期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 265, 期 -, 页码 34-41出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2006.12.032
关键词
menin; MEN1; cell proliferation; apoptosis; genome stability; transcription; epigenetics
资金
- NCI NIH HHS [R01 CA100912, R01 CA113962, CA113962] Funding Source: Medline
Human hereditary tumor syndromes serve as an ideal model for studying molecular pathways regulating tumorigenesis. Multiple endocrine neoplasia type 1 (MEN1), a human familial tumor syndrome, results from mutations in the Men1 gene. Men1 encodes a novel tumor suppressor, menin, of unknown biochemical function. Recently, significant progress has been made in identifying menin as a regulator of gene transcription, cell proliferation, apoptosis, and genome stability, leading to a new model of understanding menin's tumor-suppressing function. These findings suggest that menin's diverse functions depend on its association with chromatin and its control over gene transcription. This knowledge will likely be translated into new strategies to improve therapeutic interventions against MEN I and other related cancers. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
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