Sunita K Agarwal

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e37952. 2012
  2. pmc Rare germline mutations in cyclin-dependent kinase inhibitor genes in multiple endocrine neoplasia type 1 and related states
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1802, USA
    J Clin Endocrinol Metab 94:1826-34. 2009
  3. pmc Distribution of menin-occupied regions in chromatin specifies a broad role of menin in transcriptional regulation
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1802, USA
    Neoplasia 9:101-7. 2007
  4. pmc The parafibromin tumor suppressor protein interacts with actin-binding proteins actinin-2 and actinin-3
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA
    Mol Cancer 7:65. 2008
  5. ncbi request reprint Parafibromin, product of the hyperparathyroidism-jaw tumor syndrome gene HRPT2, regulates cyclin D1/PRAD1 expression
    Geoffrey E Woodard
    1Metabolic Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Oncogene 24:1272-6. 2005
  6. pmc The 32-kilodalton subunit of replication protein A interacts with menin, the product of the MEN1 tumor suppressor gene
    Karen E Sukhodolets
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1802, USA
    Mol Cell Biol 23:493-509. 2003
  7. pmc Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 100:10770-5. 2003
  8. pmc Parathyroid tumor development involves deregulation of homeobox genes
    H C Jennifer Shen
    Tumor Angiogenesis Section, Surgery Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Endocr Relat Cancer 15:267-75. 2008
  9. ncbi request reprint The parathyroid/pituitary variant of multiple endocrine neoplasia type 1 usually has causes other than p27Kip1 mutations
    Atsushi Ozawa
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1802, USA
    J Clin Endocrinol Metab 92:1948-51. 2007
  10. ncbi request reprint Hyperparathyroidism in hereditary syndromes: special expressions and special managements
    Stephen J Marx
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1802, USA
    J Bone Miner Res 17:N37-43. 2002

