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Genomes and Genes | SPRED1SummaryGene Symbol: SPRED1 Description: sprouty-related, EVH1 domain containing 1 Alias: NFLS, hSpred1, spred-1, sprouty-related, EVH1 domain-containing protein 1, suppressor of Ras/MAPK activation Species: human Top Publications
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Publications
Spred is a Sprouty-related suppressor of Ras signallingT Wakioka
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Nature 412:647-51. 2001..Instead, Spred inhibited the activation of MAP kinase by suppressing phosphorylation and activation of Raf. Spred may represent a class of proteins that modulate Ras-Raf interaction and MAP kinase signalling...- Molecular cloning of mammalian Spred-3 which suppresses tyrosine kinase-mediated Erk activationReiko Kato
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 302:767-72. 2003..The finding of Spred-3 revealed the presence of a novel family of regulators for the Ras/MAP kinase pathway, each member of which may have different specificities for extracellular signals... 
Café-au-lait macules and intertriginous freckling in piebaldism: clinical overlap with neurofibromatosis type 1 and Legius syndromeCathy A Stevens
Department of Pediatrics, University of Tennessee College of Medicine, Chattanooga, Tennessee, USA
Am J Med Genet A 158:1195-9. 2012..affected with piebaldism; the proband meeting diagnostic criteria for NF1 also underwent comprehensive NF1 and SPRED1 testing with no mutations detected...
A shared molecular mechanism underlies the human rasopathies Legius syndrome and Neurofibromatosis-1Irma B Stowe
Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94158, USA
Genes Dev 26:1421-6. 2012..Loss-of-function mutations in one feedback regulator of Ras/MAPK signaling, SPRED1 (Sprouty-related protein with an EVH1 domain), cause Legius syndrome, an autosomal dominant human disorder that ..- A cost savings approach to SPRED1 mutational analysis in individuals at risk for neurofibromatosis type 1Talia M Muram
Department of Pathology, University of Utah, Utah, USA
Am J Med Genet A 161:467-72. 2013..Two genetic testing algorithms (SPRED1 testing alone, and NF1 mutation analysis with reflex to SPRED1) were compared against a baseline of no genetic .. - SPRED proteins provide a NF-ty link to Ras suppressionAndrea I McClatchey
Massachusetts General Hospital Center for Cancer Research, Department of Pathology, Harvard Medical School, Charlestown, Massachusetts 02129, USA
Genes Dev 26:1515-9. 2012Mutations in the SPRED1 (Sprouty-related protein with an EVH [Ena/Vasp homology] domain 1) and NF1 (neurofibromatosis 1) genes underlie clinically related human disorders... - Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formationSeema Singh
Center of Excellence in Stem Cell Biology and Regenerative Medicine Maine Medical Center Research Institute, Scarborough, Maine, United States of America
PLoS ONE 7:e38530. 2012..For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components... - Review and update of SPRED1 mutations causing Legius syndromeHilde Brems
Department of Human Genetics, Catholic University Leuven, Leuven, Belgium
Hum Mutat 33:1538-46. 2012..Legius syndrome is caused by germline loss-of-function SPRED1 mutations, resulting in overactivation of the RAS-MAPK signal transduction cascade... - Effects of environmentally relevant mixtures of persistent organic pollutants on the developmental neurobiology in ratsSantokh Gill
Toxicology Research Division, Health Products and Foods Branch, Health Canada, Ottawa, Ontario, Canada
Toxicol Pathol 41:38-47. 2013..In addition, structural genes including neurofilaments (NFLs) and microtubule-associated protein (MAP-2) were downregulated at least 2-fold or greater... - Peripheral blood gene expression as a novel genomic biomarker in complicated sarcoidosisTong Zhou
