Skip to search form
Skip to main content
Skip to account menu
Semantic Scholar
Semantic Scholar's Logo
Search 217,275,347 papers from all fields of science
Search
Sign In
Create Free Account
p73 protein, human
Known as:
p53-Like Transcription Factor
, P73
, p53-Related Protein
Expand
Tumor protein p73 (636 aa, ~70 kDa) is encoded by the human TP73 gene. This protein is involved in the regulation of transcription, DNA damage…
Expand
National Institutes of Health
Create Alert
Alert
Related topics
Related topics
13 relations
ATM Signaling Pathway
Apoptosis Promoter
DNA-Binding Proteins
Genes, Regulator
Expand
Broader (2)
TRANSCRIPTION FACTOR
tumor suppressor protein p73
Papers overview
Semantic Scholar uses AI to extract papers important to this topic.
Highly Cited
2014
Highly Cited
2014
Identification of distinct basal and luminal subtypes of muscle-invasive bladder cancer with different sensitivities to frontline chemotherapy.
W. Choi
,
S. Porten
,
+17 authors
D. McConkey
Cancer Cell
2014
Corpus ID: 26997111
Review
2004
Review
2004
p63 and p73: roles in development and tumor formation.
U. Moll
,
N. Slade
Molecular Cancer Research
2004
Corpus ID: 13094677
The tumor suppressor p53 is critically important in the cellular damage response and is the founding member of a family of…
Expand
Highly Cited
2003
Highly Cited
2003
Akt phosphorylates the Yes-associated protein, YAP, to induce interaction with 14-3-3 and attenuation of p73-mediated apoptosis.
S. Basu
,
N. Totty
,
M. Irwin
,
M. Sudol
,
J. Downward
Molecules and Cells
2003
Corpus ID: 38691695
Highly Cited
2002
Highly Cited
2002
p63 and p73 are required for p53-dependent apoptosis in response to DNA damage
E. Flores
,
K. Tsai
,
+4 authors
T. Jacks
Nature
2002
Corpus ID: 4408567
The tumour-suppressor gene p53 is frequently mutated in human cancers and is important in the cellular response to DNA damage…
Expand
Highly Cited
2000
Highly Cited
2000
Role for the p53 homologue p73 in E2F-1-induced apoptosis
M. Irwin
,
M. Marin
,
+8 authors
W. Kaelin
Nature
2000
Corpus ID: 205009583
The transcription factor E2F-1 induces both cell-cycle progression and, in certain settings, apoptosis. E2F-1 uses both p53…
Expand
Review
2000
Review
2000
The p53/p63/p73 family of transcription factors: overlapping and distinct functions.
M. Levrero
,
V. Laurenzi
,
A. Costanzo
,
J. Gong
,
J. Wang
,
G. Melino
Journal of Cell Science
2000
Corpus ID: 7466726
The p53 gene is the most frequently mutated gene in human cancer. The identification of two homologues, p63 and p73, revealed…
Expand
Highly Cited
2000
Highly Cited
2000
p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours
A. Yang
,
N. Walker
,
+9 authors
D. Caput
Nature
2000
Corpus ID: 4428591
p73 (ref. 1) has high homology with the tumour suppressor p53 (refs 2,3,4), as well as with p63, a gene implicated in the…
Expand
Highly Cited
1999
Highly Cited
1999
The tyrosine kinase c-Abl regulates p73 in apoptotic response to cisplatin-induced DNA damage
J. Gong
,
A. Costanzo
,
+4 authors
Jean Y. J. Wang
Nature
1999
Corpus ID: 4384959
Cancer chemotherapeutic agents such as cisplatin exert their cytotoxic effect by inducing DNA damage and activating programmed…
Expand
Highly Cited
1999
Highly Cited
1999
p73 Function Is Inhibited by Tumor-Derived p53 Mutants in Mammalian Cells
C. J. Di Como
,
C. Gaiddon
,
C. Prives
Molecular and Cellular Biology
1999
Corpus ID: 12151078
ABSTRACT The p53 tumor suppressor protein, found mutated in over 50% of all human tumors, is a sequence-specific transcriptional…
Expand
Highly Cited
1997
Highly Cited
1997
p73 is a human p53-related protein that can induce apoptosis
C. A. Jost
,
M. Marin
,
W. Kaelin
Nature
1997
Corpus ID: 205026418
The protein p53 is the most frequently mutated tumour suppressor to be identified so far in human cancers,. The ability of p53 to…
Expand
By clicking accept or continuing to use the site, you agree to the terms outlined in our
Privacy Policy
(opens in a new tab)
,
Terms of Service
(opens in a new tab)
, and
Dataset License
(opens in a new tab)
ACCEPT & CONTINUE