[1] HUANG J. Current developments of targeting the p53 signaling pathway for cancer treatment[J]. Pharmacol Ther, 2021, 220:107720. [2] LIU Y, TAVANA O, GU W. p53 modifications:exquisite decorations of the powerful guardian[J]. J Mol Cell Biol, 2019, 11(7):564-577. [3] 安冬. 重视燃煤污染型地方性砷中毒的防治管理[J]. 中华地方病学杂志, 2015, 34(1):1-2. [4] WEN W H, LU L, HE Y F, et al. LincRNAs and base modifications of p53 induced by arsenic methylation in workers[J]. Chem Biol Interact, 2016, 246:1-10. [5] LIU Y Q, TAVANA O, GU W. p53 modifications:exquisite decorations of the powerful guardian[J]. J Mol Cell Biol, 2019, 11(7):564-577. [6] WANG S M, ZHAO Y J, AGUILAR A, et al. Targeting the MDM2-p53 protein-protein interaction for new cancer therapy:progress and challenges[J]. Cold Spring Harb Perspect Med, 2017, 7(5):a026245. [7] WU D Y, PRIVES C. Relevance of the p53-MDM2 axis to aging[J]. Cell Death Differ, 2018, 25(1):169-179. [8] ZHOU Z, JI Z, WANG Y, et al. TRIM59 is up-regulated in gastric tumors, promoting ubiquitination and degradation of p53[J]. Gastroenterology, 2014, 147(5):1043-1054. [9] SHEN J J, LI P Y, SHAO X J, et al. The E3 ligase RING1 targets p53 for degradation and promotes cancer cell proliferation and survival[J]. Cancer Res, 2018, 78(2):359-371. [10] KRUSE J P, GU W. MSL2 promotes Mdm2-independent cytoplasmic localization of p53[J]. J Biol Chem, 2009, 284(5):3250-3263. [11] SLUSS H K, ARMATA H, GALLANT J, et al. Phosphorylation of serine 18 regulates distinct p53 functions in mice[J]. Mol Cell Biol, 2004, 24(3):976-984. [12] MACPHERSON D, KIM J, KIM T, et al. Defective apoptosis and B-cell lymphomas in mice with p53 point mutation at Ser 23[J]. EMBO J, 2004, 23(18):3689-3699. [13] KAWARADA Y, INOUE Y, KAWASAKI F, et al. TGF-β induces p53/Smads complex formation in the PAI-1 promoter to activate transcription[J]. Sci Rep, 2016, 6:35483. [14] LAPRESA R, AGULLA J, SÁNCHEZ-MORÁN I, et al. Amyloid-ß promotes neurotoxicity by Cdk5-induced p53 stabilization[J]. Neuropharmacology, 2019, 146:19-27. [15] LEE E W, OH W, SONG H P, et al. Phosphorylation of p53 at threonine 155 is required for Jab1-mediated nuclear export of p53[J]. BMB Rep, 2017, 50(7):373-378. [16] CRAIG A L, CHRYSTAL J A, FRASER J A, et al. The MDM2 ubiquitination signal in the DNA-binding domain of p53 forms a docking site for calcium calmodulin kinase superfamily members[J]. Mol Cell Biol, 2007, 27(9):3542-3555. [17] DEMIR Ö, BARROS E P, OFFUTT T L, et al. An integrated view of p53 dynamics, function, and reactivation[J]. Curr Opin Struct Biol, 2021, 67:187-194. [18] REED S M, QUELLE D E. p53 acetylation:regulation and consequences[J]. Cancers (Basel), 2014, 7(1):30-69. [19] WANG D L, KON N, LASSO G, et al. Acetylation-regulated interaction between p53 and SET reveals a widespread regulatory mode[J]. Nature, 2016, 538(7623):118-122. [20] CHEN S, KAPILASHRAMI K, SENEVIRATHNE C, et al. Substrate-differentiated transition states of SET7/9-catalyzed lysine methylation[J]. J Am Chem Soc, 2019, 141(20):8064-8067. [21] VESCHI V, LIU Z H, VOSS T C, et al. Epigenetic siRNA and chemical screens identify SETD8 inhibition as a therapeutic strategy for p53 activation in high-risk neuroblastoma[J]. Cancer Cell, 2017, 31(1):50-63. [22] CHANDRAMOULI B, MELINO G, CHILLEMI G. Smyd2 conformational changes in response to p53 binding:role of the C-terminal domain[J]. Mol Oncol, 2019, 13(6):1450-1461. [23] CUI G F, PARK S, BADEAUX A I, et al. PHF20 is an effector protein of p53 double lysine methylation that stabilizes and activates p53[J]. Nat Struct Mol Biol, 2012, 19(9):916-924. [24] HWANG J W, KIM S N, MYUNG N, et al. PRMT5 promotes DNA repair through methylation of 53BP1 and is regulated by Src-mediated phosphorylation[J]. Commun Biol, 2020, 3(1):428. [25] CHAO C, HERR D, CHUN J, et al. Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression[J]. EMBO J, 2006, 25(11):2615-2622. [26] LI H M, BI Y R, LI Y, et al. A potent CBP/p300-Snail interaction inhibitor suppresses tumor growth and metastasis in wild-type p53-expressing cancer[J]. Sci Adv, 2020, 6(17):eaaw8500. [27] RODIER G, KIRSH O, BARAIBAR M, et al. The transcription factor E4F1 coordinates CHK1-dependent checkpoint and mitochondrial functions[J]. Cell Rep, 2015, 11(2):220-233. [28] LIU X, TAN Y, ZHANG C, et al. NAT10 regulates p53 activation through acetylating p53 at K120 and ubiquitinating Mdm2[J]. EMBO Rep, 2016, 17(3):349-366. [29] ZHAO T, SUN D, ZHAO M, et al. N6-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation[J]. Environ Pollut, 2020, 259:113908. [30] LI Y, JIANG R, ZHAO Y, et al. Opposed arsenite-mediated regulation of p53-survivin is involved in neoplastic transformation, DNA damage, or apoptosis in human keratinocytes[J]. Toxicology, 2012, 300(3):121-131. [31] HUANG Y L, ZHANG J L, MCHENRY K T, et al. Induction of cytoplasmic accumulation of p53:a mechanism for low levels of arsenic exposure to predispose cells for malignant transformation[J]. Cancer Res, 2008, 68(22):9131-9136. [32] YANG Y, LIU C Y, XIE T T, et al. Role of inhibiting Chk1-p53 pathway in hepatotoxicity caused by chronic arsenic exposure from coal-burning[J/OL]. Hum Exp Toxicol, 2021. DOI:10.1177/096032712098888. [33] LI Y, ZHAO Y, JIANG R R, et al. DNA-PKcs-mediated stabilization of p53 by JNK2 is involved in arsenite-induced DNA damage and apoptosis in human embryo lung fibroblast cells[J]. Toxicol Lett, 2012, 210(3):302-310. [34] CHEN S, WU J L, LIANG Y, et al. Arsenic trioxide rescues structural p53 mutations through a cryptic allosteric site[J]. Cancer Cell, 2021, 39(2):225-239.e8. [35] 张爱华, 潘雪莉, 夏玉洁, 等. p53基因甲基化和突变与燃煤污染型砷中毒关系研究[J]. 中华预防医学杂志, 2011, 45(5):393-398. [36] ZHANG A H, FENG H, YANG G H, et al. Unventilated indoor coal-fired stoves in Guizhou Province, China:cellular and genetic damage in villagers exposed to arsenic in food and air[J]. Environ Health Perspect, 2007, 115(4):653-658. [37] DE CHAUDHURI S, KUNDU M, BANERJEE M, et al. Arsenic-induced health effects and genetic damage in keratotic individuals:involvement of p53 arginine variant and chromosomal aberrations in arsenic susceptibility[J]. Mutat Res, 2008, 659(1/2):118-125. [38] MULLARD A. p53 programmes plough on[J]. Nat Rev Drug Discov, 2020, 19(8):497-500. [39] 张爱华, 曾奇兵. 新形势下地方性砷中毒科学防治的新机遇与挑战[J]. 中华地方病学杂志, 2019, 38(2):87-90. [40] XIA S Q, SUN Q, ZOU Z L, et al. Ginkgo biloba extract attenuates the disruption of pro-and anti-inflammatory T-cell balance in peripheral blood of arsenicosis patients[J]. Int J Biol Sci, 2020, 16(3):483-494. [41] CHEN X, WANG D P, SUN B F, et al. GBE attenuates arsenite-induced hepatotoxicity by regulating E2F1-autophagy-E2F7a pathway and restoring lysosomal activity[J]. J Cell Physiol, 2021, 236(5):4050-4065. [42] BAHRAMI A, SATHYAPALAN T, MOALLEM S A, et al. Counteracting arsenic toxicity:Curcumin to the rescue?[J]. J Hazard Mater, 2020, 400:123160. |