Search Results - (Author, Cooperation:A. M. Chan)
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1Latest Papers from Table of Contents or Articles in PressR. Possemato ; K. M. Marks ; Y. D. Shaul ; M. E. Pacold ; D. Kim ; K. Birsoy ; S. Sethumadhavan ; H. K. Woo ; H. G. Jang ; A. K. Jha ; W. W. Chen ; F. G. Barrett ; N. Stransky ; Z. Y. Tsun ; G. S. Cowley ; J. Barretina ; N. Y. Kalaany ; P. P. Hsu ; K. Ottina ; A. M. Chan ; B. Yuan ; L. A. Garraway ; D. E. Root ; M. Mino-Kenudson ; E. F. Brachtel ; E. M. Driggers ; D. M. Sabatini
Nature Publishing Group (NPG)
Published 2011Staff ViewPublication Date: 2011-07-16Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/enzymology/*genetics/*metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation ; Citric Acid Cycle/physiology ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; *Genomics ; Glutamic Acid/metabolism ; Humans ; Ketoglutaric Acids/metabolism ; Melanoma/enzymology/genetics ; Mice ; Neoplasm Transplantation ; Phosphoglycerate Dehydrogenase/genetics/metabolism ; RNA Interference ; Serine/*biosynthesisPublished by: -
2Latest Papers from Table of Contents or Articles in PressStaff View
Publication Date: 2015-10-10Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: *Lakes ; *MarsPublished by: -
3Articles: DFG German National LicensesStaff View
ISSN: 1432-0827Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesStaff View
ISSN: 1573-675XKeywords: Apoptosis ; ERK ; JNK ; p53 ; RbSource: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract The molecular events associated with apoptosis induced by two distinct triggers (1) serum withdrawal and (2) etoposide treatment were investigated in the human lung carcinoma cell line A549. Although both serum withdrawal and etoposide treatment resulted in internucleosomal DNA fragmentation, the morphologic features were distinct. Serum deprived apoptotic cells appeared small, round and refractile, with little evidence of nuclear fragmentation; etoposide-induced apoptotic cells appeared enlarged and flattened and displayed prominent nuclear fragmentation. p53 and p21/waf1 protein levels were elevated in etoposide-treated cells, but not in cells subjected to serum with-drawal. Apoptosis induced by both treatments was accompanied by a significant reduction in Rb protein levels. However, etoposide treatment led to hypo-phosphorylation of Rb, while serum withdrawal did not alter the Rb phosphorylation pattern. Serum withdrawal-induced apoptosis was correlated with activation of JNK and suppression of ERK activities, while both JNK and ERK activities were slightly elevated during etoposid- induced apoptosis. Together, these results support the hypothesis that apoptosis induced by serum withdrawal and etoposide treatment occurs through different pathways and involves distinct mediators.Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesChan, A. M. -L. ; Hilkens, J. ; Kroezen, V. ; Mitchell, P. J. ; Scambler, P. ; Wainwright, B. J. ; Williamson, R. ; Cooper, C. S.
Springer
Published 1989Staff ViewISSN: 1572-9931Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract The human INT1L1 gene, which exhibits homology to the protooncogene INT1 is very closely linked to the MET gene and cystic fibrosis locus on human chromosome 7. In the present study we have isolated overlapping genomic clones that correspond to the mouse homolog of the INT1L1 gene and have used the cloned DNA as probes to examine the distribution of the mouse INT1L1 gene within a series of 35 mouse-hamster somatic cell hybrids. These analyses have localized the INT1L1 gene to mouse chromosome 6. In addition, we demonstrate that the mouse INT1L1 and MET genes are coamplified in lines of spontaneously transformed mouse NIH3T3 cells, indicating that these genes may remain closely linked within the mouse genome.Type of Medium: Electronic ResourceURL: