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Tumor protein p73

p73, TP73
This gene encodes a member of the p53 family of transcription factors involved in cellular responses to stress and development. It maps to a region on chromosome 1p36 that is frequently deleted in neuroblastoma and other tumors, and thought to contain multiple tumor suppressor genes. The demonstration that this gene is monoallelically expressed (likely from the maternal allele), supports the notion that it is a candidate gene for neuroblastoma. Many transcript variants resulting from alternative splicing and/or use of alternate promoters have been found for this gene, but the biological validity and the full-length nature of some variants have not been determined. [provided by RefSeq, Feb 2011] (from NCBI)
Top mentioned proteins: p53, p63, CAN, V1a, p21
Papers using p73 antibodies
DNA damage-dependent acetylation of p73 dictates the selective activation of apoptotic target genes.
Gao Shou-Jiang, In PLoS Pathogens, 2001
... antibodies reactive to E2F1 (C-20), Apaf-1 (H-324), Cyclin E (M-20) Ubiquitin (FL-76); goat polyclonal antibody against p73 (S-20); and mouse monoclonal antibodies against PARP1 (F-2) and GFP (F56-BA1) were obtained from Santa Cruz Biotechnology, Inc ...
Papers on p73
Small molecule prodigiosin restores p53 tumor suppressor activity in chemoresistant colorectal cancer stem cells via c-Jun-mediated ΔNp73 inhibition and p73 activation.
El-Deiry et al., Penn Hills, United States. In Cancer Res, Feb 2016
In contrast, p53 family member p73 is rarely mutated in CRC, and p73 activation elicits p53-like tumor suppression.
Impact of Polymorphic Variations of Gemcitabine Metabolism, DNA Damage Repair, and Drug Resistance Genes on the Effect of High-Dose Chemotherapy for Relapsed or Refractory Lymphoid Malignancies.
Nieto et al., Houston, United States. In Biol Blood Marrow Transplant, Jan 2016
EXPERIMENTAL DESIGN: We evaluated 21 germline SNPs of the gemcitabine metabolism genes CDA, dCK, and hCNT3, DNA damage repair genes RECQL, XRCC1, RAD54L, ATM, ATR, MLH1, MSH2, MSH3, TREX1, EXO1, and TP73, and multidrug resistance genes MRP2 and MRP5, as well as glutathione-S-transferase GSTP1 in 153 patients with relapsed or refractory lymphoma or myeloma receiving Gem/Bu/Mel.
p73 - a positive or negative regulator of angiogenesis, or both?
Sabapathy, Singapore, Singapore. In Mol Cell Biol, Jan 2016
UNASSIGNED: The role of p73, the homologue of the tumor suppressor p53, in regulating angiogenesis has recently been extensively investigated, resulting in the publication of five articles.
DNA repair and aging: the impact of the p53 family.
Raschellà et al., Roma, Italy. In Aging (albany Ny), Jan 2016
Among the key factors of the DDR, the related proteins p53, p63 and p73, all belonging to the same family of transcription factors, play multiple relevant roles.
Novel therapeutic interventions for p53-altered tumors through manipulation of its family members, p63 and p73.
Flores et al., Houston, United States. In Cell Cycle, Jan 2016
We utilized the p53-family members, p63 and p73, which are not frequently mutated in cancer, to treat p53-defective cancers.
Integrated molecular analysis of adult T cell leukemia/lymphoma.
Ogawa et al., Kyoto, Japan. In Nat Genet, Nov 2015
We also discovered frequent intragenic deletions involving IKZF2, CARD11 and TP73 and mutations in GATA3, HNRNPA2B1, GPR183, CSNK2A1, CSNK2B and CSNK1A1.
Comprehensive genomic profiles of small cell lung cancer.
Thomas et al., Köln, Germany. In Nature, Sep 2015
We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Δex2/3.
Association of p73 G4C14-to-A4T14 polymorphism with non-small cell lung cancer risk.
Tang et al., Zhuzhou, China. In Oncol Lett, Aug 2015
UNASSIGNED: The p73 gene is a structural and functional homolog of the p53 gene, which has a crucial role in mediating cell cycle arrest and apoptosis.
