• KOL
    • Men1 Gene
    • A Lee Burns
    • A LEE Burns: Influence Statistics

      A LEE Burns

      A LEE Burns

      Metabolic Diseases Branch (A.O., S.K.A., C.M.M., A.L.B., T.S.R., P.A.K., C.M.Q., W.F.S., L.S.W., A.M.S., S.J.M.), National Institute of Diabetes and Digestive and Kidney ...

      Is this your profile? manage_accounts Claim your profile content_copy Copy URL code Embed Link to your profile

      A LEE Burns:Expert Impact

      Concepts for whichA LEE Burnshas direct influence:Men1 gene,Multiple endocrine,Membrane fusion,Human synexin,Endocrine neoplasia,Type 1,Neoplasia type,Transcription factor jund.

      A LEE Burns:KOL impact

      Concepts related to the work of other authors for whichfor which A LEE Burns has influence:Multiple endocrine,Men1 gene,Neoplasia type,Primary hyperparathyroidism,Pituitary adenomas,Tumor suppressor,Parathyroid carcinoma.

      KOL Resume for A LEE Burns

      Year
      2007

      Metabolic Diseases Branch (A.O., S.K.A., C.M.M., A.L.B., T.S.R., P.A.K., C.M.Q., W.F.S., L.S.W., A.M.S., S.J.M.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, Maryland 20892

      2005

      Surgery Branch, National Cancer Institute, Building 10, Room 4W-5940, 10 Center Drive, 20892, Bethesda, Maryland

      2003

      National Institute of Diabetes and Digestive and Kidney Diseases

      2001

      Metabolic Diseases Branch, NIDDK, NIH, U.S.A.

      2000

      Metabolic Diseases Branch, NIDDK, NIH, 20892, Bethesda, Maryland, USA

      1999

      Metabolic Diseases Branch, NIDDK, 20892, Bethesda, Maryland, MD, USA

      1998

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland

      1997

      Metabolic Diseases Branch, NIDDK, Building 10, Room 9C-101, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA

      1996

      Genetics and Endocrinology Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Maryland, 20892

      1994

      Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, U.S.A

      1992

      Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA

      1991

      Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.

      1990

      Cardiorenal Division, Food and Drug Administration, Bethesda, Maryland.

      Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, 20892, Bethesda, Maryland

      1989

      Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA

      1988

      Laboratory of Cell Biology and Genetics, National Institutes of Diabetes, and Digestive Diseases, National Institutes of Health, Bethesda, MD, USA

      1987

      Laboratory of Cell Biology and Genetics National Institute of Diabetes, Digestive and Kidney Diseases National Institutes of Health Bethesda, Maryland 20205

      1986

      Laboratory of Cell Biology, NIADDK, National Institutes of Health, 20892, Bethesda, Maryland, USA

      Sign-in to see all concepts, it's free!
      Sample of concepts for which A LEE Burns is among the top experts in the world.
      Concept World rank
      synexins #2
      annexin vii polymorphisms #2
      nucleolin cdna #2
      iii mice models #2
      human synexin mrna #2
      iii molecular escherichia #2
      cloned human synexin #2
      analysis synexin #2
      synexins sets #2
      recombinant synexins #2
      mrna cassette #2
      muscle lung isoforms #2
      annexin vii gene #2
      muscle synexin #2
      mouse synexin cdnas #2
      cassette exon brain #2
      mouse synexin #2
      type synexin mrna #2
      longer 3noncoding region #2
      synexin mrna #2
      synexin cdnas #2
      synexin clones #2
      alternate polya signal #2
      human synexin #2
      liposomes synexin #3
      parathyroid neoplasia #3
      facts synexin #3
      recombinant human synexin #3
      parathyroid adenoma carcinoma #3
      purification human menin #3
      annexin viib #3
      artificial bilayer #3
      synexin plasma membranes #3
      synexin annexin #3
      synexin biological phospholipids #3
      splice junctions annexins #3
      synexin calcium #3
      purified human synexin #3
      potential fusion site #3
      Sign-in to see all concepts, it's free!

      Prominent publications by A LEE Burns

      KOL-Index: 12741

      Lung carcinoids occur sporadically and rarely in association with multiple endocrine neoplasia type 1 (MEN1). There are no well defined genetic abnormalities known to occur in these tumors. We studied 11 sporadic lung carcinoids for loss of heterozygosity (LOH) at the locus of the MEN1 gene on chromosome 11q13, and for mutations of the MEN1 gene using dideoxy fingerprinting. Additionally, a lung carcinoid from a MEN1 patient was studied. In four of 11 (36%) sporadic tumors, both copies ...

      Known for Men1 Gene | Carcinoid Tumors | Heterozygosity Lung | 1 Neoplasm | Mutation Loss
      KOL-Index: 11861

      Primary hyperparathyroidism is a common disorder with an annual incidence of approximately 0.5 in 1,000 (ref. 1). In more than 95% of cases, the disease is caused by sporadic parathyroid adenoma or sporadic hyperplasia. Some cases are caused by inherited syndromes, such as multiple endocrine neoplasia type 1 (MEN1; ref. 2). In most cases, the molecular basis of parathyroid neoplasia is unknown. Parathyroid adenomas are usually monoclonal3,4, suggesting that one important step in tumour ...