Institute for Personalized Respiratory Medicine, The University of Illinois at Chicago, Chicago, Illinois, United States of America
PLoS ONE 7:e44818. 2012..TSHZ2; T cell/JAK-STAT pathway genes such as AKT3, CBLB, DLG1, IFNG, IL2RA, IL7R, ITK, JUN, MALT1, NFATC2, PLCG1, SPRED1)... - Association of Piebaldism, Multiple Café-au-lait Macules, and Intertriginous Freckling: Clinical Evidence of a Common Pathway between KIT and Sprouty-Related, Ena/Vasodilator-Stimulated Phosphoprotein Homology-1 Domain Containing Protein 1 (SPRED1)Yvonne E Chiu
Division of Pediatric Dermatology, Department of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin Genetics Center, Children s Hospital of Wisconsin, Milwaukee, Wisconsin Division of Genetics, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin
Pediatr Dermatol 30:379-82. 2013..caused by Sprouty-related, Ena/vasodilator-stimulated phosphoprotein homology-1 domain containing protein 1 (SPRED1) mutations that also has multiple café-au-lait macules and intertriginous freckling... - Evidence for downregulation of the negative regulator SPRED2 in clinical prostate cancerN Kachroo
Translational Prostate Cancer Group, Hutchison MRC Research Centre, University of Cambridge, Cambridge CB1 0XZ, UK
Br J Cancer 108:597-601. 2013b>SPRED1 and 2 are key negative regulators of MAPK signalling in mammalian cells. Here, we investigate the expression and functional role of SPREDs in prostate cancer. - Fgf9 signalling stimulates Spred and Sprouty expression in embryonic mouse pancreas mesenchymeKathrine B Sylvestersen
Hagedorn Research Institute, Department of Developmental Biology, Gentofte, Denmark
Gene Expr Patterns 11:105-11. 2011..that several members of the Spred and Sprouty families are expressed in embryonic mouse pancreas and find Spred1 and -2 as well as Spry2 and -4 to be predominantly expressed in pancreatic mesenchyme... - Andes virus regulation of cellular microRNAs contributes to hantavirus-induced endothelial cell permeabilityTimothy Pepini
Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794 5222, USA
J Virol 84:11929-36. 2010..We further analyzed changes in miR-126, an EC-specific miRNA that regulates vascular integrity by suppressing SPRED1 and PIK3R2 mRNAs... - Direct association of Sprouty-related protein with an EVH1 domain (SPRED) 1 or SPRED2 with DYRK1A modifies substrate/kinase interactionsDan Li
Institute of Molecular and Cell Biology, Signal Transduction Laboratory, 61 Biopolis Drive, Proteos 138673, Singapore
J Biol Chem 285:35374-85. 2010The mammalian SPRED (Sprouty-related protein with an EVH1 domain) proteins include a family of three members, SPRED1-3. Currently, little is known about their biochemistry... - NF1 exon 22 analysis of individuals with the clinical diagnosis of neurofibromatosis type 1Talia M Muram-Zborovski
Department of Pathology, University of Utah, SLC, Utah, USA
Am J Med Genet A 152:1973-8. 2010..b>SPRED1 mutations cause Legius syndrome, which clinically overlaps with this attenuated NF1 phenotype... - SPRED 1 mutations in a neurofibromatosis clinicTalia M Muram-Zborovski
Department of Pathology, University of Utah, Salt Lake City, Utah, USA
J Child Neurol 25:1203-9. 2010Legius syndrome, caused by SPRED1 mutations, has phenotypic overlap with neurofibromatosis type 1 (NF1) without tumorigenic manifestations... - Legius syndrome in fourteen familiesEllen Denayer
Department of Human Genetics, Catholic University of Leuven, Belgium
Hum Mutat 32:E1985-98. 2011..It is caused by germline loss-of-function SPRED1 mutations and is a member of the RAS-MAPK pathway syndromes... - What is the 'objective' differential factor of diarrhea in infancy?: Normal state versus diarrheal illness in infants with chronic frequent and loose stoolJin Bok Hwang
Department of Pediatrics, Keimyung University, School of Medicine, Daegu, Korea