TBCRC009: A Multicenter Phase II Clinical Trial of Platinum Monotherapy With Biomarker Assessment in Metastatic Triple-Negative Breast Cancer.
Ellisen et al., Danvers, United States. In J Clin Oncol, Jul 2015
Coprimary end points were objective response rate (RR) and response prediction by p63/p73 gene expression.
IAPP-driven metabolic reprogramming induces regression of p53-deficient tumours in vivo.
Flores et al., Houston, United States. In Nature, Mar 2015
This strategy has proven difficult to implement therapeutically, and here we examine an alternative strategy by manipulating the p53 family members, Tp63 and Tp73 (also known as p63 and p73, respectively).
Neuroblastoma: oncogenic mechanisms and therapeutic exploitation of necroptosis.
Raschellà et al., Roma, Italy. In Cell Death Dis, 2014
In this short review, we will discuss the most relevant genomic rearrangements that define high-risk NB and the role that destabilization of p53 and p73 can have in NB aggressiveness.
ASPP and iASPP: Implication in cancer development and progression.
Sarkar et al., Detroit, United States. In Cell Mol Biol (noisy-le-grand), 2014
By binding to apoptosis regulating proteins such as p53, p63, p73, Bcl—2, NF—κB p65, etc., ASPP1 and ASPP2 promote apoptosis while overexpression of iASPP inhibits apoptotic cell death typically after DNA damage.
P63 in health and cancer.
Iannizzotto et al., Roma, Italy. In Int J Dev Biol, 2014
The p53 family comprises three transcription factors (p53/p63/p73).
Role of heme oxygenase-1 in demethylating effects on SKM-1 cells induced by decitabine.
Fang et al., Guiyang, China. In Genet Mol Res, 2014
The expressions of p16, p15, TP73, CDH1, ESR1, and PDLIM4 mRNAs were detected by real-time PCR, and those of HO-1, DNMT1, DNMT3A, DNMT3B, HDAC, and p15 proteins were measured by western blot.
Mutant p53 drives pancreatic cancer metastasis through cell-autonomous PDGF receptor β signaling.
Lowe et al., United States. In Cell, 2014
Mutant p53 induced PDGFRb through a cell-autonomous mechanism involving inhibition of a p73/NF-Y complex that represses PDGFRb expression in p53-deficient, noninvasive cells.
Transcription factors Sp1 and p73 control the expression of the proapoptotic protein NOXA in the response of testicular embryonal carcinoma cells to cisplatin.
Fernandez-Luna et al., Santander, Spain. In J Biol Chem, 2012
detailed analysis of the Noxa promoter revealed that p73 and Sp1-like factors, Sp1 and KLF6, played key roles in the transcriptional control of this gene
iASPP inhibits p53-independent apoptosis by inhibiting transcriptional activity of p63/p73 on promoters of proapoptotic genes.
Liu et al., Chongqing, China. In Apoptosis, 2012
iASPP inhibited apoptosis independently of p53 in tumor cells, mainly by inhibiting the transcriptional activity of p63/p73 on the promoters of proapoptotic genes
p73 expression is regulated by RNPC1, a target of the p53 family, via mRNA stability.
Chen et al., Davis, United States. In Mol Cell Biol, 2012
knockdown of p73 or p21, another target of RNPC1, attenuates the inhibitory effect of RNPC1 on cell proliferation and premature senescence, whereas combined knockdown of p73 and p21 completely abolishes it
Tumor suppressors p53, p63TAα, p63TAy, p73α, and p73β use distinct pathways to repress telomerase expression.
Nicot et al., Kansas City, United States. In J Biol Chem, 2012
Tumor suppressors p53, p63TAalpha, p63TAy, p73alpha, and p73beta use distinct pathways to repress telomerase expression.
Association of combined p73 and p53 genetic variants with tumor HPV16-positive oropharyngeal cancer.
Li et al., Houston, United States. In Plos One, 2011
findings suggest that variant genotypes of p53 and p73 genes may be individually, or more likely jointly, associated with tumor HPV16-positive oropharyngeal cancer patients, particularly in never smokers
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