Mechanisms of Disease: multiple endocrine neoplasia type 1—relation to chromatin modifications and transcription regulation

[1]  K. Mulder,et al.  Menin links estrogen receptor activation to histone H3K4 trimethylation. , 2006, Cancer research.

[2]  Matthew Meyerson,et al.  The Menin Tumor Suppressor Protein Is an Essential Oncogenic Cofactor for MLL-Associated Leukemogenesis , 2005, Cell.

[3]  O. Rozenblatt-Rosen,et al.  Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[4]  M. Blasco.  Telomeres and human disease: ageing, cancer and beyond , 2005, Nature Reviews Genetics.

[5]  S. Horvath,et al.  Global histone modification patterns predict risk of prostate cancer recurrence , 2005, Nature.

[6]  Richard A Young,et al.  Global and Hox-specific roles for the MLL1 methyltransferase. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[7]  M. Fraga,et al.  Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer , 2005, Nature Genetics.

[8]  O. Rozenblatt-Rosen,et al.  Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[9]  Yigong Shi,et al.  Direct Binding of DNA by Tumor Suppressor Menin* , 2004, Journal of Biological Chemistry.

[10]  T. Xu,et al.  Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1. , 2004, Human Molecular Genetics.

[11]  H. Masai,et al.  Functional Interaction between Tumor Suppressor Menin and Activator of S-Phase Kinase , 2004, Cancer Research.

[12]  Maho Takahashi,et al.  Menin Missense Mutants Associated with Multiple Endocrine Neoplasia Type 1 Are Rapidly Degraded via the Ubiquitin-Proteasome Pathway , 2004, Molecular and Cellular Biology.

[13]  W. Herr,et al.  Leukemia Proto-Oncoprotein MLL Forms a SET1-Like Histone Methyltransferase Complex with Menin To Regulate Hox Gene Expression , 2004, Molecular and Cellular Biology.

[14]  G. Hendy,et al.  Activin inhibits pituitary prolactin expression and cell growth through Smads, Pit-1 and menin. , 2004, Molecular endocrinology.

[15]  R. Kitazawa,et al.  Menin Inactivation Leads to Loss of Transforming Growth Factor β Inhibition of Parathyroid Cell Proliferation and Parathyroid Hormone Secretion , 2004, Cancer Research.

[16]  G. Kay,et al.  Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. , 2004, Molecular cell.

[17]  A. Vortmeyer,et al.  Meningiomas May Be a Component Tumor of Multiple Endocrine Neoplasia Type 1 , 2004, Clinical Cancer Research.

[18]  R. B. van der Luijt,et al.  Do patients with multiple endocrine neoplasia syndrome type 1 benefit from periodical screening? , 2003, European journal of endocrinology.

[19]  Jun O. Liu,et al.  Menin, a tumor suppressor, represses JunD-mediated transcriptional activity by association with an mSin3A-histone deacetylase complex. , 2003, Cancer research.

[20]  R. Adelstein,et al.  Menin, a tumor suppressor, associates with nonmuscle myosin II-A heavy chain , 2003, Oncogene.

[21]  F. Collins,et al.  Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[22]  A. D’Andrea,et al.  Menin associates with FANCD2, a protein involved in repair of DNA damage. , 2003, Cancer research.

[23]  S. Elledge,et al.  Multiple Tumor Suppressor Pathways Negatively Regulate Telomerase , 2003, Cell.

[24]  S. Chandrasekharappa,et al.  Functional studies of the MEN1 gene , 2003, Journal of internal medicine.

[25]  S. Forbes,et al.  Multiple endocrine neoplasia type 1 (MEN1) germline mutations in familial isolated primary hyperparathyroidism , 2003, Clinical endocrinology.

[26]  F. Collins,et al.  The 32-Kilodalton Subunit of Replication Protein A Interacts with Menin, the Product of the MEN1 Tumor Suppressor Gene , 2003, Molecular and Cellular Biology.

[27]  Stuart L. Schreiber,et al.  Active genes are tri-methylated at K4 of histone H3 , 2002, Nature.

