Zobrazeno 1 - 10
of 82
pro vyhledávání: '"Martin L. Hooper"'
Autor:
Rossant, Janet
Publikováno v:
The Quarterly Review of Biology, 1986 Dec 01. 61(4), 540-541.
Externí odkaz:
https://www.jstor.org/stable/2827775
Autor:
Janet Rossant
Publikováno v:
The Quarterly Review of Biology. 61:540-541
Autor:
Uta Francke
Publikováno v:
BioScience. 37:741-742
Autor:
Owen J. Sansom, Sarah J. Plowman, Mark J. Arends, David J. Harrison, Walter Kolch, William A Wallace, David G. Brownstein, Marion F Walker, Paul S. Devenney, Martin L. Hooper, Feijun Luo, Charles E. Patek, Rachel L. Berry, Lorraine Rose, Suzanne Hagan
Publikováno v:
Experimental Cell Research. 314:1105-1114
To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with
Autor:
Charles E. Patek, Rachel L. Berry, Ann-Marie Ritchie, Feijun Luo, Paul S. Devenney, Lorraine Rose, Sarah J. Plowman, Mark J. Arends, Martin L. Hooper, David G. Brownstein, David J. Harrison
Publikováno v:
Experimental Cell Research. 312:16-26
Ras proteins function as molecular switches in signal transduction pathways, and, here, we examined the effects of the K-ras4A and 413 splice variants on cell function by comparing wild-type embryonic stem (ES) cells with K-ras(tm Delta 4A/tm Delta 4
Autor:
Rachel L. Berry, Charles E. Patek, Richard M. Sharpe, Colin G. Miles, Nicholas D. Hastie, Martin L. Hooper, Philippa T. K. Saunders
Publikováno v:
Transgenic Research. 14:691-702
Gonadal effects of the Denys-Drash syndrome (DDS) mutation Wt1(tmT396 )were examined in chimaeric and heterozygous mice. Since the only heterozygote was 41,XXY, Sertoli cell function was assessed by comparison with age-matched control XXY testes. Con
Autor:
Charles E. Patek, Martin L. Hooper, Colin G. Miles, Lee Spraggon, Nicholas D. Hastie, Christopher Bellamy, Stewart Fleming, John J. Mullins, Michael Ladomery
Publikováno v:
Human Molecular Genetics. 12:2379-2394
Denys-Drash syndrome (DDS) is caused by dominant mutations of the Wilms' tumour suppressor gene, WT1, and characterized by a nephropathy involving diffuse mesangial sclerosis, male pseudohermaphroditism and/or Wilms' tumourigenesis. Previously, we re
Autor:
Marion Walker, Brian Hendrich, Andrew H. Wyllie, Scott Bader, Martin L. Hooper, Colin C. Bird, Adrian Bird
Publikováno v:
Oncogene. 18:8044-8047
Defects of mismatch repair are thought to be responsible for carcinogenesis in hereditary non-polyposis colorectal cancer and about 15% of sporadic colon cancers. The phenotype is seen as microsatellite instability and is known to be caused either by
Autor:
Sheila Christie, Alan Richard Clarke, Jean Paul Charlieu, Melissa H. Little, Martin L. Hooper, Nicholas D. Hastie, Colin G. Miles, David J. Harrison, David J. Porteous, Jennifer Doig, Stewart Fleming, Kiyoshi Miyagawa, Anthony J. Brookes, Charles E. Patek
Publikováno v:
Proceedings of the National Academy of Sciences. 96:2931-2936
The Wilms tumor-suppressor gene, WT1 , plays a key role in urogenital development, and WT1 dysfunction is implicated in both neoplastic (Wilms tumor, mesothelioma, leukemias, and breast cancer) and nonneoplastic (glomerulosclerosis) disease. The anal
Autor:
Anthony M. Ford, S D Griffiths, Martin L. Hooper, Mel Greaves, Andrew H. Wyllie, Alan Richard Clarke, Lyn E. Healy, G Ross
Publikováno v:
Oncogene. 14:523-531
Much evidence has been gathered in support of a critical role for p53 in the cellular response to DNA damage. p53 dysfunction is associated with progression and poor prognosis of many human cancers and with a high incidence of tumours in p53 knockout