      Known for Parathyroid Tumours | Men1 Gene | Somatic Mutation | Molecular Basis | Neoplasm Proteins
      KOL-Index: 11183

      MEN1 is a tumor suppressor gene that encodes a 610 amino acid nuclear protein (menin) of previously unknown function. Using a yeast two-hybrid screen with menin as the bait, we have identified the transcription factor JunD as a direct menin-interacting partner. Menin did not interact directly with other Jun and Fos family members. The menin-JunD interaction was confirmed in vitro and in vivo. Menin repressed transcriptional activation mediated by JunD fused to the Gal4 DNA-binding domain ...

      Known for Transcription Factor Jund | Proto Oncogene | Jun Fos | Menin Interaction | Factor Ap1
      KOL-Index: 10945

      CONTEXT: One variant of multiple endocrine neoplasia type 1 (MEN1) is defined by sporadic tumors of both the parathyroids and pituitary. 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.

      OBJECTIVE: The objective was to test p27 in germline DNA from cases with tumors of both the parathyroids and pituitary.

      DESIGN: Medical ...

      Known for Multiple Endocrine | Neoplasia Type | Germline Mutation | P27 Gene | Sporadic Tumors
      KOL-Index: 10655

      Familial multiple endocrine neoplasia type 1 (FMEN1) is an autosomal dominant trait characterized by tumors of the parathyroids, gastro-intestinal endocrine tissue, anterior pituitary and other tissues. We recently cloned the MEN1 gene and confirmed its identity by finding mutations in FMEN1. We have now extended our mutation analysis to 34 more unrelated FMEN1 probands and to two related states, sporadic MEN1 and familial hyperparathyroidism. There was a high prevalence of heterozygous ...

      Known for Men1 Gene | Germline Mutations | Familial Hyperparathyroidism | Type 1 | Endocrine Neoplasia
      KOL-Index: 10533

      Menin, the product of the MEN1 tumor suppressor gene, binds to the AP1 transcription factor JunD and represses JunD transcriptional activity. The effects of human or mouse JunD missense mutations upon menin interaction were studied by random and alanine scanning mutagenesis of the menin binding region of JunD (amino acids 1–70). JunD mutant proteins were tested for menin binding in a reverse yeast two-hybrid assay, and for transcriptional regulation by menin in AP1-reporter assays. ...

      Known for Jund Menin | Amino Acid | Protein Binding | Transcriptional Regulation | Proto Oncogene
      KOL-Index: 10208

      Menin is a 70-kDa protein encoded by MEN1, the tumor suppressor gene disrupted in multiple endocrine neoplasia type 1. In a yeast two-hybrid system based on reconstitution of Ras signaling, menin was found to interact with the 32-kDa subunit (RPA2) of replication protein A (RPA), a heterotrimeric protein required for DNA replication, recombination, and repair. The menin-RPA2 interaction was confirmed in a conventional yeast two-hybrid system and by direct interaction between purified ...

      Known for Replication Protein | Tumor Suppressor Gene | Dna Binding | Rpa1 Rpa2 | Multiple Endocrine Neoplasia
      KOL-Index: 9868

      Different components of the AP1 transcription factor complex appear to have distinct effects on cell proliferation and transformation. In contrast to other AP1 components, JunD has been shown to inhibit cell proliferation. Also, in prior studies, JunD alone bound menin, product of the MEN1 tumor suppressor gene, and JunD's transcriptional activity was inhibited by menin, suggesting that JunD might achieve all or most of its unique properties through binding to menin. Analyses of JunD and ...

      Known for Jund Menin | Growth Suppressor | Cell Proliferation | Cyclin D1 | Proto Oncogene
      KOL-Index: 9162

      Patients with multiple endocrine neoplasia type 1 (MEN1) develop multiple endocrine tumors, primarily affecting the parathyroid, pituitary, and endocrine pancreas, due to the inactivation of the MEN1 gene. A conditional mouse model was developed to evaluate the loss of the mouse homolog, Men1, in the pancreatic beta cell. Men1 in these mice contains exons 3 to 8 flanked by loxP sites, such that, when the mice are crossed to transgenic mice expressing cre from the rat insulin promoter ...

      Known for Men1 Mice | Beta Cells | Loxp Sites | Mouse Homolog | Multiple Endocrine Neoplasia

      Key People For Men1 Gene

      Top KOLs in the world
      #1
      Stephen J Marx∘∘
      multiple endocrine men1 gene primary hyperparathyroidism
      #2
      Allen M Spiegel
      men1 gene multiple endocrine adenylate cyclase
      #3
      Sunita Kishore Agarwal
      men1 gene multiple endocrine neoplasia type
      #4
      Francis S Collins
      type 2 diabetes cystic fibrosis men1 gene
      #5
      Settara C Chandrasekharappa
      fanconi anemia men1 gene multiple endocrine
      #6
      A LEE Burns
      men1 gene multiple endocrine membrane fusion

      Metabolic Diseases Branch (A.O., S.K.A., C.M.M., A.L.B., T.S.R., P.A.K., C.M.Q., W.F.S., L.S.W., A.M.S., S.J.M.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, Maryland 20892 | Surger

    Download on the App StoreGet it on Google Play

    Copyright © 2023 Key Opinion Leaders, LLC.