[28]  D. Bonofiglio,et al.  Menin uncouples Elk-1, JunD and c-Jun phosphorylation from MAP kinase activation , 2002, Oncogene.

[29]  E. Bongcam-Rudloff,et al.  Menin's interaction with glial fibrillary acidic protein and vimentin suggests a role for the intermediate filament network in regulating menin activity. , 2002, Experimental cell research.

[30]  C. Béroud,et al.  Germline mutation profile of MEN1 in multiple endocrine neoplasia type 1: search for correlation between phenotype and the functional domains of the MEN1 protein , 2002, Human mutation.

[31]  Jeffrey E. Lee,et al.  Genotype-phenotype analysis in multiple endocrine neoplasia type 1. , 2002, Archives of surgery.

[32]  B. Ponder,et al.  Guidelines for diagnosis and therapy of MEN type 1 and type 2. , 2001, The Journal of clinical endocrinology and metabolism.

[33]  John P. Bilezikian,et al.  CONSENSUS: Guidelines for Diagnosis and Therapy of MEN Type 1 and Type 2 , 2001 .

[34]  C. Larsson,et al.  Menin interacts directly with the homeobox-containing protein Pem. , 2001, Biochemical and biophysical research communications.

[35]  F. Collins,et al.  The tumor suppressor protein menin interacts with NF-κB proteins and inhibits NF-κB-mediated transactivation , 2001, Oncogene.

[36]  N. Ohkura,et al.  Menin, a gene product responsible for multiple endocrine neoplasia type 1, interacts with the putative tumor metastasis suppressor nm23. , 2001, Biochemical and biophysical research communications.

[37]  G. Hendy,et al.  Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type β signaling , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[38]  O. Yazgan,et al.  Differential binding of the Menin tumor suppressor protein to JunD isoforms. , 2001, Cancer research.

[39]  F. Collins,et al.  A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[40]  V. Godfrey,et al.  Functional Collaboration between Different Cyclin-Dependent Kinase Inhibitors Suppresses Tumor Growth with Distinct Tissue Specificity , 2000, Molecular and Cellular Biology.

[41]  Roijers,et al.  Criteria for mutation analysis in MEN 1‐suspected patients: MEN 1 case‐finding , 2000, European journal of clinical investigation.

[42]  M. Berg,et al.  Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism. , 1999, Biochimica et biophysica acta.

[43]  J. Burgess,et al.  Osteoporosis in multiple endocrine neoplasia type 1: severity, clinical significance, relationship to primary hyperparathyroidism, and response to parathyroidectomy. , 1999, Archives of Surgery.

[44]  F. Collins,et al.  Menin Interacts with the AP1 Transcription Factor JunD and Represses JunD-Activated Transcription , 1999, Cell.

[45]  Thompson.  Current concepts in the surgical management of multiple endocrine neoplasia type 1 pancreatic‐duodenal disease. Results in the treatment of 40 patients with Zollinger–Ellison syndrome, hypoglycaemia or both , 1998, Journal of internal medicine.

[46]  F. Collins,et al.  Menin, the product of the MEN1 gene, is a nuclear protein. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[47]  F. Collins,et al.  Somatic mutations of the MEN1 tumor suppressor gene in sporadic gastrinomas and insulinomas. , 1997, Cancer research.

[48]  F. Collins,et al.  Somatic mutation of the MEN1 gene in parathyroid tumours , 1997, Nature Genetics.

[49]  Y Wang,et al.  Positional cloning of the gene for multiple endocrine neoplasia-type 1. , 1997, Science.

[50]  C. Larsson,et al.  Multiple endocrine neoplasia type 1 gene maps to chromosome 11 and is lost in insulinoma , 1988, Nature.

[51]  F. Collins,et al.  Common ancestral mutations in the MEN1 gene is likely responsible for the prolactinoma variant of MEN1 (MEN1Burin) in four kindreds from Newfoundland , 1998, Human mutation.