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1、RNA结合蛋白与转录后调控结合蛋白与转录后调控王文恭王文恭mRNA turnover Translation level Post-translation levelTranscription levelGene RegulationDNA and chromatin levelsPost-transcriptional levelMaturation mRNA export Regulatory factors for mRNA decay and translation1. RNA binding proteins2. microRNAs RNA binding proteins (RBP
2、s) RNA结合蛋白种类很多，估计占细胞编码蛋结合蛋白种类很多，估计占细胞编码蛋白白6-8%者为者为RNA结合蛋白结合蛋白, 但迄今只需为数不多但迄今只需为数不多的几种的几种RNA结合蛋白如结合蛋白如HuR，AUF1，TTP，TIA1，CUGBP2等被证明可特异参与等被证明可特异参与mRNA稳稳定性、翻译、或其它层面的基因调控。定性、翻译、或其它层面的基因调控。 HuR Hu /ELAV RNA 结合蛋白家族包括合蛋白家族包括HuA/HuR，Hel-N1，HuC，HuD 的主要成的主要成员。与其它成。与其它成员仅表达于神表达于神经细胞不同，胞不同，HuR几乎在一切几乎在一切组织 都有表达。主要
3、位于都有表达。主要位于细胞核，但可穿越于胞核，但可穿越于细胞胞浆/核核间，且只需，且只需细胞胞浆HuR 可可调控控mRNA稳定性及翻定性及翻译。核内。核内HuR那么与那么与mRNA成熟及成熟及export有关。有关。 结合一切三合一切三类AREs。结合后的合后的结局主要局主要为稳定目的。因此也被定目的。因此也被 称称为mRNA 稳定因子。定因子。 结合并合并稳定定VEGF, COX-2, p21, cyclin A, cyclin B1, c-fos, TNF ，IL-1， MyoD，Myogenin，bcl-2等等mRNA。因此可。因此可调理理应激反响，激反响，细胞周期，胞周期，肿瘤，瘤，
4、分化，分化，调亡等亡等过程。程。 HuR也可也可结合目的并合目的并调理其翻理其翻译。 1调控翻控翻译效率，效率， 如如 p53，p27 mRNA, c-myc。 2调控控mRNA export, 如如 CD83，c-fos, COX-2。AUF1 1.也叫也叫HnRNPDheterogeneous nuclear ribonucleoprotein D).2.主要位于核内，但可穿越于核主要位于核内，但可穿越于核/细胞浆间，细胞浆间，结合结合I，II类类AREs。3.结合目的结合目的mRNA 后使之不稳定易于降后使之不稳定易于降解，如解，如P21， CyclinD1，也可使目的，也可使目的稳定，
5、如稳定，如TNF-alpha。TTP与与HuR及及AUF1不同，不同，TTP主要位于细胞浆，主要位于细胞浆，结合结合II类类AREs。结合目的后主要使目的不稳定。如：结合目的后主要使目的不稳定。如：COX-2，TNF-alpha,GM-CSF,等。等。 Effect of ARE-BPs on the stability and translation of ARE-containing mRNAsARE-BPs mRNA stability Protein expression Translational efficiency Abundance Increase Decrease Incr
6、ease Decrease Up regulated Down regulated AUF1 c-myc (42) c-myc (46) GMCSF (55) c-fos (42,67) c-fos (53) IL-3 (55) PTH (56) p21 (48) GMCSF (42) Cyclin D1 (48) TNF-alpha (42) GMCSF (53,54) IL-3 (55) HuR c-fos(59,63,67) p53(99,) TNF-alpha () p21 (69) TNF-alpha () MyoD (68) Cox-2 () Cyclin A (70) p21 (
7、48,68,69) Cyclin B1 (70) Cyclin A (70) NOS II/iNOS (64) Cyclin B1 (70) GMCSF (55) Cyclin D1 (48) Cox-2 (71,173) NOS II/iNOS (64) IL-3 (55) GMCSF (59) VEGF (173) TNF-alpha (65,74,) p53 (99,) Cox-2 (71,) IL-3 (55,66) VEGF (62) Myogenin (68)Hel-N1 TNF-alpha (74) NF-M (73) NF-M (73) GLUT1 (72) GLUT1 (72
8、) GLUT1 (72)HuD GAP-43 (7577) GAP-43 (75,76)TTP c-fos (90) GMCSF (81) GMCSF (18,81,8385,91) TNF-alpha (80) TNF-alpha (18,81,8386,89,90) IL-2 (82) Cox-2 (87) IL-3 (88) IL-2 (82,90) IL-3 (18,66,83,84,88)BRF1 TNF-alpha (89,93) GMCSF (55) IL-3 (55,92,93) IL-3 (55)TIA-1 TNF-alpha (120) TNF-alpha (120) Co
9、x-2 (121) Cox-2 (121) KSRP c-fos (90,93) NOS II/iNOS (102) NOS II/iNOS (102) TNF-alpha (90,93) IL-2 (90,93) c-jun (93)CUG-BP2 Cox-2 (150) Cox-2 (150) Cox-2 (150) Nucleolin bcl-2 (175)TINO bcl-2 (176) PAIP2 VEGF (177) VEGF (177)Interaction of the factors involving in post-transcriptional regulation1.
10、 RNA结合蛋白相互作用。合蛋白相互作用。如，如， HuR与与AUF1均可均可结合于合于p21 与与cyclin D1 3UTR， 但二者有但二者有竞争，且功能相反。争，且功能相反。2. RNA结合蛋白与合蛋白与microRNA间相互作用。相互作用。如，如， HuR与与let-7, miR-122, TTP与与miR-16 。AU-rich Elements (AREs)1.主要指位于主要指位于3-非翻非翻译区的富含区的富含AU的序列。的序列。2. 被被RNA结合蛋白合蛋白识别，结合。合。3. 主要主要为mRNA 不不稳定元件，是定元件，是mRNA 在完成使命后快在完成使命后快速降解的构造根底
11、。速降解的构造根底。4. 依构成分依构成分为三三类1含含1-5个分散的个分散的AUUUA。2至少有两个至少有两个Overlapping UUAUUUA(U/A)(U/A). 依依AUUUA的反复方式分的反复方式分为5类，IIA，IIB，IIC，等。，等。3富含富含U，但无，但无AUUUA。注：注： 除一除一级构造外，构造外， mRNA的二的二级构造也与构造也与RNA-蛋白蛋白质相相互作用互作用亲密相关。密相关。 如，如，约70-80% HuR或或AUF1结合序合序列具有列具有类似的二似的二级构造构造mRNAs ARE-BPsClass Motif Examples I 1 to 5个散在个散在
12、 AUUUA c-myc AUF1 , HuR ，Hel-N1， HuC， HuD， AUH，GAPDH，Hsp70 c-fos AUF1，HuR， Hel-N1， HuD ，KSRP，AUH Beta1-AR AUF1 PTH AUF1 Interferon-gamma GAPDH，Hsp70 MyoD HuR p21 AUF1， HuR， HuD Cyclin A HuR Cyclin B1 HuR Cyclin D1 AUF1，HuR PAI-2 HuR NOS II/iNOS HuR， KSRPIIA (AUUU)5A GMCSF AUF1， HuR， Hel-N1， TTP， BRF
13、1， TIAR，KSRP，AUH，GAPDH，Hsp70，hnRNP-A1， hnRNP-C TNF-alpha AUF1，HuR， TTP， BRF1，TIA-1， TIAR，KSRPIIB(AUUU)4A Interferon-alpha hnRNP-A1， hnRNP-A2, hnRNP-A3IIC(A/U)(AUUU)3A(A/U) Cox-2 AUF1, HuR, HuD, TTP, TIA-1, TIAR, hnRNP-A1， hnRNP-A2, hnRNP-A3，CUDBP2 IL-2 AUF1， HuR， HuD， TTP。Hsp70， Hsp110， hnRNP-A1 IL-
14、3 HuR， BEF1， AUH，Nucleolin，TINO bcl-2 AUF1， HuR， VEGF HuR HuC， HuD，PAIP2IIINo AUUUA, c-jun TIAR，CUGBP1 U-rich region GLUT1 Hel-N1，hnRNP-A2， hnRNP-L p53 HuR， Id Hel-N1 hsp70 HuR Myogenin HuR NF-M Hel-N1 GAP-43 HuD A matrix presentation has been used to represent the identified associations between AR
15、E-BPs and ARE-containing mRNAs. The mRNAs containing identified functional AREs are listed vertically and are grouped according to the classifications proposed by (24) and (26). The ARE-BPs are displayed horizontally. Where appropriate the different names used to denote the same protein or mRNA are
16、given. The lists of ARE-containing mRNAs and of ARE-BPs are not exhaustive and only direct interactions have been considered. Where the experimental methods used identified endogenous interactions, these are indicated by an asterisk. Data on the experimental methods are presented in the Supplementar
17、y data. Numbers correspond to listed references.Interaction between ARE and RBPsRNA-蛋白质相互作用蛋白质相互作用(结合结合)的特点的特点可在可在细胞核胞核, 也可在也可在细胞胞浆发生在核与胞生在核与胞浆的的结合功能截然不同合功能截然不同, 如在胞如在胞浆与与翻翻译及及mRNA稳定性有关定性有关, 在核能在核能够与拼接或成熟与拼接或成熟有关有关.RNA结合蛋白合蛋白对目的的序列要求不如目的的序列要求不如DNA 结合蛋合蛋白般白般严厉.结合部位大多在合部位大多在3-UTR, 少数在少数在5-UTR,绝少少见于于CD
18、S.mRNA稳定性稳定性turnover研讨的特殊技术研讨的特殊技术蛋白质蛋白质-RNA结合实验：结合实验： 1目的目的Transcript 的体外转录与标志的体外转录与标志 2细胞浆抽提物的制备。细胞浆抽提物的制备。 3) EMSA (gel-shift, supershift) 4) rChip, pull-down assays (using paramagnetic streptavidin dynabeads, biotinyl-labeled transcripts)mRNA半衰期测定半衰期测定 根本思绪根本思绪:终止转录后终止转录后,收取不同时间点之收取不同时间点之RNA, 定量
19、分定量分析析RNA降解速率降解速率. 1用用ActinomycinD终止转录终止转录 2Tet-off/on 或类似报告基因系统或类似报告基因系统 3) in vitro RNA降解分析降解分析Tet-on system is activated in the presence of doxycyclinethe DNA binding domain of the Tet-on regulator (rTetR) contains mutations repressorthatonlybindsDNAintheabsenceofligandisconvertedtoaligand-depend
