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p21WAF1/CIP1

p21WAF1/CIP1的相关文献在1997年到2020年内共计132篇,主要集中在肿瘤学、基础医学、分子生物学 等领域,其中期刊论文131篇、会议论文1篇、专利文献567篇;相关期刊92种,包括中国组织化学与细胞化学杂志、中华实用中西医杂志、现代生物医学进展等; 相关会议1种,包括2007生命科学领域青年科学家年会暨第五届北京生命科学领域联合年会等;p21WAF1/CIP1的相关文献由383位作者贡献,包括廖威明、周伟强、施公胜等。

p21WAF1/CIP1—发文量

期刊论文>

论文:131 占比:18.74%

会议论文>

论文:1 占比:0.14%

专利文献>

论文:567 占比:81.12%

总计:699篇

p21WAF1/CIP1—发文趋势图

p21WAF1/CIP1

-研究学者

  • 廖威明
  • 周伟强
  • 施公胜
  • 邓卓霖
  • 丘钜世
  • 于世英
  • 何煦
  • 刘丽
  • 刘凯
  • 刘斌
  • 期刊论文
  • 会议论文
  • 专利文献

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    • Ya-Nan Wang; Xu Zhao; Xue-Wei Qi; Xiongzhi Wu; Cuihong Zhu; Tian-Yan Wen
    • 摘要: Background:Our previous work demonstrated that Gekko sulfated glycopeptide extracted from the Chinese gecko Shou gong(Gekko swinhonis Guenther)could inhibit tumor growth by regulating basic fibroblast growth factor.However,basic fibroblast growth factor has opposing effects on growth in breast and liver cancers.Direct effects and mechanisms of Gekko sulfated glycopeptide on tumor growth remain unclear and are ripe for further exploration.Methods:Differential regulation by Gekko sulfated glycopeptide and bFGF were studied in established human breast cancer MCF-7 cells and hepatocarcinoma HepG2 cells.Cell proliferation was evaluated with a Trypan blue exclusion assay.Cell cycle phases were measured by flow cytometry.Basic fibroblast growth factor,transforming growth factor-β1,and p21WAF1/CIP1 mRNA and protein expression levels were detected by real-time PCR(mRNA)and ELISA(protein).Changes in phosphorylated extracellular signal-regulated kinase levels were analyzed by Western blot.Results:Data indicated that Gekko sulfated glycopeptide inhibited the proliferation of HepG2 cells(P<0.001)and also blocked basic fibroblast growth factor-stimulated proliferation of these cells(P=0.001).Gekko sulfated glycopeptide was shown to increase transforming growth factor-β1 and p21WAF1/CiP1 expression(P<0.01)and partially compensate for reductions therein induced by basic fibroblast growth factor.Conversely,in MCF-7 cells,Gekko sulfated glycopeptide alone had no observable effect on transforming growth factor-β1 and p21WAF1/CiP1 expression.Gekko sulfated glycopeptide did,however,enhance basic fibroblast growth factor-induced inhibition of cell proliferation and transforming growth factor-β1 and p21WAF1/CiP1 expression in the MCF-7 cells(P=0.001,P<0.01,P<0.01,respectively).Gekko sulfated glycopeptide was shown to suppress basic fibroblast growth factor secretion in both HepG2 and MCF-7 cell lines(P<0.05 and P<0.01,respectively)and inhibited extracellular signal-regulated kinase 1/2 phosphorylation facilitated by basic fibroblast growth factor.Gekko sulfated glycopeptide alone decreased phosphorylated extracellular signal-regulated kinase in HepG2 cells but did not visibly affect phosphorylated extracellular signal-regulated kinase levels in MCF-7 cells.Conclusions:Gekko sulfated glycopeptide,a basic fibroblast growth factor inhibitor,differentially regulates growth in different cancer cell lines,and these differences may be determined by the opposing effects of basic fibroblast growth factor on transforming growth factor-β1 and p21WAF1/CiP1 levels in breast and liver cancer cells.
