Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Shin Yuen Nam"'
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 6, Iss 5, Pp 546-557 (2004)
Although p73 is a structural and functional homologue of the tumor-suppressor gene p53, it is not mutated in many human cancers as p53. Besides, p73 was shown to be activated by only a subset of signals that activate p53, such as y-irradiation and ci
Externí odkaz:
https://doaj.org/article/88818be9cf344ba2aa83e0675bb02833
Autor:
Shin Yuen Nam, K Sabapathy
Publikováno v:
Oncogene. 30:4476-4486
A variety of cellular insults activate the tumour suppressor p53, leading generally to cell-cycle arrest or apoptosis. However, it is not inconceivable that cellular protective mechanisms may be required to keep cells alive while cell-fate decisions
Publikováno v:
Cell Death & Differentiation. 17:787-800
The molecular mechanisms regulating cell death during mitosis are poorly understood. We show here a critical role for p73, but not p53, in regulating mitotic cell death induced by various means. Prolonged mitotic arrest and the activation of spindle
Autor:
Shin Yuen Nam, Kanaga Sabapathy
Publikováno v:
Cell death and differentiation. 15(9)
Defects in Major Histocompatibility class I cell surface expression is thought to allow escape of tumor cells from immune surveillance. Hitherto, it is unclear whether this deficiency confers immune-independent survival advantage. We show here that c
Publikováno v:
The Journal of physiology. 586(2)
Immune-independent diabetes often occurs via pancreatic beta cell dysfunction. However, the role of the tumour suppressor p53 that regulates cellular life and death in multiple tissues, in pancreatic cell death and diabetes has not been clarified. We
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 6, Iss 5, Pp 546-557 (2004)
Although p73 is a structural and functional homologue of the tumor-suppressor gene p53, it is not mutated in many human cancers as p53. Besides, p73 was shown to be activated by only a subset of signals that activate p53, such as y-irradiation and ci
Autor:
Shin Yuen Nam, Anton Bauer, Erwin F. Wagner, Kanaga Sabapathy, Konrad Hochedlinger, Michael Karin
Publikováno v:
Molecular cell. 15(5)
Different c-Jun N-terminal kinases (JNKs) are activated by a plethora of signals and phosphorylate substrates such as c-Jun, which is required for efficient cell cycle progression. Although JNK1 and JNK2 were shown to differentially regulate fibrobla