20、entDNAbindingprotein.RNA-polTetracycline controlled transactivator (tTA)TET-OFF in detailsManfredGossenandHermannBujardbiochem.arizona.edu The Tet-off system is repressed in the presence of the doxycyclineTET-VP producing vectorGene of interest expressing vectorVP RNA pol interacting partTetR - tet
21、binding partTET-OFF systemTetracycline controlled transactivator (tTA)如：EGFP-interest target chimericmRNA 翻译研讨特用技术翻译研讨特用技术新生蛋白分析。新生蛋白分析。Polysome 分别，分别， Polysomal RNA, Polysomal 蛋白质分别。蛋白质分别。其它经典技术。其它经典技术。 Reference 1)Barreau, etal; Nucleic Acids Research,2)33(22): 7-7150, 20053)2) 4)3) Wang, et al; M
22、CB, 20:760-769, 20005)4) Lal, et al; EMBO J., 23:3092-3102, 2004gmu.edu/departments/mmb/baranova/pages/ppt/biotech-lec5.ppt HuR Regulates p21 mRNA Stabilization by UV LightWang, et al; Mol Cell Biol. 2000， 20(3): 760769. 细胞暴露于多种应激细胞暴露于多种应激Stresses如如short-wavelength UV light (UVC)时时, cyclin-dependent
23、 kinase inhibitor p21的表达明显被诱导。的表达明显被诱导。P21 的调控，尤其的调控，尤其P53调理的转录已被广泛，深化研讨。调理的转录已被广泛，深化研讨。先前的研讨发现，先前的研讨发现，UVC可经过可经过P53-不依赖的方式诱导不依赖的方式诱导P21。研讨还发现，细胞暴露于。研讨还发现，细胞暴露于UVC后，后，p21 mRNA 稳稳定性添加。定性添加。问题：问题：UVC诱导诱导P21表达稳定性添加的机制如何？表达稳定性添加的机制如何？ 与与HuR有关否？有关否？ Background:Example UVC 辐射射诱导蛋白蛋白-P21 RNA复合物构成。复合物构成。复合物
24、构成复合物构成为P53不依不依赖性的，性的，由于无由于无论RKO细胞能否有野生胞能否有野生型型P53，复合物的构成无区，复合物的构成无区别。复合物由蛋白复合物由蛋白质与与3UTR间结合而成。合而成。5UTR及缺失及缺失ARE的的3-UTRA1，C5几乎无蛋白几乎无蛋白结合。核与合。核与细胞胞浆蛋白均可与蛋白均可与P21 3UTR 构成复合物，但只构成复合物，但只需胞需胞浆中的复合物构成可被中的复合物构成可被UVC诱导。UVC induces the formation of p213-UTR-protein complex in the cytoplasmA。复合物构成在。复合物构成在UVC
25、辐射半小射半小时后明后明显被被诱导，与，与P21 被被诱导相吻合。相吻合。B。 竞争争抑制抑制实验阐明复合物的特异性，明复合物的特异性，Cold 探探针可可竞争抑制复合物构成。争抑制复合物构成。C。 EMSA 后，后，UV交交联，SDS-PAGE 分分别复合物，复合物，发现复合物中一条大复合物中一条大约40Kd 的复合物的复合物单一蛋白与大一蛋白与大约10个碱基的短个碱基的短片断片断转录物构成，物构成，阐明有一明有一35-40 Kd RNA结合蛋白被合蛋白被UVC诱导并与并与P21 3-UTR 结合。合。 D。 UVC 诱导该未知复合物未知复合物的的趋势与与P21被被诱导一致。一致。Eleva
26、tion of p21 by UVC is accompanied with increased formation of P21 3UTR-protein complexHuR 结合p21 mRNA in vivo and in vitro (A)， (B) HuR抗体可特异结合细胞浆蛋白与B2构成的复合物。(C) RNase T1 Selection Assay was carried out with B2 and A1, incubated with 10 nM GST or GST-HuR (see Materials and Methods). T1, digestions wit
27、h RNase T1 alone; M, molecular weight markers. (D) Gel retardation assays using B2 and the indicated concentrations of either GST or GST-HuR. (E) EMSA-Western Assay: Left, cytoplasmic fractions were either incubated with B2 or not, cross-linked, digested with RNase T1, resolved by SDS-PAGE (15% gel)
28、, and transferred onto polyvinylidene difluoride membranes, which were sequentially exposed to X-ray film for 24 h (Radioactive signal) and subjected to Western blot analysis to detect HuR (Western signal); exposure time, 30 s. Right, Lysates from UVC-treated or untreated cells were incubated with B
29、2 and then subjected to Western blot analysis. Estimated size of the HuR-p21 complexes, 37 to 40 kDa.HuR binds to the 3UTR of p21 mRNAHuR表达降低后， p21 3 UTR 与细胞浆蛋白间构成的复合物在UVC辐射后降低， p21 mRNA 稳定性降低半衰期缩短，表达降低。Decreased HuR expression lowers binding to the p21 3 UTR and reduces p21 mRNA stability and p21 i
