| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Karina J Matissek, Mohanad Mossalam, Abood Okal, Carol S Li. The DNA binding domain of p53 is sufficient to trigger a potent apoptotic response at the mitochondria. Molecular pharmaceutics. vol 10. issue 10. 2014-05-22. PMID:23968395. |
the tumor suppressor p53 is one of the most studied proteins in human cancer.1-3 while nuclear p53 has been utilized for cancer gene therapy, mitochondrial targeting of p53 has not been fully exploited to date.4,5 in response to cellular stress, p53 translocates to the mitochondria and directly interacts with bcl-2 family proteins including antiapoptotic bcl-xl and bcl-2 and proapoptotic bak and bax.6 antiapoptotic bcl-xl forms inhibitory complexes with proapoptotic bak and bax preventing their homo-oligomerization.7 upon translocation to the mitochondria, p53 binds to bcl-xl, releases bak and bax from the inhibitory complex and enhances their homo-oligomerization.8 bak and bax homotetramer formation disrupts the mitochondrial outer membrane, releases antiapoptotic factors such as cytochrome c and triggers a rapid apoptotic response mediated by caspase induction.9 it is still unclear if the mdm2 binding domain (mbd), the proline-rich domain (prd) and/or dna binding domain (dbd) of p53 are the domains responsible for interaction with bcl-xl.10-17 the purpose of this work is to determine if a smaller functional domain of p53 is capable of inducing apoptosis similarly to full length p53. |
2014-05-22 |
2023-08-12 |
human |
| Karina J Matissek, Mohanad Mossalam, Abood Okal, Carol S Li. The DNA binding domain of p53 is sufficient to trigger a potent apoptotic response at the mitochondria. Molecular pharmaceutics. vol 10. issue 10. 2014-05-22. PMID:23968395. |
taken together, our data demonstrates for the first time that the dbd of p53 may be the minimally necessary domain for achieving apoptosis at the mitochondria in multiple cell lines. |
2014-05-22 |
2023-08-12 |
human |
| Larisa Pereboeva, Erik Westin, Toral Patel, Ian Flaniken, Lawrence Lamb, Aloysius Klingelhutz, Frederick Goldma. DNA damage responses and oxidative stress in dyskeratosis congenita. PloS one. vol 8. issue 10. 2014-05-22. PMID:24124565. |
apoptosis and reactive oxygen species (ros) were assessed by flow cytometry, and western blotting was used to measure expression of dna damage response (ddr) proteins, including total p53, p53s15, and p21(waf). |
2014-05-22 |
2023-08-12 |
human |
| Zhe Cheng, Huimin Tian, Hongran Chu, Jianjian Wu, Yingying Li, Yanhai Wan. The effect of tributyltin chloride on Caenorhabditis elegans germline is mediated by a conserved DNA damage checkpoint pathway. Toxicology letters. vol 225. issue 3. 2014-05-21. PMID:24445071. |
this apoptotic response was blocked in loss-of-function mutants of hus-1 (op241), mrt-2 (e2663) and p53/cep-1 (gk138), indicating that checkpoints and p53 are essential for mediating tbtcl-induced germ cell apoptosis. |
2014-05-21 |
2023-08-12 |
caenorhabditis_elegans |
| Wei Qiang, Tianbo Jin, Qi Yang, Wei Liu, Shu Liu, Meiju Ji, Nongyue He, Chao Chen, Bingyin Shi, Peng Ho. PRIMA-1 selectively induces global DNA demethylation in p53 mutant-type thyroid cancer cells. Journal of biomedical nanotechnology. vol 10. issue 7. 2014-05-21. PMID:24804545. |
the p53 tumor suppressor pathway blocks carcinogenesis by triggering apoptosis and cellular senescence in response to oncogenic stress. |
2014-05-21 |
2023-08-13 |
human |
| Wei Qiang, Tianbo Jin, Qi Yang, Wei Liu, Shu Liu, Meiju Ji, Nongyue He, Chao Chen, Bingyin Shi, Peng Ho. PRIMA-1 selectively induces global DNA demethylation in p53 mutant-type thyroid cancer cells. Journal of biomedical nanotechnology. vol 10. issue 7. 2014-05-21. PMID:24804545. |
recently, the identification of mutant p53-reactivating small molecules such as prima-1 (p53 reactivation and induction of massive apoptosis) renders possibilities for the development of more efficient anticancer drugs. |
