Dr Nicholas J Dibb

Publications


Journals

  • Kapustin Y; Chan E; Sarkar R; Wong F; Vorechovsky I; Winston RM; Tatusova T; Dibb NJ. (1 Aug 2011). Cryptic splice sites and split genes. NUCLEIC ACIDS RESEARCH. 39:5837-5844. Author weblink DOI.
  • Kapustin Y; Chan E; Sarkar R; Wong F; Vorechovsky I; Winston RM; Tatusova T; Dibb NJ. (Aug 2011). Cryptic splice sites and split genes. Nucleic Acids Res. 39:5837-5844. DOI.
  • Zhou AY; Ichaso N; Adamarek A; Zila V; Forstova J; Dibb NJ; Dilworth SM. (Apr 2011). Polyomavirus middle T-antigen is a transmembrane protein that binds signaling proteins in discrete subcellular membrane sites. J Virol. 85:3046-3054. DOI.
  • Lee KC; Ouwehand I; Giannini AL; Thomas NS; Dibb NJ; Bijlmakers MJ. (Apr 2010). Lck is a key target of imatinib and dasatinib in T-cell activation. Leukemia. 24:896-900. DOI.
  • Skobridis K; Kinigopoulou M; Theodorou V; Giannousi E; Russell A; Chauhan R; Sala R; Brownlow N; et alKiriakidis S; Domin J; Tzakos AG; Dibb NJ. (Jan 2010). Novel imatinib derivatives with altered specificity between Bcr-Abl and FMS, KIT, and PDGF receptors. ChemMedChem. 5:130-139. DOI.
  • Brownlow N; Mol C; Hayford C; Ghaem-Maghami S; Dibb NJ. (1 Mar 2009). Dasatinib is a potent inhibitor of tumour-associated macrophages, osteoclasts and the FMS receptor. LEUKEMIA. 23:590-594. Author weblink DOI.
  • Brownlow N; Vaid M; Dibb NJ. (1 Jul 2008). Tandutinib inhibits FMS receptor signalling, and macrophage and osteoclast formation in vitro. LEUKEMIA. 22:1452-1453. Author weblink DOI.
  • Lo AS; Taylor JR; Farzaneh F; Kemeny DM; Dibb NJ; Maher J. (Mar 2008). Harnessing the tumour-derived cytokine, CSF-1, to co-stimulate T-cell growth and activation. Mol Immunol. 45:1276-1287. DOI.
  • Brownlow N; Russell AE; Saravanapavan H; Wiesmann M; Murray JM; Manley PW; Dibb NJ. (Mar 2008). Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis. Leukemia. 22:649-652. DOI.
  • Taylor JR; Brownlow N; Domin J; Dibb NJ. (5 Jan 2006). FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance. Oncogene. 25:147-151. DOI.
  • Dibb NJ; Dilworth SM; Mol CD. (Sep 2004). Switching on kinases: oncogenic activation of BRAF and the PDGFR family. Nat Rev Cancer. 4:718-727. DOI.
  • Sadusky T; Newman AJ; Dibb NJ. (23 Mar 2004). Exon junction sequences as cryptic splice sites: implications for intron origin. Curr Biol. 14:505-509. DOI.
  • Baker DA; Mille-Baker B; Wainwright SM; Ish-Horowicz D; Dibb NJ. (17 May 2001). Mae mediates MAP kinase phosphorylation of Ets transcription factors in Drosophila. Nature. 411:330-334. DOI.
  • Taylor DM; Handyside AH; Ray PF; Dibb NJ; Winston RM; Ao A. (Feb 2001). Quantitative measurement of transcript levels throughout human preimplantation development: analysis of hypoxanthine phosphoribosyl transferase. Mol Hum Reprod. 7:147-154.
  • Maher J; Lo ASY; Dibb NJ; Farzaneh F; Sadelain M; Kemeny DM. (16 Nov 2000). Harnessing the tumor-derived cytokine, macrophage colony-stimulating factor (M-CSF), to costimulate genetically modified T cells. BLOOD. 96:294A-294A. Author weblink.
  • Uden M; Morley GM; Dibb NJ. (1 Jul 1999). Evidence that downregulation of the M-CSF receptor is not dependent upon receptor kinase activity. Oncogene. 18:3846-3851. DOI.
  • Morley GM; Uden M; Gullick WJ; Dibb NJ. (20 May 1999). Cell specific transformation by c-fms activating loop mutations is attributable to constitutive receptor degradation. Oncogene. 18:3076-3084. DOI.
  • Takeda S; Soutter WP; Dibb NJ; White JO. (Mar 1996). Biological activity of the receptor for macrophage colony-stimulating factor in the human endometrial cancer cell line, Ishikawa. Br J Cancer. 73:615-619.
  • Maher J; Baker D; Dibb N; Roberts I. (Jan 1996). Mutant ras promotes haemopoietic cell proliferation or differentiation in a cell-specific manner. Leukemia. 10:83-90.