Korean J Pediatr 53:1006-11. 2010This study aimed to identify 'objective' differential factors for normal frequent loose stool (NFLS) and diarrheal illness with dehydration and nutritional deficiency (DIDN) among infants with chronic frequent loose stool (CFLS). - Sprouty2 and Spred1-2 proteins inhibit the activation of the ERK pathway elicited by cyclopentenone prostanoidsCarlota A García-Domínguez
Unidad de Biologia Celular, Área de Biología Celular y del Desarrollo, Centro Nacional de Microbiologia, Instituto de Salud Carlos III ISCIII, Majadahonda, Madrid, Spain
PLoS ONE 6:e16787. 2011..We therefore found that ectopic overexpression in HeLa cells of human Sprouty2, or human Spred1 or 2, inhibits ERK1/2 and Elk-1 activation triggered by the cyclopentenone prostanoids PGA(1) and 15d-PGJ(2)... - KITLG mutations cause familial progressive hyper- and hypopigmentationMustapha Amyere
Laboratory of Human Molecular Genetics, de Duve Institute, Universite Catholique de Louvain, Brussels, Belgium
J Invest Dermatol 131:1234-9. 2011..the Legius syndrome, characterized by familial café-au-lait spots and skin fold freckling, caused by mutations in SPRED1. We performed a genome-wide linkage analysis in seven families with FPHH, and identified linkage on 12q21... - Identification of SPRED1 deletions using RT-PCR, multiplex ligation-dependent probe amplification and quantitative PCREmily Spencer
University of Alabama at Birmingham, Dept of Genetics, 35294 0024, USA
Am J Med Genet A 155:1352-9. 2011Legius syndrome, is a recently identified autosomal dominant disorder caused by loss of function mutations in the SPRED1 gene, with individuals mainly presenting with multiple café-au-lait macules (CALM), freckling and macrocephaly... - Interaction of the receptor FGFRL1 with the negative regulator Spred1Lei Zhuang
Department of Clinical Research, University of Bern, 3010 Bern, Switzerland
Cell Signal 23:1496-504. 2011..we used the yeast two-hybrid system to demonstrate that FGFRL1 binds with its C-terminal, histidine-rich domain to Spred1 and to other proteins of the Sprouty/Spred family... - miR126 positively regulates mast cell proliferation and cytokine production through suppressing Spred1Takuma Ishizaki
Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku ku, Tokyo, Japan
Genes Cells 16:803-14. 2011The protein known as Spred1 (Sprouty-related Ena/VASP homology-1 domain-containing protein) has been identified as a negative regulator of growth factor-induced ERK/mitogen-activated protein kinase activation... - The Sprouty-related protein, Spred-1, localizes in a lipid raft/caveola and inhibits ERK activation in collaboration with caveolin-1Atsushi Nonami
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
Genes Cells 10:887-95. 2005..Furthermore, forced expression of exogenous Spred-1 in Cav-1-expressing cells further suppressed proliferation and ERK activation. These data suggest that Spred-1 inhibits ERK activation in collaboration with Cav-1... - Sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein (SPRED1), a tyrosine-protein phosphatase non-receptor type 11 (SHP2) substrate in the Ras/extracellular signal-regulated kinase (ERK) pathwayMartina Quintanar-Audelo
Institute of Molecular and Cell Biology, Signal Transduction Laboratory, 61 Biopolis Drive, Proteos 138673, Singapore
J Biol Chem 286:23102-12. 2011..Finally, we found two tyrosine residues on SPRED1 that are required, when phosphorylated, to inhibit Ras/ERK activation and identified Tyr-420 as a specific .. - Spred1, a negative regulator of Ras-MAPK-ERK, is enriched in CNS germinal zones, dampens NSC proliferation, and maintains ventricular zone structureTimothy N Phoenix
New York Neural Stem Cell Institute, Rensselaer, New York 12144, USA
Genes Dev 24:45-56. 2010..Sprouty-related protein with an EVH1 domain (Spred1) is a recently discovered negative Ras-MAPK-ERK regulator linked to a neurofibromatosis 1 (NF-1)-like human .. - Expanding the phenotype of a neurofibromatosis type 1-like syndrome: a patient with a SPRED1 mutation and orbital manifestationsKatherine A Lane