    • 顾磊; 文斐; 李瀚
    • 摘要: 目的 探讨喉癌患者的p21 WAF1/CIP1和p53表达情况并对其临床病理价值进行研究.方法 采用回顾性研究方法,选取2015年1月至2017年1月接收治疗的100例喉癌患者作为研究组,另外选取100例未患有喉癌的急性喉炎患者作为对照组.使用免疫组织化学方法(即S-P法)检测两组患者p21WAF1/CIP1和p53的表达情况,观察研究组p21WAF1/CIP1、p53表达同临床病理参数之间的关系,以及p53蛋白的表达与p21WAF1/CIP1表达的相关性.结果 随着分化程度的增加,p21WAF1/CIP1的阳性表达率逐渐增加,高分化患者的阳性表达率明显高于低分化患者(P<0.05);患者p21WAF1/CIP1、p53的阳性表达率与性别、临床分型、T分期以及临床分期之间的差异无显著性(P>0.05);p21WAF1/CIP1在对照组及研究组中的阳性表达率分别为94.0%、64.0%,对照组明显高于研究组,p53在对照组中的阳性表达率为0,研究组为62.0%,研究组明显高于对照组,两组差异有显著性(P<0.05);p53蛋白的表达同p21WAF1/CIP1表达不存在相关性.结论 p21WAF1/CIP1蛋白受到抑制、p53基因表达均与喉癌的发生存在密切的关系,但p21WAF1/CIP1的表达同p53基因的表达之间不存在相关性,明确二者在喉癌患者体内的表达对于临床诊治有重要意义.
    • 郑淑荣; 张亚卓; 高华
    • 摘要: Objective To explore the levels of p21Waf1/cip1and p27Kip1in functional pituitary adenomas,and analyse the relationship between the levels of p 21Waf1/cip1and p27Kip1and clinical features.Method Tissue microarray technology was performed among 6 cases with normal pituitaries, 36 invasive pituitary adenomas and 58 non-invasive pituitary adenomas. Immunohistochemistry experiment was used to detect the protein levels of p 21Waf1/cip1and p27Kip1.The clinicopathologic data of 94 patients was collected and followed up.Methylation-specific polymerase chain reaction and sequencing were detected among 3 normal pituitaries and 24 adenomas cases. Results High-p21Waf1/cip1level cases were featured by 8/36 and H-Score 148 ±28.4 in invasive functional adenomas,and 39/58 and 217.2 ±43.2 in non-invasive adenomas(χ2=18.017,P=0.000).High-p27Kip1level cases were featured by 10/36 and H-Score 122.1 ±31.1 in invasive functional adenomas, and 37/58 and 187.2 ±36.6 in non-invasive adenomas(χ2=9.446,P =0.002).The p27Kip1level was negative with serum prolactin levels in prolactinoma patients(r =-0.237,P50%的为7/33,其中4个位点的差异有统计学意义(P<0.01).结论 功能性垂体腺瘤的p21Waf1/cip1和p27Kip1表达水平降低与肿瘤的侵袭行为有明显关系;启动子甲基化程度影响p27Kip1的表达水平.
    • 邹丹; 周伟强
    • 摘要: Aim Toinvestigatethespecificbinding sites that HDAC1 can be recruited to regulate the tran-scriptional activity of p21 WAF1/CIP1 promoter in the breast cancer MCF-7 cells.Methods ThebreastcancerMCF-7 cells in logarithmic growth phase were starved with FBS free medium for 24 hours,and treated with 20 μmol·L-1 SAHA(S group)or 0. 625 nmol·L-1 Leptin(L group)for 24 hours,and the cells that were cultured in the complete RPMI 1640 medium without any treatment were assigned as control group (B group).The DNA-ChIP was followed the manufactur-er′s protocol for the assay.The cell lysis was prepared and incubated with anti-HDAC1 antibody overnight at 4°C.DNA fragments binding anti-HDAC1 antibody were gathered and purified.The relative expression level of DNA fragments from TSS to the upstream of the p21 WAF1/CIP1 promoter region(+2 ~-4000 bp)bind-ing with antibody was detected by Real-time PCR and analyzedby2-ΔΔCTmethod.Results