Signaling to p53
نویسندگان
چکیده
منابع مشابه
Signaling to p53 Breaking the MDM2–p53 Circuit
general transcriptional machinery, such as TAFs. Third, a number of phosphorylation sites have been identified in the vicinity of this region that are highly likely to be involved in regulating p53. How does MDM2 mediate p53 degradation? There have been a number of attempts to address this ques-The p53 tumor suppressor protein transmits signals aris-tion. Honda et al. (1997) reported that MDM2 ...
متن کاملNon-canonical p53 signaling to promote invasion
It has been known for a number of years that mutated "inactive" p53 proteins still capable of binding to DNA per se, can bind to DNA sequences that are non-canonical for p53, with for example, a resultant increase in the transcription and expression of growth factor receptors such as ERBB1, (1)(,) (2) i.e., mutation of p53 not merely results in "no p53 function" but in fact results in "oncogeni...
متن کاملMitotic Kinases and p53 Signaling
Mitosis is tightly regulated and any errors in this process often lead to aneuploidy, genomic instability, and tumorigenesis. Deregulation of mitotic kinases is significantly associated with improper cell division and aneuploidy. Because of their importance during mitosis and the relevance to cancer, mitotic kinase signaling has been extensively studied over the past few decades and, as a resul...
متن کاملp53-Dependent Transcriptional Responses to Interleukin-3 Signaling
p53 is critical in the normal response to a variety of cellular stresses including DNA damage and loss of p53 function is a common feature of many cancers. In hematological malignancies, p53 deletion is less common than in solid malignancies but is associated with poor prognosis and resistance to chemotherapy. Compared to their wild-type (WT) counterparts, hematopoietic progenitor cells lacking...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cell
سال: 1998
ISSN: 0092-8674
DOI: 10.1016/s0092-8674(00)81774-2