2014-05-21 |
2023-08-13 |
human |
| Noriko Kobayashi, Mohammadreza Abedini, Noriaki Sakuragi, Benjamin K Tsan. PRIMA-1 increases cisplatin sensitivity in chemoresistant ovarian cancer cells with p53 mutation: a requirement for Akt down-regulation. Journal of ovarian research. vol 6. 2014-05-20. PMID:23351152. |
since ovarian cancer is associated with high frequency of p53 mutation, the availability of p53 reactivation and induction of massive apoptosis (prima-1) offers a possible new therapeutic strategy for overcoming this devastating disease. |
2014-05-20 |
2023-08-12 |
Not clear |
| Kai Liu, Jinli Lou, Tao Wen, Jiming Yin, Bin Xu, Wei Ding, Anna Wang, Daojie Liu, Chao Zhang, Dexi Chen, Ning L. Depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either DRAM-induced autophagy or BAX. Liver international : official journal of the International Association for the Study of the Liver. vol 33. issue 10. 2014-05-19. PMID:23875779. |
depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either dram-induced autophagy or bax. |
2014-05-19 |
2023-08-12 |
Not clear |
| Kai Liu, Jinli Lou, Tao Wen, Jiming Yin, Bin Xu, Wei Ding, Anna Wang, Daojie Liu, Chao Zhang, Dexi Chen, Ning L. Depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either DRAM-induced autophagy or BAX. Liver international : official journal of the International Association for the Study of the Liver. vol 33. issue 10. 2014-05-19. PMID:23875779. |
apoptosis mediated by p53 plays a pathological role in the progression of hepatosteatosis. |
2014-05-19 |
2023-08-12 |
Not clear |
| Kai Liu, Jinli Lou, Tao Wen, Jiming Yin, Bin Xu, Wei Ding, Anna Wang, Daojie Liu, Chao Zhang, Dexi Chen, Ning L. Depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either DRAM-induced autophagy or BAX. Liver international : official journal of the International Association for the Study of the Liver. vol 33. issue 10. 2014-05-19. PMID:23875779. |
it is noteworthy that p53 can promote the expression of damage-regulated autophagy modulator (dram), an inducer of autophagy-mediated apoptosis. |
2014-05-19 |
2023-08-12 |
Not clear |
| Kai Liu, Jinli Lou, Tao Wen, Jiming Yin, Bin Xu, Wei Ding, Anna Wang, Daojie Liu, Chao Zhang, Dexi Chen, Ning L. Depending on the stage of hepatosteatosis, p53 causes apoptosis primarily through either DRAM-induced autophagy or BAX. Liver international : official journal of the International Association for the Study of the Liver. vol 33. issue 10. 2014-05-19. PMID:23875779. |
this study aimed to examine how p53 orchestrates autophagy and apoptosis to affect hepatosteatosis. |
2014-05-19 |
2023-08-12 |
Not clear |
| Sascha Venturelli, Alexander Berger, Timo Weiland, Frank Essmann, Michaela Waibel, Tina Nuebling, Sabine Häcker, Martin Schenk, Klaus Schulze-Osthoff, Helmut R Salih, Simone Fulda, Bence Sipos, Ricky W Johnstone, Ulrich M Lauer, Michael Bitze. Differential induction of apoptosis and senescence by the DNA methyltransferase inhibitors 5-azacytidine and 5-aza-2'-deoxycytidine in solid tumor cells. Molecular cancer therapeutics. vol 12. issue 10. 2014-05-19. PMID:23924947. |
in contrast, 5-aza-cr downregulated p53, induced caspase activation and apoptosis. |
2014-05-19 |
2023-08-12 |
human |
| Chae Won Kim, Jing Nan Lu, Se-Il Go, Ji Hyun Jung, Sang Mi Yi, Jae-Hoon Jeong, Young-Sool Hah, Myung Shin Han, Jeong Woo Park, Won Sup Lee, Young Joo Mi. p53 restoration can overcome cisplatin resistance through inhibition of Akt as well as induction of Bax. International journal of oncology. vol 43. issue 5. 2014-05-19. PMID:23970333. |
the induction of wild-type p53 can enhance cddp-induced apoptosis not only by inducing bax protein but also by suppressing anti-apoptotic proteins through inhibition of akt. |
2014-05-19 |
2023-08-12 |