Children s Hospital of Philadelphia, University of Pennsylvania Hospital System, Philadelphia, Pennsylvania 19104 4399, USA
Ophthal Plast Reconstr Surg 25:399-401. 2009..Further investigation revealed a loss of function mutation in SPRED1 on chromosome 15... - [Gene screening in five Chinese families with hereditary spastic paraplegia with thin corpus callosum]Guo Hua Zhao
Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008 PR China
Zhonghua Yi Xue Yi Chuan Xue Za Zhi 24:677-80. 2007..To screen all ten genes between D15S971 and D15S1012 in five Chinese families with hereditary spastic paraplegia with thin corpus callosum (HSP-TCC)... - Tesk1 interacts with Spry2 to abrogate its inhibition of ERK phosphorylation downstream of receptor tyrosine kinase signalingSumana Chandramouli
Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673
J Biol Chem 283:1679-91. 2008..By selectively modulating the downstream effects of Spry2, Tesk1 may thus serve as a molecular determinant of the signaling outcome... - Germline loss-of-function mutations in SPRED1 cause a neurofibromatosis 1-like phenotypeHilde Brems
Department of Human Genetics, Catholic University Leuven, 3000 Leuven, Belgium
Nat Genet 39:1120-6. 2007We report germline loss-of-function mutations in SPRED1 in a newly identified autosomal dominant human disorder... - Interobserver reliability of video recording in the diagnosis of nocturnal frontal lobe seizuresLuca Vignatelli
Department of Neurological Sciences, University of Bologna, Via Ugo Foscolo 7, 40123 Bologna, Italy
Epilepsia 48:1506-11. 2007Nocturnal frontal lobe seizures (NFLS) show one or all of the following semeiological patterns: (1) paroxysmal arousals (PA: brief and sudden recurrent motor paroxysmal behavior); (2) hyperkinetic seizures (HS: motor attacks with complex .. - Spred-2 steady-state levels are regulated by phosphorylation and Cbl-mediated ubiquitinationPeter Lock
Cell Signaling Laboratory, Department of Surgery, University of Melbourne, Royal Melbourne Hospital, Parkville 3050, Australia
Biochem Biophys Res Commun 351:1018-23. 2006..These results suggest a role for Spred-2 tyrosine phosphorylation and ubiquitination in controlling Spred-2 expression levels... - Spreds, inhibitors of the Ras/ERK signal transduction, are dysregulated in human hepatocellular carcinoma and linked to the malignant phenotype of tumorsT Yoshida
Department of Medicine, Kurume University School of Medicine, Liver Cancer Division, Research Center for Innovative Cancer Therapy, and Center of the 21st Century COE Program for Medical Science, Kurume, Japan
Oncogene 25:6056-66. 2006..These data indicate that the reduction of Spred expression in HCC is one of the causes of the acquisition of malignant features. Thus, Spred could be not only a novel prognostic factor but also a new therapeutic target for human HCC... - FGF signaling inhibitor, SPRY4, is evolutionarily conserved target of WNT signaling pathway in progenitor cellsYuriko Katoh
M and M Medical BioInformatics, Hongo, Japan
Int J Mol Med 17:529-32. 2006..Here, transcriptional regulation of SPRY1, SPRY2, SPRY3, SPRY4, SPRED1, SPRED2, and SPRED3 genes by WNT/beta-catenin signaling cascade was investigated by using bioinformatics and human .. - 1.15 A crystal structure of the X. tropicalis Spred1 EVH1 domain suggests a fourth distinct peptide-binding mechanism within the EVH1 familyNicholas J Harmer
Department of Biochemistry, 80 Tennis Court Road, Cambridge, CB2 1GA, UK
FEBS Lett 579:1161-6. 2005..structure of the Enabled/vasodilator-stimulated phosphoprotein homology-1 (EVH1) domain from Xenopus tropicalis Spred1, solved to 1.15 A resolution... - Distinct requirements for the Sprouty domain for functional activity of Spred proteinsJames A J King
