PMID- 10203277
OWN - NLM
STAT- MEDLINE
DCOM- 19990420
LR  - 20190513
IS  - 0027-8874 (Print)
IS  - 0027-8874 (Linking)
VI  - 91
IP  - 7
DP  - 1999 Apr 7
TI  - The emerging p53 gene family.
PG  - 594-8
AB  - Perturbation of p53 protein function is a common, if not universal, finding in
      human cancer. Tumor suppression by p53 is due, at least in part, to its ability
      to activate transcription of certain genes involved in cell cycle control and
      apoptosis (programmed cell death). Two additional members of the mammalian p53
      family, p73 and p51, which is also known as p40, p63, KET, or p73L, were recently
      identified. Both of these proteins share substantial sequence homology with p53
      and can, at least when overproduced, activate p53-responsive promoters and induce
      apoptosis. Nonetheless, data on differences between these proteins and p53 are
      emerging. For example, p73 is not induced by DNA damage and is not targeted for
      inactivation by viral oncoproteins such as simian virus 40 (SV40) T antigen,
      adenovirus E1B 55K, and human papillomavirus E6. In contrast to p53, neither p73 
      nor p51 appears to be frequently mutated in human cancers on the basis of the
      limited studies reported to date. Finally, unlike p53, cells produce multiple p73
      and p51 isoforms as a result of alternative splicing, and production of p73 and
      p51 appears to be restricted to certain tissues. Additional studies are required 
      to determine the role, if any, that p73 and p51 play in cell growth control and
      carcinogenesis.
FAU - Kaelin, W G Jr
AU  - Kaelin WG Jr
AD  - Howard Hughes Medical Institute and Dana-Farber Cancer Institute and Harvard
      Medical School, Boston, MA 02115, USA. william_kaelin@dfci.harvard.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Natl Cancer Inst
JT  - Journal of the National Cancer Institute
JID - 7503089
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (TP63 protein, human)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Protein p73)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (p73 protein, human)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - DNA-Binding Proteins/genetics/*metabolism
MH  - *Genes, Tumor Suppressor
MH  - *Genes, p53/genetics
MH  - Humans
MH  - Neoplasms/*genetics/metabolism
MH  - Nuclear Proteins/genetics/*metabolism
MH  - *Phosphoproteins
MH  - *Trans-Activators
MH  - Transcription Factors
MH  - Tumor Protein p73
MH  - Tumor Suppressor Protein p53/genetics/*metabolism
MH  - Tumor Suppressor Proteins
RF  - 86
EDAT- 1999/04/15 02:02
MHDA- 2001/03/28 10:01
CRDT- 1999/04/15 02:02
PHST- 1999/04/15 02:02 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1999/04/15 02:02 [entrez]
AID - 10.1093/jnci/91.7.594 [doi]
PST - ppublish
SO  - J Natl Cancer Inst. 1999 Apr 7;91(7):594-8. doi: 10.1093/jnci/91.7.594.