  • Baker DA; Uden M; White JO; Dibb NJ. (15 Nov 1995). M-CSF autocrine loop stimulates the proliferation of AML and CML leukaemic cell lines. BLOOD. 86:2884-2884.
  • Maher J; Baker DA; Manning M; Dibb NJ; Roberts IA. (19 Oct 1995). Evidence for cell-specific differences in transformation by N-, H- and K-ras. Oncogene. 11:1639-1647.
  • Glover HR; Baker DA; Celetti A; Dibb NJ. (5 Oct 1995). Selection of activating mutations of c-fms in FDC-P1 cells. Oncogene. 11:1347-1356.
  • BAKER DA; MAHER J; ROBERTS IAG; DIBB NJ. (15 Nov 1994). EVIDENCE THAT RAS AND MYC MEDIATE THE SYNERGY BETWEEN SCF OR M-CSF AND OTHER HEMATOPOIETIC GROWTH-FACTORS. BLOOD. 84:A423-A423. Author weblink.
  • MAHER J; BAKER DA; DIBB NJ; ROBERTS IAG. (15 Nov 1994). N-RAS, H-RAS, AND K-RAS - A DIFFERENCE IN TRANSFORMING POTENTIAL. BLOOD. 84:A295-A295. Author weblink.
  • Baker DA; Maher J; Roberts IA; Dibb NJ. (Nov 1994). Evidence that ras and myc mediate the synergy between SCF or M-CSF and other haemopoietic growth factors. Leukemia. 8:1970-1981.
  • Baker DA; Glover HR; Dibb NJ. (Jan 1994). Synergy between SCF or M-CSF with IL-3 or GM-CSF in FDC-P1 cells: a sensitive assay of transforming mutations of c-fms. Leukemia. 8:141-150.
  • Dibb NJ. (28 Jun 1993). Why do genes have introns?. FEBS Lett. 325:135-139.
  • MAHER J; BAKER D; DIBB N; ROBERTS IAG. (1 Jan 1993). THE ROLE OF RAS IN STEM-CELL FACTOR-MEDIATED SYNERGY. BRITISH JOURNAL OF HAEMATOLOGY. 84:68-68. Author weblink.
  • Dibb NJ. (7 Aug 1991). Proto-splice site model of intron origin. J Theor Biol. 151:405-416.
  • Dibb NJ; Green SM; Ralph P. (1990). Expression of v-fms and c-fms in the hemopoietic cell line FDC-P1. Growth Factors. 2:301-311.
  • Dibb NJ; Newman AJ. (Jul 1989). Evidence that introns arose at proto-splice sites. EMBO J. 8:2015-2021.
  • Dibb NJ; Maruyama IN; Krause M; Karn J. (5 Feb 1989). Sequence analysis of the complete Caenorhabditis elegans myosin heavy chain gene family. J Mol Biol. 205:603-613.
  • Wickner W; Moore K; Dibb N; Geissert D; Rice M. (Aug 1987). Inhibition of purified Escherichia coli leader peptidase by the leader (signal) peptide of bacteriophage M13 procoat. J Bacteriol. 169:3821-3822.
  • Dibb NJ; Wolfe PB. (Apr 1986). lep operon proximal gene is not required for growth or secretion by Escherichia coli. J Bacteriol. 166:83-87.
  • Dibb NJ; Brown DM; Karn J; Moerman DG; Bolten SL; Waterston RH. (25 Jun 1985). Sequence analysis of mutations that affect the synthesis, assembly and enzymatic activity of the unc-54 myosin heavy chain of Caenorhabditis elegans. J Mol Biol. 183:543-551.
  • Karn J; Dibb NJ; Miller DM. (1985). Cloning nematode myosin genes. Cell Muscle Motil. 6:185-237.
  • DIBB NJ. (1 Jan 1985). CORRECTION. JOURNAL OF MOLECULAR BIOLOGY. 185:653-653. Author weblink.
  • Dibb NJ; Downie JA; Brewin NJ. (May 1984). Identification of a rhizosphere protein encoded by the symbiotic plasmid of Rhizobium leguminosarum. J Bacteriol. 158:621-627.
  • HOMBRECHER G; GOTZ R; DIBB NJ; DOWNIE JA; JOHNSTON AWB; BREWIN NJ. (1 Jan 1984). CLONING AND MUTAGENESIS OF NODULATION GENES FROM RHIZOBIUM-LEGUMINOSARUM TOM, A STRAIN WITH EXTENDED HOST RANGE. MOLECULAR & GENERAL GENETICS. 194:293-298. Author weblink DOI.
  • BREWIN NJ; WOOD EA; JOHNSTON AWB; DIBB NJ; HOMBRECHER G. (1 Jan 1982). RECOMBINANT NODULATION PLASMIDS IN RHIZOBIUM-LEGUMINOSARUM. JOURNAL OF GENERAL MICROBIOLOGY. 128:1817-1827. Author weblink.

Conferences

  • Khorashad JS; Lipton JH; Marin D; Milojkovic D; Cross NCP; Dibb N; Melo JV; Kamel-Reid S; et alGoldman JM; Apperley JF; Kaeda JS. Abnormally small BCR-ABL transcripts in CML patients before and during imatinib treatment. 48th Annual Meeting of the American-Society-of-Hematology, 9 Dec 2006 - 12 Dec 2006. 108:611A-611A. AMER SOC HEMATOLOGY (16 Nov 2006). Author weblink.
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