Abstract
p53 controls crucial stress responses that play a major role in preventing malignant transformation. Hence, inactivation of p53 is the single most common genetic defect in human cancer. With the recent discovery of two close structural homologs, p63 en p73, we are getting a broader view of a fascinating gene family that links developmental biology with tumor biology. While unique roles are apparent for each of these genes, intimate biochemical cross-talk among family members suggests a functional network that might influence many different aspects of individual gene action. The most interesting part of this family network derives from the fact that the p63 and p73 genes are based on the 'two-genes-in-one' idea, encoding both agonist and antagonist in the same open reading frame. In this review, we attempt to present an overview of the current status of this fast moving field.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 47-59 |
| Number of pages | 13 |
| Journal | Biochimica et Biophysica Acta - Reviews on Cancer |
| Volume | 1552 |
| Issue number | 2 |
| DOIs | |
| State | Published - Dec 28 2001 |
| Externally published | Yes |
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Keywords
- Oncogene
- p53
- p63
- p73
- Transcription factor
- Tumor suppressor gene
ASJC Scopus subject areas
- Biophysics
- Cancer Research
- Oncology
Cite this
p53, p63 and p73 - Solos, alliances and feuds among family members. / Moll, Ute M.; Erster, Susan; Zaika, Alexander.
In: Biochimica et Biophysica Acta - Reviews on Cancer, Vol. 1552, No. 2, 28.12.2001, p. 47-59.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - p53, p63 and p73 - Solos, alliances and feuds among family members
AU - Moll, Ute M.
AU - Erster, Susan
AU - Zaika, Alexander
PY - 2001/12/28
Y1 - 2001/12/28
N2 - p53 controls crucial stress responses that play a major role in preventing malignant transformation. Hence, inactivation of p53 is the single most common genetic defect in human cancer. With the recent discovery of two close structural homologs, p63 en p73, we are getting a broader view of a fascinating gene family that links developmental biology with tumor biology. While unique roles are apparent for each of these genes, intimate biochemical cross-talk among family members suggests a functional network that might influence many different aspects of individual gene action. The most interesting part of this family network derives from the fact that the p63 and p73 genes are based on the 'two-genes-in-one' idea, encoding both agonist and antagonist in the same open reading frame. In this review, we attempt to present an overview of the current status of this fast moving field.
AB - p53 controls crucial stress responses that play a major role in preventing malignant transformation. Hence, inactivation of p53 is the single most common genetic defect in human cancer. With the recent discovery of two close structural homologs, p63 en p73, we are getting a broader view of a fascinating gene family that links developmental biology with tumor biology. While unique roles are apparent for each of these genes, intimate biochemical cross-talk among family members suggests a functional network that might influence many different aspects of individual gene action. The most interesting part of this family network derives from the fact that the p63 and p73 genes are based on the 'two-genes-in-one' idea, encoding both agonist and antagonist in the same open reading frame. In this review, we attempt to present an overview of the current status of this fast moving field.
KW - Oncogene
KW - p53
KW - p63
KW - p73
KW - Transcription factor
KW - Tumor suppressor gene
UR - http://www.scopus.com/inward/record.url?scp=0035966345&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035966345&partnerID=8YFLogxK
U2 - 10.1016/S0304-419X(01)00036-1
DO - 10.1016/S0304-419X(01)00036-1
M3 - Review article
C2 - 11825686
AN - SCOPUS:0035966345
VL - 1552
SP - 47
EP - 59
JO - Biochimica et Biophysica Acta - Reviews on Cancer
JF - Biochimica et Biophysica Acta - Reviews on Cancer
SN - 0304-419X
IS - 2
ER -