InBgroup, HDAC1 had high affinity with the f1 and f 8 fragmentsof p21 WAF1/CIP1 promoter compared to the other fragemts,and showed the highest affinity with the f8 fragment.In S group,the binding ability of HDAC1 to the f1 ~f10 fragment of p21 WAF1/CIP1 promoter was sig-nificantly lower than that of the control.The binding activity of HDAC1 to f8 fragment was the lowest,while reversing to reach the peak after leptin treatment.Con-clusions HDAC1canberecruitedtop21WAF1/CIP1pro-moter by the cell proliferation signal during the prolifer-ation of breast cancer MCF-7 cells.The DNA fragment from -2800 to -3200 bp in the upstream of p21 WAF1/CIP1 promoter is the target functional region for the binding with HDAC1 .%目的 研究乳腺癌MCF-7细胞中组蛋白去乙酰化酶1(histone deacetylases 1,HDAC1)募集于p21WAF1/CIP1启动子区调控其转录活性的特异性结合位点.方法 将处于对数生长期的乳腺癌MCF-7细胞在无血清培养基中饥饿24 h后,分别用20μmol·L-10.88μL SAHA(S组)、0.625 nmol·L-110μL Leptin(L组)处理24 h,对照组(B组)细胞培养在完全型RPMI 1640培养基中.各组细胞裂解液与HDAC1抗体孵育,收集纯化结合HDAC1抗体的DNA片段,应用Real-time PCR法检测p21 WAF1/CIP1启动子区从TSS到其上游(+2~-4000 bp)f1~f10片段的DNA相对表达量并用2-ΔΔCT法分析.结果 B组中,HDAC1抗体在p21WAF1/CIP1启动子区f1、f8片段有高亲和力,f8片段达最高.S组中,HDAC1抗体与p21 WAF1/CIP1启动子区f1~f10片段结合量明显低于对照组,f8片段达最低,而在L组此片段与HDAC1抗体结合量达最大值.结论 乳腺癌MCF-7细胞增殖过程中,HDAC1可被招募至p21 WAF1/CIP1启动子区,该启动子区上游-2800 bp至-3200 bp DNA片段是与HDAC1高度结合的靶功能区.
    • 邹丹; 冯秀艳; 周伟强
    • 摘要: Aim To investigate the specific binding sites that histone deacetylases 1(HDAC1) and estrogen receptor α(ERα)can be recruited to regulate the transcriptional activity of p21WAF1/CIP1 promoter in the breast cancer MCF-7 cells, and to clarify the molecular mechanism of suberoylanilide hydroxamic acid(SAHA) and leptin regulating p21WAF1/CIP1 promoter function.Methods The breast cancer MCF-7 cells in logarithmic growth phase were starved with FBS free medium for 24 hours, and treated with 20 μmol·L-1 SAHA(SAHA group) or 0.625 nmol·L-1 leptin(Leptin group) for 24 hours.The cells that were cultured in complete RPMI 1640 medium without any treatment were assigned as control group(Basal group).The cell lysis was prepared and incubated respectively with anti-HDAC1 and anti-ERα antibody by chromatin-immunoprecipitation(ChIP) method overnight at 4°C.The DNA-ChIP was followed the manufacturer′s protocol for the assay.DNA fragments binding anti-HDAC1 and anti-ERα antibody were gathered and purified.The relative expression level of DNA fragments from TSS to the upstream of the p21WAF1/CIP1 promoter region(+2~-4 000 bp) binding with antibody was detected by real-time PCR and analyzed by 2-△△CT method.Results In basal group, HDAC1 and ERα had high affinity with the f1 and f8 fragments of p21WAF1/CIP1 promoter compared to the f4 fragment.In SAHA group, the binding ability of HDAC1 and ERα to the f1 and f8 fragments of p21WAF1/CIP1 promoter was significantly lower than that of the control, while reversing to reach the peak after leptin treatment.Conclusions HDAC1 and ERα can be recruited to p21WAF1/CIP1 promoter by the cell proliferation signal during the proliferation of breast cancer MCF-7 cells.The DNA f1(from 0 to-400 bp) and f8(from-2 800 to-3 200 bp) fragment in the upstream of p21WAF1/CIP1 promoter are the target functional region for the binding with HDAC1and ERα.