Department of Surgery, 5th Floor Clinical Sciences Building, University of Melbourne, Royal Melbourne Hospital, Parkville, VIC 3050, Australia
Biochem J 388:445-54. 2005.... - Spred-1 negatively regulates interleukin-3-mediated ERK/mitogen-activated protein (MAP) kinase activation in hematopoietic cellsAtsushi Nonami
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
J Biol Chem 279:52543-51. 2004..These data suggest that Spred-1 negatively regulates hematopoiesis by suppressing not only SCF-induced but also IL-3-induced ERK activation... - The Sprouty-related protein, Spred, inhibits cell motility, metastasis, and Rho-mediated actin reorganizationKanta Miyoshi
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Oncogene 23:5567-76. 2004..Using stably highly metastatic LM8 cells infected with the Spred1-Sendai virus vector, we demonstrated that Spred1 inhibits the metastasis of LM8 cells in nude mice... - Experimental validation of circumferential, longitudinal, and radial 2-dimensional strain during dobutamine stress echocardiography in ischemic conditionsPatricia Reant
INSERM U828 and IFR4, University of Bordeaux 2, Bordeaux, France
J Am Coll Cardiol 51:149-57. 2008..The aim of this study was to assess and validate 2-dimensional (2D) strain for the detection of ischemia during dobutamine stress echocardiography (DSE)... - Spred1 and TESK1--two new interaction partners of the kinase MARKK/TAO1 that link the microtubule and actin cytoskeletonCindy Johne
Max Planck Unit for Structural Molecular Biology, D 22607 Hamburg, Germany
Mol Biol Cell 19:1391-403. 2008..and identified two new interaction partners of MARKK, the regulatory Sprouty-related protein with EVH-1 domain1 (Spred1) and the testis-specific protein kinase (TESK1)... - Effects of silibinin on cell growth and invasive properties of a human hepatocellular carcinoma cell line, HepG-2, through inhibition of extracellular signal-regulated kinase 1/2 phosphorylationMajid Momeny
Department of Medical Genetics, University of Tehran, Tehran, Iran
Eur J Pharmacol 591:13-20. 2008..In addition, cell growth and proliferation may be inhibited by silibinin through down-regulation of Hec1... - Down regulation of genes involved in T cell polarity and motility during the induction of heart allograft tolerance by allochimeric MHC IWojciech Lisik
Department of General and Transplantation Surgery, Warsaw Medical University, Warsaw, Poland
PLoS ONE 4:e8020. 2009..The immune response in allograft rejection involves a cascade of molecular events leading to the formation of immunological synapses between T cells and the antigen-presenting cells... - Clinical and mutational spectrum of neurofibromatosis type 1-like syndromeLudwine Messiaen
Medical Genomics Laboratory, Department of Genetics, University of Alabama at Birmingham, 720 20th St S, Birmingham, AL 35294, USA
JAMA 302:2111-8. 2009Autosomal dominant inactivating sprouty-related EVH1 domain-containing protein 1 (SPRED1) mutations have recently been described in individuals presenting mainly with café au lait macules (CALMs), axillary freckling, and macrocephaly... - Identification of LATS transcriptional targets in HeLa cells using whole human genome oligonucleotide microarrayStacy Visser
Department of Pathology and Molecular Medicine, Queen s University, Kingston, ON, Canada K7L 3N6
Gene 449:22-9. 2010..known tumor suppressor genes and oncogenes such as CDKN1A, WISP2, SLIT2, TP53INP1, BIRC4BP, SPRY2, SPRY4, SPRED1, FAT4, and CYR61 were confirmed by qRT-PCR to be significantly differentially expressed... - SPRED1 mutations (Legius syndrome): another clinically useful genotype for dissecting the neurofibromatosis type 1 phenotypeG Spurlock
Institute of Medical Genetics, Cardiff University, Cardiff, UK
J Med Genet 46:431-7. 2009Mutations of the SPRED1 gene, one of a family of Sprouty (Spry)/Spred proteins known to "downregulate" mitogen activated protein kinase (MAPK) signalling, have been identified in patients with a mild neurofibromatosis type 1 (.. - SPRED1 germline mutations caused a neurofibromatosis type 1 overlapping phenotypeE Pasmant
