Results 11 to 20 of about 653,143 (286)

p53-Induced DNA Bending: The Interplay between p53−DNA and p53−p53 Interactions [PDF]

The Journal of Physical Chemistry B, 2008
Specific p53 binding-induced DNA bending and its underlying responsible forces are crucial for the understanding of selective transcription activation. Diverse p53-response elements exist in the genome; however, it is not known what determines the DNA bending and to what extent.
Yongping, Pan, Ruth, Nussinov
openaire   +2 more sources

Living with p53, Dying of p53 [PDF]

Cell, 2007
The p53 tumor suppressor protein acts as a major defense against cancer. Among its most distinctive features is the ability to elicit both apoptotic death and cell cycle arrest. In this issue of Cell, Das et al. (2007) and Tanaka et al. (2007) provide new insights into the mechanisms that dictate the life and death decisions of p53.
Aylon, Yael, Oren, Moshe
openaire   +2 more sources

p53 β-hydroxybutyrylation attenuates p53 activity [PDF]

Cell Death & Disease, 2019
Abstractp53 is an essential tumor suppressor, whose activity is finely tuned by the posttranslational modifications. Previous research has reported that β-hydroxybutyrate (BHB) induces β-hydroxybutyrylation (Kbhb), which is a novel histone posttranslational modification.
Kun Liu, Fangzhou Li, Qianqian Sun, Ning Lin, Haichao Han, Kaiqiang You, Feng Tian, Zebin Mao, Tingting Li, Tanjun Tong, Meiyu Geng, Yingming Zhao, Wei Gu, Wenhui Zhao   +13 more
openaire   +2 more sources

p53 α-Helix mimetics antagonize p53/MDM2 interaction and activate p53 [PDF]

Molecular Cancer Therapeutics, 2005
Abstract Overexpression or hyperactivation of MDM2 contributes to functional inactivation of wild-type p53 in nearly 50% of tumors. Inhibition of p53 by MDM2 depends on binding between an NH2-terminal (residues 16–28) p53 α-helical peptide and a hydrophobic pocket on MDM2, presenting an attractive target for development of inhibitors ...
Lihong, Chen, Hang, Yin, Bilal, Farooqi, Said, Sebti, Andrew D, Hamilton, Jiandong, Chen   +5 more
openaire   +2 more sources

p53 isoforms change p53 paradigm [PDF]

Molecular & Cellular Oncology, 2014
Although p53 defines cellular responses to cancer treatment it is not clear how p53 can be used to control cell fate outcome. Data demonstrate that so-called p53 does not exist as a single protein, but is in fact a group of p53 protein isoforms whose expression can be manipulated to control the cellular response to treatment.
openaire   +3 more sources

p53 isoforms can regulate p53 transcriptional activity [PDF]

Genes & Development, 2005
The recently discovered p53-related genes, p73 and p63, express multiple splice variants and N-terminally truncated forms initiated from an alternative promoter in intron 3. To date, no alternative promoter and multiple splice variants have been described for the p53 gene.
Bourdon, J C, Fernandes, K, Murray-Zmijewski, F, Liu, G, Diot, A, Xirodimas, D P, Saville, M K, Lane, David P.   +7 more
openaire   +3 more sources

USP11 regulates p53 stability by deubiquitinating p53 [PDF]

Journal of Zhejiang University SCIENCE B, 2014
The p53 tumor suppressor protein coordinates the cellular responses to a broad range of cellular stresses, leading to DNA repair, cell cycle arrest or apoptosis. The stability of p53 is essential for its tumor suppressor function, which is tightly controlled by ubiquitin-dependent degradation primarily through its negative regulator murine double ...
Jia-ying, Ke, Cong-jie, Dai, Wen-lin, Wu, Jin-hua, Gao, Ai-juan, Xia, Guang-ping, Liu, Kao-sheng, Lv, Chun-lin, Wu   +7 more
openaire   +2 more sources

Monitoring flux in signalling pathways through measurements of 4EBP1-mediated eIF4F complex assembly

BMC Biology, 2019
Background The most commonly occurring cancer mutations, including oncogenes such as MYC, Ras and PIK3C, are found in signal transductions pathways feeding into the translational machinery.
Yuri Frosi, Rachael Usher, Dawn Thean Gek Lian, David P. Lane, Christopher J. Brown   +4 more
doaj   +1 more source

The degradation of p53 and its major E3 ligase Mdm2 is differentially dependent on the proteasomal ubiquitin receptor S5a. [PDF]

, 2013
p53 and its major E3 ligase Mdm2 are both ubiquitinated and targeted to the proteasome for degradation. Despite the importance of this in regulating the p53 pathway, little is known about the mechanisms of proteasomal recognition of ubiquitinated p53 and
A Arlt, A Haririnia, A Hishiya, A Peth, A Sparks, AK Hock, AM Ruschak, AS Fatimababy, B Cross, C Brignone, C Wojcik, CF Cheok, D Finley, D Pei, EG Mimnaugh, G Lozano, GL Bond, H Fu, H Fu, H Higashitsuji, H Hiyama, H Inuzuka, H Inuzuka, H Kawahara, HT Kim, I Dikic, J Boehringer, J Das, J Hamazaki, JD Oliner, JD Shaughnessy Jr., JM Stommel, JM Winget, K Husnjak, K Itahana, L Bedford, LF Stevenson, LJ Crawford, LK Linares, LR Dick, LT Vassilev, M Elangovan, M Elangovan, M Isasa, M K Saville, M Kaur, M Wade, M Wade, MD Kaeser, MF Kleijnen, MH Glickman, MJ Lee, MK Saville, MP Bousquet-Dubouch, N Allende-Vega, N Allende-Vega, N Allende-Vega, N Gallastegui, NP Dantuma, NP Dantuma, P Robertson, P Sdek, P Young, PG Santamaria, Q Xu, Q Zhu, R Kulikov, R Verma, S Carter, S Dayal, S Dayal, S Elsasser, S Glockzin, S Menendez, S Nickell, S Raasi, SJ Wei, T Kaneko, T Mayor, T Szlanka, TA Gomez, V Su, VD Nair, XM Sun, Y Jin, Y Kravtsova-Ivantsiv, Y Midorikawa, Y Saeki, Y Wan, YA Lam, YH Shen, YV Wang, Z Lipinszki, Z Lipinszki   +93 more
core   +3 more sources

The Basally Expressed p53-Mediated Homeostatic Function

Frontiers in Cell and Developmental Biology, 2021
Apart from mutations in the p53 gene, p53 functions can be alternatively compromised by a decrease in nuclear p53 protein levels or activities. In accordance, enhanced p53 protein turnover due to elevated expression of the critical p53 E3 ligase MDM2 or ...
Isha Nagpal, Zhi-Min Yuan
doaj   +1 more source