Not clear |
| Chae Won Kim, Jing Nan Lu, Se-Il Go, Ji Hyun Jung, Sang Mi Yi, Jae-Hoon Jeong, Young-Sool Hah, Myung Shin Han, Jeong Woo Park, Won Sup Lee, Young Joo Mi. p53 restoration can overcome cisplatin resistance through inhibition of Akt as well as induction of Bax. International journal of oncology. vol 43. issue 5. 2014-05-19. PMID:23970333. |
in conclusion, this study suggests that the primary contributor to resistance to cddp in snu-16 cells may well be a failure of induction of apoptosis due to a lack of induction of pro-apoptotic proteins rather than suppression of anti-apoptotic proteins, and that restoration of p53 function can overcome the resistance to cddp not only by augmenting the pro-apoptotic drive through p53-mediated transcriptional activation but also by inhibiting the anti-apoptotic drive through inhibition of akt activity. |
2014-05-19 |
2023-08-12 |
Not clear |
| Masahiro Takahashi, Yuichi Kakudo, Shin Takahashi, Yasuhiro Sakamoto, Shunsuke Kato, Chikashi Ishiok. Overexpression of DRAM enhances p53-dependent apoptosis. Cancer medicine. vol 2. issue 1. 2014-05-19. PMID:24133622. |
till date, "super p53" mutants exhibiting more potent ability to induce apoptosis than wild-type p53 have been reported. |
2014-05-19 |
2023-08-12 |
human |
| Maija Pesonen, Merja Häkkinen, Kirsi Rilla, Risto Juvonen, Tapio Kuitunen, Markku Pasanen, Kirsi Vähäkanga. Chloropicrin-induced toxic responses in human lung epithelial cells. Toxicology letters. vol 226. issue 2. 2014-05-19. PMID:24548678. |
immunoblotting analysis revealed increases in the amount of four proteins (p53, p21, p27 and phospho-erk1/2) that are involved in dna-damage, cell cycle regulation and apoptosis. |
2014-05-19 |
2023-08-12 |
human |
| X Y Song, J F Hu, M N Sun, Z P Li, D H Wu, H J Ji, Y H Yuan, Z X Zhu, N Han, G Liu, N H Che. IMM-H004, a novel coumarin derivative compound, protects against amyloid beta-induced neurotoxicity through a mitochondrial-dependent pathway. Neuroscience. vol 242. 2014-05-16. PMID:23523945. |
further study indicated that imm-h004 significantly inhibited aβ-induced cytotoxicity and apoptosis by reversing aβ-induced mitochondrial dysfunction, including mmp (mitochondrial membrane potential) decrease, reactive oxygen species production, and mitochondrial release of cytochrome c. imm-h004 can regulate the interaction between bax and bcl-2, decreased levels of p53 and active caspase-3 protein induced by aβ25-35. |
2014-05-16 |
2023-08-12 |
Not clear |
| Gregory Azzam, Xuting Wang, Douglas Bell, Maureen E Murph. CSF1 is a novel p53 target gene whose protein product functions in a feed-forward manner to suppress apoptosis and enhance p53-mediated growth arrest. PloS one. vol 8. issue 9. 2014-05-16. PMID:24019961. |
csf1 is a novel p53 target gene whose protein product functions in a feed-forward manner to suppress apoptosis and enhance p53-mediated growth arrest. |
2014-05-16 |
2023-08-12 |
Not clear |
| Rana Elkholi, Jerry E Chipu. How do I kill thee? Let me count the ways: p53 regulates PARP-1 dependent necrosis. BioEssays : news and reviews in molecular, cellular and developmental biology. vol 36. issue 1. 2014-05-16. PMID:24323920. |
it appears that the p53 pathway is a central node for nearly all cell stress responses, including: gene expression, dna repair, cell cycle arrest, metabolic adjustments, apoptosis, and senescence. |
2014-05-16 |
2023-08-12 |
Not clear |
| K Kurokawa, Y Akaike, K Masuda, Y Kuwano, K Nishida, N Yamagishi, K Kajita, T Tanahashi, K Rokuta. Downregulation of serine/arginine-rich splicing factor 3 induces G1 cell cycle arrest and apoptosis in colon cancer cells. Oncogene. vol 33. issue 11. 2014-05-15. PMID:23503458. |
interestingly, selective knockdown of hipk2 fl induced apoptosis in various colon cancer cells expressing wild-type or mutated p53. |
2014-05-15 |
2023-08-12 |
Not clear |