30、nduction by UVC. (A) Western blot analysis of HuR expression in RKO cells, either untransfected (untr.) or transfected with pZeoSV2()HuR, expressing AS HuR. Chosen clonal isolates are shown. Blots were sequentially stripped and rehybridized with an antibody recognizing actin (43 kDa), to visualize d
31、ifferences in loading and transfer, and with an antibody recognizing hnRNP C (43 kDa). (B) B5 binding activity in lysates from untransfected and AS HuR-expressing cells 6 h after UVC irradiation. (C) Northern blot analysis of p21 mRNA expression in untransfected and AS HuR-expressing RKO cells 8 h a
32、fter either no treatment () or exposure to the indicated UVC doses. Evenness in loading and transfer among samples was assessed after stripping the membrane and rehybridizing it with an oligomer probe recognizing 18S rRNA. (D) Western blot analysis to assess the expression of p21, c-Jun (39 kDa), an
33、d actin in untransfected and AS HuR-expressing RKO cells 10 h after either no treatment or exposure to 20 J/m2 UVC. p-jun, phosphorylated Jun. (E) Graphs depict the rate of loss of p21 and -actin mRNAs in cells with different HuR levels after actinomycin D (2 g/ml) addition with or without UVC irrad
34、iation. At the times indicated, total RNA was extracted and p21 and -actin mRNAs were monitored by Northern blotting; signals were quantitated with a PhosphorImager, normalized against 18S (not shown), and plotted on a logarithmic scale. The mRNA half-life in each treatment group is indicated in par
35、entheses. Values represent means standard errors of the means of three independent experiments.Ectopic expression of the antisense HuR inhibited the interaction of HuR with p21 mRNA and reduced the levels as well as the half-life of p21 mRNAUVC 辐射下，B2 含HuR结合位点赋予P21 mRNA 稳定性。用反义方法降低内源性HuR 表达后，由B2赋予的稳
36、定性消逝。Effect of the full-length and mutant p21 3 UTR on expression of a luciferase reporter construct. (Top) Expression vectors pGL3, pGL3-FL, and pGL3-B2 (see Materials and Methods) were transiently cotransfected into RKO parental (untransfected Untr.), AS.2, or AS.7 cells along with pSV-gal (used t
37、o normalize for transfection efficiency); cells were irradiated with UVC (20 J/m2) or left untreated, and luciferase and -galactosidase activities were examined 24 h later. (Bottom) Relative fold increase in luciferase activity after UVC exposure, seen with either pGL3-FL or pGL3-B2 compared with th
38、at seen with the control vector pGL3. Values represent means standard errors of the means of five independent experiments The B2 fragment confers PGL3-B2 reporter ability to respond to the down-regulation of HuR Western blot analysis of HuR expression and subcellular localization. (A) Six hours afte
39、r irradiation with the indicated doses of UVC, whole-cell (20 g), cytoplasmic (40 g), nuclear (10 g), and cytosolic (40 g) lysates were prepared and subjected to Western blot analysis to monitor the expression of HuR, hnRNP C, AUF1, BAF57c (57 kDa), and actin. Cell lysates were collected at the time