Collaborators

Detail Information

Publications22

  1. pmc Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e37952. 2012
    ....
  2. pmc Rare germline mutations in cyclin-dependent kinase inhibitor genes in multiple endocrine neoplasia type 1 and related states
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1802, USA
    J Clin Endocrinol Metab 94:1826-34. 2009
    ..However, the prevalence of identifiable germline MEN1 mutations in familial MEN1 cases is only 70%. Some cases may have a germline mutation in another gene such as the p27 cyclin-dependent kinase inhibitor (CDKI)...
  3. pmc Distribution of menin-occupied regions in chromatin specifies a broad role of menin in transcriptional regulation
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1802, USA
    Neoplasia 9:101-7. 2007
    ..These unbiased data also suggest that menin could play a broad role in transcriptional regulation...
  4. pmc The parafibromin tumor suppressor protein interacts with actin-binding proteins actinin-2 and actinin-3
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA
    Mol Cancer 7:65. 2008
    ..HRPT2 encodes parafibromin. To identify parafibromin interacting proteins we used the yeast two-hybrid system for screening a heart cDNA library with parafibromin as the bait...
  5. ncbi request reprint Parafibromin, product of the hyperparathyroidism-jaw tumor syndrome gene HRPT2, regulates cyclin D1/PRAD1 expression
    Geoffrey E Woodard
    1Metabolic Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Oncogene 24:1272-6. 2005
    ..These results demonstrate that human parafibromin is a nucleocytoplasmic protein with functions consistent with its postulated role as a tumor suppressor protein...
  6. pmc The 32-kilodalton subunit of replication protein A interacts with menin, the product of the MEN1 tumor suppressor gene
    Karen E Sukhodolets
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1802, USA
    Mol Cell Biol 23:493-509. 2003
    ..This finding was consistent with the extensive overlap in the nuclear localization patterns of endogenous menin, RPA2, and RPA1 observed by immunofluorescence...
  7. pmc Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 100:10770-5. 2003
    ..To conclude, JunD changed from growth suppressor to growth promoter when its binding to menin was prevented by a JunD mutant unable to bind menin or by Men1-null genetic background...
  8. pmc Parathyroid tumor development involves deregulation of homeobox genes
    H C Jennifer Shen
    Tumor Angiogenesis Section, Surgery Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Endocr Relat Cancer 15:267-75. 2008
    ..Our results strongly reinforce the idea that abnormal expression of developmental HOX genes can be critical in human cancer progression...
  9. ncbi request reprint The parathyroid/pituitary variant of multiple endocrine neoplasia type 1 usually has causes other than p27Kip1 mutations
    Atsushi Ozawa
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1802, USA
    J Clin Endocrinol Metab 92:1948-51. 2007
    ..The prevalence of identified MEN1 mutations in this variant is lower than in familial MEN1 (7% vs. 90%), suggesting different causes. Recently, one case of this variant had a germline mutation of p27(Kip1)/CDKN1B...
  10. ncbi request reprint Hyperparathyroidism in hereditary syndromes: special expressions and special managements
    Stephen J Marx
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1802, USA
    J Bone Miner Res 17:N37-43. 2002
    ..The CASR test, perhaps least urgent, has largely been unavailable. Further progress in molecular genetics will enhance understandings, diagnosis, and therapy of HPT...
  11. ncbi request reprint Familial isolated hyperparathyroidism is rarely caused by germline mutation in HRPT2, the gene for the hyperparathyroidism-jaw tumor syndrome
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 89:96-102. 2004
    ..Even accounting for families with one of the three occult syndromes and false negative biochemical or DNA testing, these results indicate that an unexpectedly large fraction of FIHP has currently unrecognized causes...
  12. doi request reprint The embryonic transcription factor Hlxb9 is a menin interacting partner that controls pancreatic β-cell proliferation and the expression of insulin regulators
    Kerong Shi
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Endocr Relat Cancer 20:111-22. 2013
    ..Also, our findings identify Hlxb9 as an important factor for β-cell proliferation and insulin regulation...
  13. doi request reprint The MEN1 gene and pituitary tumours
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Horm Res 71:131-8. 2009
    ..We present recent clinical and basic findings about the MEN1 gene, particularly concerning hereditary vs. common variety pituitary tumours...
  14. ncbi request reprint Multiple endocrine neoplasia type 1 variant with frequent prolactinoma and rare gastrinoma
    Wei Hao
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 89:3776-84. 2004
    ..MEN1 carriers in such families should have periodic monitoring adjusted for the expected penetrance of tumors...
  15. ncbi request reprint Molecular pathology of the MEN1 gene
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 1014:189-98. 2004
    ..The Men1+/- mouse has robust MEN1; its most important difference from human MEN1 is marked hyperplasia of pancreatic islets, a tumor precursor stage...
  16. ncbi request reprint Menin, a tumor suppressor, associates with nonmuscle myosin II-A heavy chain
    Victor H Obungu
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Oncogene 22:6347-58. 2003
    ..These data indicate that menin through binding to NMHC II-A could participate in cell division and in other processes that involve NMHC II-A...
  17. pmc The tumor suppressor protein menin inhibits AKT activation by regulating its cellular localization
    Yan Wang
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 71:371-82. 2011
    ..Together, our results suggest menin as an important novel negative regulator of AKT kinase activity...
  18. pmc Genome-wide analysis of menin binding provides insights into MEN1 tumorigenesis
    Peter C Scacheri
    Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA
    PLoS Genet 2:e51. 2006
    ..Our findings expand the realm of menin-targeted genes several hundred-fold beyond that previously described and provide potential insights to the endocrine tumor bias observed in MEN1 patients...
  19. ncbi request reprint Mouse embryo fibroblasts lacking the tumor suppressor menin show altered expression of extracellular matrix protein genes
    Youngmi Ji
    Genome Technology Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA
    Mol Cancer Res 5:1041-51. 2007
    ..The expression changes associated with the loss of the tumor suppressor menin provide insights into the defective organogenesis observed during early embryonic development in Men1-null mouse embryos...
  20. ncbi request reprint Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Medicine (Baltimore) 81:1-26. 2002
  21. doi request reprint Multiple endocrine neoplasia type 1
    Sunita K Agarwal
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA SunitaA mail nih gov
    Front Horm Res 41:1-15. 2013
    ..This chapter covers clinical, genetic and basic findings about the MEN1 syndrome, MEN1 gene and its product protein menin...
  22. doi request reprint GSK-3β protein phosphorylates and stabilizes HLXB9 protein in insulinoma cells to form a targetable mechanism of controlling insulinoma cell proliferation
    Shruti S Desai
    From the Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 and
    J Biol Chem 289:5386-98. 2014
    ..Our results reveal that GSK-3β and pHLXB9 can serve as novel targets for insulinoma treatment and have implications for understanding the pathways associated with β cell proliferation. ..