ArticleNeoplasia (New York, N.Y.)
An N-terminal region of mot-2 binds to p53 in vitro.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 64 citations in OpenAlex.
- Synthetic Small Molecule Modulators of Hsp70 and Hsp40 Chaperones as Promising Anticancer Agents.International journal of molecular sciences · 2023Review
- The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022Review
- Identification of a new member of Mortaparib class of inhibitors that target mortalin and PARP1.Frontiers in cell and developmental biology · 2022Article
- Abrogating the Interaction Between p53 and Mortalin (Grp75/HSPA9/mtHsp70) for Cancer Therapy: The Story so far.Frontiers in cell and developmental biology · 2022Review
- Comparative computational and experimental analyses of some natural small molecules to restore transcriptional activation function of p53 in cancer cells harbouring wild type and p53Current research in structural biology · 2022Article
- Experimental Evidence for Therapeutic Potentials of Propolis.Nutrients · 2021Review
- Identification and Characterization of MortaparibCancers · 2021Article
- Wild type p53 function in p53Journal of experimental & clinical cancer research : CR · 2019Article
- Structural studies of UBXN2A and mortalin interaction and the putative role of silenced UBXN2A in preventing response to chemotherapy.Cell stress & chaperones · 2016Article
- Selective Mitochondrial Uptake of MKT-077 Can Suppress Medullary Thyroid Carcinoma Cell Survival In Vitro and In Vivo.Endocrinology and metabolism (Seoul, Korea) · 2015Article
- Reduced levels of Hspa9 attenuate Stat5 activation in mouse B cells.Experimental hematology · 2015Article
- Crystal structure of the nucleotide-binding domain of mortalin, the mitochondrial Hsp70 chaperone.Protein science : a publication of the Protein Society · 2014Article
- Ubiquitin-like (UBX)-domain-containing protein, UBXN2A, promotes cell death by interfering with the p53-Mortalin interactions in colon cancer cells.Cell death & disease · 2014Article
- Targeting GRP75 improves HSP90 inhibitor efficacy by enhancing p53-mediated apoptosis in hepatocellular carcinoma.PloS one · 2014Article
- Resveratrol protects DAergic PC12 cells from high glucose-induced oxidative stress and apoptosis: effect on p53 and GRP75 localization.Neurotoxicity research · 2014Article
- Aurora kinase-A inactivates DNA damage-induced apoptosis and spindle assembly checkpoint response functions of p73.Cancer cell · 2012Article
- Differential activities of the two closely related withanolides, Withaferin A and Withanone: bioinformatics and experimental evidences.PloS one · 2012Article
- Uptake rate of cationic mitochondrial inhibitor MKT-077 determines cellular oxygen consumption change in carcinoma cells.PloS one · 2012Article
- Knockdown of Hspa9, a del(5q31.2) gene, results in a decrease in hematopoietic progenitors in mice.Blood · 2011Article
- Cloning, characterization, and functional studies of a human 40-kDa catecholamine-regulated protein: implications in central nervous system disorders.Cell stress & chaperones · 2009Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mouse mot-2 protein was earlier shown to bind to the tumor suppressor protein, p53. The mot-2 binding site of p53 was mapped to C-terminal amino acid residues 312-352, which includes the cytoplasmic sequestration domain. In the present study, we have found that both mot-1 and mot-2 bind to p53 in vitro. By using His-tagged deletion mutant proteins, the p53-binding domain of mot-2 was mapped to its N-terminal amino acid residues 253-282, which are identical in mot-1 and mot-2 proteins. Some peptides containing the p53-binding region of mot-2 were able to compete with the full-length protein for p53 binding. The data provided rationale for in vitro binding of mot-1 and mot-2 proteins to p53 and supported the conclusion that inability of mot-1 protein to bind p53 in vivo depends on secondary structure or its binding to other cellular factors. Most interestingly, the p53-binding region of mot-2 was common to its MKT-077, a cationic dye that exhibits antitumor activity, binding region. Therefore it is most likely that MKT-077-induced nuclear translocation and restoration of wild-type p53 function in transformed cells takes place by a competitional mechanism.
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