40、s indicated after irradiation with UVC (20 J/m2) (B) or 6 h after irradiation with the indicated doses of UVC (C), and Western blot analysis of HuR expression performed on cytoplasmic (40 g) and nuclear (10 g) fractions. (D) Indicated doses of ionomycin (Ion.; micromolar) or lithium acetate (LiAc; m
41、illimolar) were added to cells 1 h before UVC irradiation with 20 J/m2 and Western blot analysis of cytoplasmic HuR. Hybridization using antibodies against actin and BAF57c was carried out to assess uniformity in loading and transfer among cytoplasmic and nuclear samples, respectively.UVC induces th
42、e cytoplasmic presence of HuRSubcellular localization of HuR. GFP-HuR was visualized by fluorescence microscopy in transiently transfected RKO cells that were either left untreated or treated with 20 J of UVC/m2 (4 h earlier). DAPI staining served to visualize the nucleus. Note the distinct overlap
43、of DAPI and GFP-HuR signals in untreated cells; while UVC-irradiated cells also exhibit abundant nuclear GFP-HuR, the treatment causes a substantial increase in the cytoplasmic GFP-HuR signal, not seen in untreated cells.UVC induces cytoplasmic HuRIncreased cytoplasmic HuR and p21 RNA binding after
44、exposure to stresses. (A) Western blot analysis to monitor HuR expression in cytoplasmic and nuclear fractions after treatment with the indicated agents. Samples were collected 2 h after addition of actinomycin (Act.) D (1 g/ml) or 4 h after exposure to 100 M H2O2, MMS (100 g/ml), 48 M PGA2, or UVC
45、(20 J/m2). Hybridizations using antibodies against actin and BAF57c were carried out to assess uniformity in loading and transfer among cytoplasmic and nuclear samples, respectively. (B) B2 binding activity in cytoplasmic lysates of cells treated as for panel and supershift analysis of complexes for
46、ming after exposure to such stresses.Induction of cytoplasmic HuR and its binding to p21 mRNA by UVCSummaryUVC在不影响在不影响总HuR程度的条件下程度的条件下诱导细胞胞浆HuR程度程度UVC诱导HuR与与p21 mRNA 的的结合合HuR 结合合P21 3-UTR后使后使P21mRNA 稳定定性增高，性增高，进而引起而引起P21表达增高。表达增高。人人为降低降低HuR程度可降低程度可降低HuR与与P21 3-UTR间的相互的相互结合，降低合，降低P21mRNA 稳定定性，降低性，降低P
47、21表达，提示表达，提示HuR对UVC诱导的的P21 mRNA 稳定性是必需的。定性是必需的。Example II AUF1 Regulates Replicative Senescence through Mediating p16 mRNA TurnoverWang, et al; EMBO Rep., 6 : 158-164, 2005. BackgroundCDK inhibitor p16INK4 is induced with replicative senescence. Although transcriptional regulation of p16 has been in
48、tensively studied, regulation by post-transcriptional mechanism has not been reported.RNA binding protein AUF1 is expressed as a family of four protein isoforms (p37, p40, p42 and p45) arising through alternative splicing. AUF1 binds to AU-rich elements (ARE) or AUUUA motifs in the 3-UTR of target m
49、RNAs and destabilizes them (different from HuR).Question: Is AUF1 mediated mRNA turnover involved in the regulation of p16 during cellular senescence? P16 mRNA 3-UTR contains motifs for biding by RNA binding proteinsSenescenceYoungP16 3-UTR is important for the instability of EGFP-p16 3-UTR (In youn