UMR745 INSERM, Universite Paris Descartes, Faculte des Sciences Pharmaceutiques et Biologiques, Paris, France
J Med Genet 46:425-30. 2009Germline loss-of-function mutations in the SPRED1 gene have recently been identified in patients fulfilling the National Institutes of Health (NIH) diagnostic criteria for neurofibromatosis type 1 (NF1) but with no NF1 (neurofibromin 1) .. - TGF-beta modulates the functionality of tumor-infiltrating CD8+ T cells through effects on TCR signaling and Spred1 expressionMaria Giovanna di Bari
Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 8B09, MSC 1750, Bethesda, MD 20892, USA
Cancer Immunol Immunother 58:1809-18. 2009.... - Bcl-xL gene expression correlated with lower apoptotic cell numbers and shorter progression-free survival in PCFCLRazieh Soltani-Arabshahi
INSERM, U728, Paris, F 75010, France
J Invest Dermatol 129:1703-9. 2009..an antiapoptotic member of the bcl-2 family, has been correlated with poor prognosis in nodal follicular lymphomas (NFLs)... - A severe form of Noonan syndrome and autosomal dominant café-au-lait spots - evidence for different genetic originsAnna Maja Nyström
Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden
Acta Paediatr 98:693-8. 2009..Therefore, investigations of the genetic cause of a severe phenotype in a patient with NS and the presence of multiple café-au-lait spots (CAL) spots in the patient and four members of the family were performed... - Spred1 is required for synaptic plasticity and hippocampus-dependent learningEllen Denayer
Department of Human Genetics and Laboratory of Biological Psychology, University of Leuven, B 3000 Leuven, Belgium
J Neurosci 28:14443-9. 2008Germline mutations in SPRED1, a negative regulator of Ras, have been described in a neurofibromatosis type 1 (NF1)-like syndrome (NFLS) that included learning difficulties in some affected individuals... - Attribution of vascular phenotypes of the murine Egfl7 locus to the microRNA miR-126Frank Kuhnert
Division of Hematology, Department of Medicine, Stanford University School of Medicine, CCSR 1155, 269 Campus Drive, Stanford, CA 94305, USA
Development 135:3989-93. 2008..inhibited VEGF-dependent Akt and Erk signaling by derepression of the p85beta subunit of PI3 kinase and of Spred1, respectively... - miR-126 regulates angiogenic signaling and vascular integrityJason E Fish
Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA
Dev Cell 15:272-84. 2008..in part by directly repressing negative regulators of the VEGF pathway, including the Sprouty-related protein SPRED1 and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2/p85-beta)... - Identification of endogenous phosphorylation sites of bovine medium and low molecular weight neurofilament proteins by tandem mass spectrometrySarah Trimpin
Department of Chemistry, Oregon State University, Corvallis, Oregon 97331, USA
Biochemistry 43:2091-105. 2004..while two sites (Ser(55) and Ser(472)) are consistent with the phosphorylations observed in other mammalian NFLs. The three sites, Ser(55), Ser(66), Ser(472), are heterogeneously phosphorylated...
Research Grants
- Molecular Function of the Nf2 Tumor Suppressor, MerlinAndrea McClatchey; Fiscal Year: 2009..The results of this study will yield important insight into the mechanism of Merlin function as a tumor suppressor and identify novel targets for therapeutic intervention of NF2. ..
- Molecular Function of the Nf2 Tumor Suppressor, MerlinAndrea I McClatchey; Fiscal Year: 2010..These studies will advance our understanding of the molecular cause of NF2 and of the biology of ErbB receptors that have been widely implicated in human cancer. ..
- Comprehensive NF1 Mutational Analysis in Leukemia CellsLudwine Messiaen; Fiscal Year: 2006..abstract_text> ..