title: The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis.
abstract: The MYC family of proteins plays essential roles in embryonic development and in oncogenesis. Efforts over the past 30 years to define the transcriptional activities of MYC and how MYC functions to promote proliferation have produced evolving models of MYC function. One picture that has emerged of MYC and its partner protein MAX is of a transcription factor complex with a seemingly unique ability to stimulate the transcription of genes that are epigenetically poised for transcription and to amplify the transcription of actively transcribed genes. During lymphocyte activation, MYC is upregulated and stimulates a pro-proliferative program in part through the upregulation of a wide variety of metabolic effector genes that facilitate cell growth and cell cycle progression. MYC upregulation simultaneously sensitizes cells to apoptosis and activated lymphocytes and lymphoma cells have pro-survival attributes that allow MYC-driven proliferation to prevail. For example, the MAX-interacting protein MNT is upregulated in activated lymphocytes and was found to protect lymphocytes from MYC-dependent apoptosis. Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis. This article is part of a Special Issue entitled: Myc proteins in cell biology and pathology.
authors.affiliation: Shriners Hospitals for Children Portland, 3101 SW Sam Jackson Park Road, Portland, OR 97239, USA; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. Electronic address: linkja@ohsu.edu.
authors.forename: Jason M
authors.initials: JM
authors.lastname: Link
authors.affiliation: Shriners Hospitals for Children Portland, 3101 SW Sam Jackson Park Road, Portland, OR 97239, USA; Department of Cell and Developmental Biology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. Electronic address: pjh@shcc.org.
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Hurlin
mesh_terms: D001402:B-Lymphocytes / Q000378:metabolism; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*; D063646:Carcinogenesis / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008213:Lymphocyte Activation / Q000235:genetics; D008223:Lymphoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D060066:Protein Interaction Maps; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis / Q000378:metabolism*; D012097:Repressor Proteins / Q000235:genetics* / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism
chemical_list: D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; C499330:MAX protein, human; C106465:MNT protein, human; D016271:Proto-Oncogene Proteins c-myc; D012097:Repressor Proteins
keywords: Apoptosis; Lymphocytes; Lymphoma; MNT; MYC; Metabolism; Proliferation