All Relations between apoptosis and p53

Publication Sentence Publish Date Extraction Date Species
Nathan P Gomes, Joaquín M Espinos. Disparate chromatin landscapes and kinetics of inactivation impact differential regulation of p53 target genes. Cell cycle (Georgetown, Tex.). vol 9. issue 17. 2011-01-24. PMID:20818159. the p53 transcription factor regulates the expression of genes involved in cellular responses to stress, including cell cycle arrest and apoptosis. 2011-01-24 2023-08-12 Not clear
Wen-bin Zhang, Zhuo Wang, Fei Shu, Yong-hua Jin, Hong-yi Liu, Qiu-juan Wang, Yong Yan. Activation of AMP-activated protein kinase by temozolomide contributes to apoptosis in glioblastoma cells via p53 activation and mTORC1 inhibition. The Journal of biological chemistry. vol 285. issue 52. 2011-01-24. PMID:20880848. activation of amp-activated protein kinase by temozolomide contributes to apoptosis in glioblastoma cells via p53 activation and mtorc1 inhibition. 2011-01-24 2023-08-12 human
Wen-bin Zhang, Zhuo Wang, Fei Shu, Yong-hua Jin, Hong-yi Liu, Qiu-juan Wang, Yong Yan. Activation of AMP-activated protein kinase by temozolomide contributes to apoptosis in glioblastoma cells via p53 activation and mTORC1 inhibition. The Journal of biological chemistry. vol 285. issue 52. 2011-01-24. PMID:20880848. our study suggests that activation of ampk by tmz contributes to glioblastoma cell apoptosis, probably by promoting p53 activation and inhibiting mtorc1 signaling. 2011-01-24 2023-08-12 human
Jeng-Yuan Yao, Jan-Kan Che. TAp63 plays compensatory roles in p53-deficient cancer cells under genotoxic stress. Biochemical and biophysical research communications. vol 403. issue 3-4. 2011-01-20. PMID:21075072. p53 is involved in many anti-cancer mechanisms, such as cell cycle regulation, apoptosis, and the maintenance of genomic integrity. 2011-01-20 2023-08-12 Not clear
Natsumi Kubo, Rintaro Okoshi, Kumiko Nakashima, Osamu Shimozato, Akira Nakagawara, Toshinori Ozak. MDM2 promotes the proteasomal degradation of p73 through the interaction with Itch in HeLa cells. Biochemical and biophysical research communications. vol 403. issue 3-4. 2011-01-20. PMID:21093410. during adriamycin (adr)-mediated apoptosis, p53 and p73 were induced to stabilize in association with a significant reduction of mdm2 and itch, suggesting that, in addition to itch, mdm2 could also be involved in the stability control of p73. 2011-01-20 2023-08-12 Not clear
Julie Roy, Pragathi Pallepati, Ahmed Bettaieb, Diana A Averill-Bate. Acrolein induces apoptosis through the death receptor pathway in A549 lung cells: role of p53. Canadian journal of physiology and pharmacology. vol 88. issue 3. 2011-01-18. PMID:20393600. acrolein induces apoptosis through the death receptor pathway in a549 lung cells: role of p53. 2011-01-18 2023-08-12 human
Julie Roy, Pragathi Pallepati, Ahmed Bettaieb, Diana A Averill-Bate. Acrolein induces apoptosis through the death receptor pathway in A549 lung cells: role of p53. Canadian journal of physiology and pharmacology. vol 88. issue 3. 2011-01-18. PMID:20393600. this study shows that p53 is an initiating factor in acrolein-induced death receptor activation during apoptosis in a549 human lung cells. 2011-01-18 2023-08-12 human
Julie Roy, Pragathi Pallepati, Ahmed Bettaieb, Diana A Averill-Bate. Acrolein induces apoptosis through the death receptor pathway in A549 lung cells: role of p53. Canadian journal of physiology and pharmacology. vol 88. issue 3. 2011-01-18. PMID:20393600. activation of p53 and increased expression of p53-upregulated modulator of apoptosis (puma) occurred in response to acrolein. 2011-01-18 2023-08-12 human
Mark Band, Osnat Ashur-Fabian, Aaron Aviv. The expression of p53-target genes in the hypoxia-tolerant subterranean mole-rat is hypoxia-dependent and similar to expression patterns in solid tumors. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703075. the tumor suppressor gene, p53, in response to dna damage/hypoxia, induces growth arrest and/or apoptosis. 2011-01-18 2023-08-12 human
Mark Band, Osnat Ashur-Fabian, Aaron Aviv. The expression of p53-target genes in the hypoxia-tolerant subterranean mole-rat is hypoxia-dependent and similar to expression patterns in solid tumors. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703075. moreover, cells transfected with human p53 underwent more extensive apoptosis (44.8%) as compared to spalax p53 (23.2%) transfected cells. 2011-01-18 2023-08-12 human
