PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33310183-6 2021 Furthermore, only the C-terminal domain participates in the jump of p53 along DNA at a high salt concentration. Salts 92-96 tumor protein p53 Homo sapiens 68-71 22880817-3 2012 Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association. Salts 59-63 tumor protein p53 Homo sapiens 44-47 25647416-0 2015 Differential salt-induced dissociation of the p53 protein complexes with circular and linear plasmid DNA substrates suggest involvement of a sliding mechanism. Salts 13-17 tumor protein p53 Homo sapiens 46-49 25647416-2 2015 Salt concentrations above 200 mM strongly affected association of the p53 protein to any plasmid DNA substrate. Salts 0-4 tumor protein p53 Homo sapiens 70-73 25647416-3 2015 Strikingly different behavior was observed when dissociation of pre-formed p53-DNA complexes in increased salt concentrations was studied. Salts 106-110 tumor protein p53 Homo sapiens 75-78 32792545-3 2020 We characterized the target search dynamics of the tumor suppressor p53 along nonspecific DNA at physiological salt concentrations. Salts 111-115 tumor protein p53 Homo sapiens 68-71 32792545-5 2020 Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex. Salts 93-97 tumor protein p53 Homo sapiens 52-55 32792545-5 2020 Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex. Salts 93-97 tumor protein p53 Homo sapiens 160-163 32792545-5 2020 Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex. Salts 93-97 tumor protein p53 Homo sapiens 160-163 30834051-10 2019 Status of p53 was investigated to see their association with the result of the H. pylori, age and sex, tumor status, smoking and extra salt intake of the patients. Salts 135-139 tumor protein p53 Homo sapiens 10-13 26520021-8 2015 The support l-tyrosine Sepharose used in chromatographic experiments promotes the separation of native pVAX1-LacZ and pcDNA3-FLAG-p53 samples (oc+sc) by decreasing the salt concentration. Salts 168-172 tumor protein p53 Homo sapiens 130-133 25584700-4 2015 Altered spectral characteristics of the Trp53 residue suggest that the core of the protein attains a CH-pi interaction at a low concentration of the salt, with an increase in the packing density. Salts 149-153 tumor protein p53 Homo sapiens 40-45 22880817-3 2012 Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association. Salts 59-63 tumor protein p53 Homo sapiens 130-133 22880817-3 2012 Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association. Salts 110-114 tumor protein p53 Homo sapiens 44-47 22880817-3 2012 Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association. Salts 110-114 tumor protein p53 Homo sapiens 130-133 22880817-5 2012 In the simulation of tetrameric full-length p53, two DNA binding domains both bound to nonspecific DNA in a characteristic form at low salt concentration, whereas at physiological salt concentration, only CTD kept bound to DNA and the core domain frequently hopped on DNA. Salts 135-139 tumor protein p53 Homo sapiens 44-47 22880817-5 2012 In the simulation of tetrameric full-length p53, two DNA binding domains both bound to nonspecific DNA in a characteristic form at low salt concentration, whereas at physiological salt concentration, only CTD kept bound to DNA and the core domain frequently hopped on DNA. Salts 180-184 tumor protein p53 Homo sapiens 44-47 12891704-4 2003 Ninety-seven kiloDaltons eEF2 was found to coimmunoprecipitate in a salt-stable complex with p53. Salts 68-72 tumor protein p53 Homo sapiens 93-96 21525412-0 2011 Acetylation of lysine 120 of p53 endows DNA-binding specificity at effective physiological salt concentration. Salts 91-95 tumor protein p53 Homo sapiens 29-32 21525412-5 2011 p53 binds DNA randomly in vitro at effective physiological salt concentration and does not bind specifically to DNA or distinguish among its different response elements until higher salt concentrations. Salts 59-63 tumor protein p53 Homo sapiens 0-3 21525412-5 2011 p53 binds DNA randomly in vitro at effective physiological salt concentration and does not bind specifically to DNA or distinguish among its different response elements until higher salt concentrations. Salts 182-186 tumor protein p53 Homo sapiens 0-3 19505151-5 2009 Here we demonstrate that the interaction with a consensus DNA sequence provides the core domain of p53 with enhanced conformational stability at physiological salt concentrations (0.15 M). Salts 159-163 tumor protein p53 Homo sapiens 99-102 21604265-3 2012 High salt and sorbitol were found to activate similar molecular pathways, including the p38 MAPK and the p53-p21(WAF1)-pRb axis, that were not stimulated by high urea. Salts 5-9 tumor protein p53 Homo sapiens 105-108 21604265-5 2012 Furthermore, salt- and sorbitol-treated cells were able to phosphorylate histone H2A.X on Ser139, in contrast to cells exposed to urea, indicating a common mechanism for DNA repair, which was achieved by a p53-dependent activation of the G1 checkpoint by both solutes. Salts 13-17 tumor protein p53 Homo sapiens 206-209 17900613-5 2007 Here we present molecular dynamics simulations of wild-type p53 and the R337His mutant at several different pH and salt conditions. Salts 115-119 tumor protein p53 Homo sapiens 60-63 12834351-1 2003 The evolution of the nanosecond dynamics of the core tryptophan, Trp53, of barstar has been monitored during the induction of collapse and structure formation in the denatured D form at pH 12, by addition of increasing concentrations of the stabilizing salt Na(2)SO(4). Salts 253-257 tumor protein p53 Homo sapiens 65-70 12834351-2 2003 Time-resolved fluorescence methods have been used to monitor the dynamics of Trp53 in the intermediates that are populated during the salt-induced transition of the D form to the molten globule B form. Salts 134-138 tumor protein p53 Homo sapiens 77-82 10588903-4 1999 The interaction of p53 and the p53CD with p53CON induced a noticeable salt-dependent bending of the DNA axis. Salts 70-74 tumor protein p53 Homo sapiens 19-22 10588903-4 1999 The interaction of p53 and the p53CD with p53CON induced a noticeable salt-dependent bending of the DNA axis. Salts 70-74 tumor protein p53 Homo sapiens 31-34 10588903-7 1999 The bending angle of the p53/DNA complex under low salt conditions showed a somewhat broader distribution (sigma approximately 39 degrees ) than at high salt concentration (sigma approximately 31 degrees ) or for p53CD (sigma approximately 24-27 degrees ). Salts 51-55 tumor protein p53 Homo sapiens 25-28 10588903-7 1999 The bending angle of the p53/DNA complex under low salt conditions showed a somewhat broader distribution (sigma approximately 39 degrees ) than at high salt concentration (sigma approximately 31 degrees ) or for p53CD (sigma approximately 24-27 degrees ). Salts 153-157 tumor protein p53 Homo sapiens 25-28 7727392-9 1995 The stability of p53tet is dependent on pH and salt concentration. Salts 47-51 tumor protein p53 Homo sapiens 17-20 9154813-4 1997 Treatment of cytoplasmic extracts with RNase or puromycin in the presence of high salt, both of which are known to disrupt ribosomal function, dissociated p53 polypeptide from the ribosomes. Salts 82-86 tumor protein p53 Homo sapiens 155-158 8141761-0 1994 Increased salt concentration reversibly destabilizes p53 quaternary structure and sequence-specific DNA binding. Salts 10-14 tumor protein p53 Homo sapiens 53-56 8141761-4 1994 We conclude that high salt can reversibly destabilize the quaternary structure of p53 that is most efficient for sequence-specific DNA binding. Salts 22-26 tumor protein p53 Homo sapiens 82-85