappa,S C, AU - Burns,A L, AU - Collins,F S, AU - Spiegel,A M, AU - Marx,S J, PY - 2005/7/8/pubmed PY - 2005/9/30/medline PY - 2005/7/8/entrez SP - 369 EP - 74 JF - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme JO - Horm Metab Res VL - 37 IS - 6 N2 - Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease predisposed by heterozygous germline mutations in the MEN1 tumor suppressor gene. Biallelic loss of MEN1 resulting from small mutation and/or loss of heterozygosity occurs in a large tissue spectrum of MEN1 tumors or non-hereditary tumors. Mouse models of MEN1 underexpression or overexpression have also supported the tumor-suppressor effect of the MEN1 gene. Menin, the 610-amino-acid protein encoded by MEN1, is expressed ubiquitously and found predominantly in the nucleus. Sequence analyses do not reveal motifs of known function other than two nuclear localization sequences. Menin has been found to partner in vitro with a variety of proteins that comprise transcription factors, DNA processing factors, DNA repair proteins, and cytoskeletal proteins. The diverse functions of menin interactors suggest roles for menin in multiple biological pathways. Inactivation of menin switches its JunD partner from a downstream action of growth suppression to growth promotion. This is a plausible mechanism for menin tumorigenesis. SN - 0018-5043 UR - https://www.unboundmedicine.com/medline/citation/16001329/Menin_molecular_interactions:_insights_into_normal_functions_and_tumorigenesis_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-2005-870139 DB - PRIME DP - Unbound Medicine ER -