50、g cells)Time in Dox (h)Time in Dox (h) AUF1 binds to p16 3-UTR. Binding of AUF1 to p16 3-UTR attenuated with cellular senescence.AUF1 levels reduced with cellular senescence. AUF1 binds to AU rich region of p16 3-UTR.ABCP16 3-UTR confers instability to chimeric transcripts in lung carcinoma cells (H
51、2)Time in Dox (h)Knock-down of AUF1 stabilizes EGFP-p16 3-UTR chimeric transcripts in H2 cells Knock-down of AUF1 increases p16 expression and accelerates cellular senescence of WI-38 cellsSummarymRNA turnover is important for p16 regulation during cell aging.2. AUF1 binds to p16 3-UTR and destabili
52、zes p16 mRNA.3. AUF1 expression reduced with cellular senescence. Reduction of AUF1 during cellular senescence can lead to p16 up-regulation and accelerate cell senescent.RNA-binding protein HuR enhances p53 translation in response to ultraviolet light irradiation.Mazan-Mamczarz K, et al; 2003, PNAS
53、Example Backgroundp53是重要的抗癌基因，是重要的抗癌基因， 功能广泛。功能广泛。 在在UVC辐辐 射下，射下，p53被诱导，但机制不明。被诱导，但机制不明。2. UVC诱导细胞浆诱导细胞浆HuR。Questions： HuR能否调控能否调控p53? 如何调控如何调控? Fig. 1.UVC induces p53 expression at protein levelUVC induces p53 expressionp53 mRNA levels is not influenced by UVCp53 mRNA half-life is not altered by UV
54、CSubcellular and polysomal p53 mRNA is not altered under UVC. UVC induces p53 expression at protein levelFig. 2. Western blot analysis of p53 expression in RKO whole-cell lysates prepared at the times indicated after treatment with lactacystin (5 M), UVC (15 J/m2), or a combination of both. Signals
55、were quantitated by densitometry (graph). (B) Newly translated p53 is increased by UVC.UVC induced p53 is not associated with proteasome turnover Fig. 3.(A) REMSA (11) by using either CR or 3 UTR p53 radiolabeled transcripts and cytoplasmic lysates prepared 4 and 6 h after treatment of RKO cells wit
56、h either 15 or 30 J/m2 UVC. (B) Plasmids pGL3-Luc and pGL3-Luc-p53(3UTR) were used in transient transfections; 24 h after transfection, cells were either irradiated (15 J/m2) or left untreated, and the relative luciferase activity was calculated 6, 12, and 24 h later.Binding of cytoplasmic proteins
57、to the p53 3 UTR is linked to p53 translational up-regulation.Fig. 4.(REMSA) HuR binds to the p53 3UTR (pull-down assays) HuR binds to the p53 3UTR. (rCHip assays) HuR binds to the p53 3UTR.UVC induces the presence of HuR in the cytoplasm and polysome.HuR binds to the p53 3 UTR in a UVC-dependent ma
58、nnerFig. 5.Western blot analysis of HuR and p53 in HuR-over-expressing (S11) cells under UVC treatment. Western blot analysis of HuR and p53 in HuR-silencing cells under UVC treatment. Analysis of newly translated p53 in HuR-silenced cells.Modulation of HuR levels affects p53 translation and steady-state levels.ConclussionUVC induces p53 translation.HuR binds to the 3UTR of p53.HuR enhances p53 translation under UVC treatment.