Mark Band, Osnat Ashur-Fabian, Aaron Aviv. The expression of p53-target genes in the hypoxia-tolerant subterranean mole-rat is hypoxia-dependent and similar to expression patterns in solid tumors. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703075. we conclude that, similar to our previous in-vitro work, two parallel hypoxia-adaptive mechanisms evolved in spalax: mutated p53 and p53 response element leading to a bias against apoptosis and increased mdm2, which are analogous to observations in tumor development. 2011-01-18 2023-08-12 human
Dorothy Lo, Hua L. Nucleostemin: Another nucleolar "Twister" of the p53-MDM2 loop. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703089. several nucleolar proteins, such as arf, ribosomal protein (rp) l5, l11, l23 and s7, have been shown to induce p53 activation by inhibiting mdm2 e3 ligase activity and consequently to trigger cell cycle arrest and/or apoptosis. 2011-01-18 2023-08-12 Not clear
Omid Tavana, Cara L Benjamin, Nahum Puebla-Osorio, Mei Sang, Stephen E Ullrich, Honnavara N Ananthaswamy, Chengming Zh. Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703098. genotoxic stress triggers the p53 tumor suppressor network to activate cellular responses that lead to cell cycle arrest, dna repair, apoptosis or senescence. 2011-01-18 2023-08-12 mouse
Omid Tavana, Cara L Benjamin, Nahum Puebla-Osorio, Mei Sang, Stephen E Ullrich, Honnavara N Ananthaswamy, Chengming Zh. Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703098. this network functions mainly through transactivation of different downstream targets, including cell cycle inhibitor p21, which is required for short-term cell cycle arrest or long-term cellular senescence, or proapoptotic genes such as p53 upregulated modulator of apoptosis (puma) and noxa. 2011-01-18 2023-08-12 mouse
Omid Tavana, Cara L Benjamin, Nahum Puebla-Osorio, Mei Sang, Stephen E Ullrich, Honnavara N Ananthaswamy, Chengming Zh. Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703098. in this study, we found that mice harboring a hypomorphic mutant p53, r172p, a mutation that abrogates p53-mediated apoptosis while keeping cell cycle control mostly intact, are more susceptible to ultraviolet-b (uvb)-induced skin damage, inflammation and immunosuppression than wild-type mice. 2011-01-18 2023-08-12 mouse
Omid Tavana, Cara L Benjamin, Nahum Puebla-Osorio, Mei Sang, Stephen E Ullrich, Honnavara N Ananthaswamy, Chengming Zh. Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703098. p53(r172p) embryonic fibroblasts (mefs) are hypersensitive to uvb and prematurely senesce after uvb exposure, in stark contrast to wild-type mefs, which undergo apoptosis. 2011-01-18 2023-08-12 mouse
Omid Tavana, Cara L Benjamin, Nahum Puebla-Osorio, Mei Sang, Stephen E Ullrich, Honnavara N Ananthaswamy, Chengming Zh. Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence. Cell cycle (Georgetown, Tex.). vol 9. issue 16. 2011-01-18. PMID:20703098. importantly, p53(r172p) mefs failed to downregulate anti-apoptotic protein bcl-2, which has been shown to play an important role in p53-dependent apoptosis. 2011-01-18 2023-08-12 mouse
Giovanna D'Onofrio, Filomena Tramontano, Annalisa Susanna Dorio, Alessia Muzi, Valeria Maselli, Domenico Fulgione, Grazia Graziani, Maria Malanga, Piera Quesad. Poly(ADP-ribose) polymerase signaling of topoisomerase 1-dependent DNA damage in carcinoma cells. Biochemical pharmacology. vol 81. issue 2. 2011-01-18. PMID:20875401. furthermore, tpt-dependent induction of p53, p21 and apoptosis were found 24-72h after treatment and were increased by pj34 both in parp-1 proficient and silenced cells. 2011-01-18 2023-08-12 Not clear
Reza Behjati, Koji Kawai, Yukinori Inadome, Junko Kano, Hideyuki Akaza, Masayuki Noguch. APAF-1 is related to an undifferentiated state in the testicular germ cell tumor pathway. Cancer science. vol 102. issue 1. 2011-01-18. PMID:20977544. apoptotic protease activating factor-1 (apaf-1) is a key regulator gene of apoptosis, located downstream from p53. 2011-01-18 2023-08-12 Not clear
Yuguang Zhao, Yi Tan, Junying Dai, Bing Li, Luping Guo, Jiuwei Cui, Guanjun Wang, Xue Shi, Xiang Zhang, Nicholas Mellen, Wei Li, Lu Ca. Exacerbation of diabetes-induced testicular apoptosis by zinc deficiency is most likely associated with oxidative stress, p38 MAPK activation, and p53 activation in mice. Toxicology letters. vol 200. issue 1-2. 2011-01-18. PMID:21078376. exacerbation of diabetes-induced testicular apoptosis by zinc deficiency is most likely associated with oxidative stress, p38 mapk activation, and p53 activation in mice. 2011-01-18 2023-08-12 mouse