Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Raynard L. Bateman"'
Publikováno v:
Journal of Biological Chemistry. 283:35756-35762
Human carbonyl reductase 1 (hCBR1) is an NADPH-dependent short chain dehydrogenase/reductase with broad substrate specificity and is thought to be responsible for the in vivo reduction of quinones, prostaglandins, and other carbonyl-containing compou
Autor:
David E. Timm, Ronald W. McClard, Thomas D. Hurley, Markus Grompe, Raynard L. Bateman, L.-J. Baker, John F. Witte, Justin Ashworth, Pullooru Bhanumoorthy
Publikováno v:
Biochemical Journal. 402:251-260
FAH (fumarylacetoacetate hydrolase) catalyses the final step of tyrosine catabolism to produce fumarate and acetoacetate. HT1 (hereditary tyrosinaemia type 1) results from deficiency of this enzyme. Previously, we prepared a partial mimic of the puta
Autor:
Evangelos Hytopoulos, Eric J. Kunkel, Eugene C. Butcher, Dat Nguyen, Anthony C. Bishop, Ivan Plavec, Raynard L. Bateman, Leon T. Kao, Yuker Wang, Elen S. Rosler, Jennifer Melrose, Kevan M. Shokat, Ellen L. Berg
Publikováno v:
ASSAY and Drug Development Technologies. 2:431-442
Rapid, quantitative methods for characterizing the biological activities of kinase inhibitors in complex human cell systems could allow the biological consequences of differential target selectivity to be monitored early in development, improving the
Autor:
Meenakshi Noll, Keany Rathbun, Carol Reifsteck, Timothy Lax, Milton J. Finegold, Markus Grompe, Susan B. Olson, Kevin P. Battaile, Grover C. Bagby, Raynard L. Bateman
Publikováno v:
Experimental Hematology. 30:679-688
Objective Fanconi anemia (FA) is a genetically heterogeneous disorder associated with defects in at least eight genes. The biochemical function(s) of the FA proteins are unknown, but together they define the FA pathway, which is involved in cellular
Publikováno v:
Molecular Therapy. 3(1):14-23
Fanconi anemia (FA) is an autosomal recessive disorder characterized by birth defects, increased incidence of malignancy, progressive bone marrow failure, and cellular hypersensitivity to DNA cross-linking agents. Bone marrow transplantation is thera
Publikováno v:
Molecular and Cellular Biology. 20:8283-8289
Following introduction of DNA interstrand cross-links (ICLs), mammalian cells display chromosome breakage or cell cycle delay with a 4N DNA content. To further understand the nature of the delay, previously described as a G(2)/M arrest, we developed
Autor:
Kevin P. Battaile, Raynard L. Bateman, Derik Mortimer, Jean Mulcahy, R. Keaney Rathbun, Grover Bagby, William H. Fleming, Markus Grompe
Publikováno v:
Blood. 94:2151-2158
Fanconi anemia (FA) is an autosomal recessive disorder characterized by birth defects, increased incidence of malignancy, and progressive bone marrow failure. Bone marrow transplantation is therapeutic and, therefore, FA is a candidate disease for he
Autor:
Raynard L. Bateman, William H. Fleming, R. Keaney Rathbun, Markus Grompe, Kevin P. Battaile, Grover C. Bagby, Jean Mulcahy, Derik Mortimer
Publikováno v:
Blood. 94:2151-2158
Fanconi anemia (FA) is an autosomal recessive disorder characterized by birth defects, increased incidence of malignancy, and progressive bone marrow failure. Bone marrow transplantation is therapeutic and, therefore, FA is a candidate disease for he
Autor:
Glenn Tisman, J. Amin, Malcolm Brenner, S. Malkin, Mercedita Ramos, T. Browder, T. Vu, V. Cordts, G. Luszko, Raynard L. Bateman, V. Flener
Publikováno v:
American Journal of Hematology. 43:226-229
We have recently reported a new and rapid assay to measure plasma holotranscobalamin II (holo TC II) as a means of exploring vitamin B12 status. In order to further evaluate the significance of plasma holoTC II in determining tissue cobalamin, we hav
Autor:
Raynard L. Bateman, Markus Grompe, Ronald W. McClard, Milton J. Finegold, Karsten Wursthorn, John F. Witte
Publikováno v:
Molecular Therapy. 13
Mice deficient in the tyrosine catabolic enzyme Fah are an excellent model for liver repopulation by selection. Fah positive cells from several different origins can engraft and correct the phenotype of a Fah-mutant liver. Non-cell based gene therapy