%目的 研究乳腺癌MCF-7细胞中组蛋白去乙酰化酶1(histone deacetylases 1,HDAC1)、雌激素受体α(estrogen receptor α,ERα)共同募集于p21WAF1/CIP1启动子特定区域,调控其转录活性的具体作用位点,同时明确辛二酰苯胺异羟肟酸(suberoylanilide hydroxamic acid,SAHA)及瘦素(Leptin)在调节p21WAF1/CIP1启动子功能中的作用机制.方法 将处于对数生长期的乳腺癌MCF-7细胞在无血清培养基中饥饿24 h后,分别用20 μmol·L-1 0.88 μL SAHA (SAHA组)、0.625 nmol·L-1 10 μL Leptin(Leptin组)处理24 h,对照组(Basal组)细胞培养在完全型RPMI 1640培养基中.各组细胞裂解液先后与HDAC1抗体及ERα抗体进行染色质免疫共沉淀(chromatin-immunoprecipitation, ChIP)孵育,收集纯化结合HDAC1及ERα抗体的DNA片段,应用Real-time PCR法检测p21WAF1/CIP1 启动子区从转录起始位点(transcription start site, TSS)到其上游(+2~-4 000 bp) f1~f10片段的DNA相对表达量,并用2-△△CT法分析.结果 Basal组中,HDAC1、ERα抗体在p21WAF1/CIP1启动子区f1、f8片段有高亲和力.SAHA 组中,HDAC1、ERα抗体与p21WAF1/CIP1启动子区f1、f8片段结合量明显低于对照组,而在Leptin组两片段与HDAC1、ERα抗体结合量明显高于对照组.结论 乳腺癌MCF-7细胞增殖过程中,细胞增殖信号可招募HDAC1、ERα至p21WAF1/CIP1启动子区.该启动子区上游0~-400 bp,-2 800~-3 200 bp DNA片段是与HDAC1、ERα共同作用的靶功能区.
    • 周慧; 周伟强
    • 摘要: 目的 研究组蛋白去乙酰化酶抑制剂(histone deacetylase inhibitor,HDACI)调控p21WAF1/CIP1启动子乙酰化水平,调节乳腺癌MCF-7细胞周期的分子机制.方法 采用实时定量PCR、Western blot和DNA-ChIP方法测定SAHA对乳腺癌MCF-7细胞周期调控系统的影响;应用染色质免疫沉淀(chromatin immunoprecipitation, ChIP)技术探究SAHA调控p21WAF1/CIP1启动子乙酰化水平的情况.结果 SAHA明显影响乳腺癌细胞周期相关调控因子的表达;在针对p21WAF1/CIP1基因功能的筛查中发现,SAHA可明显诱导p21WAF1/CIP1 mRNA和蛋白的表达,并且可调节p21WAF1/CIP1启动子乙酰化水平.结论 SAHA通过影响p21WAF1/CIP1启动子乙酰化程度调节乳腺癌MCF-7细胞周期的进程.%Aim To study the regulation mechanisms of deacetylase inhibitor SAHA in p21WAF1/CIP1 promoter acetylation in breast cancer MCF-7 cells.Methods We used quantitative real-time PCR, Western blot and DNA-ChIP to determine the effects on the regulation of cell cycle with SAHA treatment in MCF-7 cells.By DNA-ChIP, we assessed the acetylation level of p21WAF1/CIP1 promoter.Results SAHA significantly affected the expression of cell cycle-related factors, and induced the mRNA and protein expression of p21WAF1/CIP1.SAHA could adjust the acetylation level of p21WAF1/CIP1 promoter.Conclusion SAHA regulates the cell cycle progression by adjusting the acetylation level of p21WAF1/CIP1 promoter in MCF-7 cells.
    • 邹丹; 冯秀艳; 周伟强
    • 摘要: Objective To investigate the specific sites that estrogen receptor (ER)α could be recruited to in the p21WAF1/CIP1 promoter region to regulate its transcriptional activity in MCF-7 cells,and to clarify the molecular mechanism of suberoylanilide hydroxamic acid (SAHA) and leptin in the regulation of p21WAFI/CIP1 promoter function.Methods MCF-7 cells were starved by culturing them in fetal calf serum-free medium for 24 hours,and then treated with 20 μmol/L of 0.88 μL SAHA (SAHA group) or 0.625 nmol/L of 10 μL leptin (leptin group) for 24 hours,or cultured in complete RPMI-1640 medium (control group).Cell lysates were incubated with anti-ERα antibody for ChIP analysis.The relative expression levels of DNA fragments,ranging from the TSS to upstream of the p21WAF1/CIP1 promoter region (+2 to-4 000 bp),that bound the antibody were detected by real-time PCR.Results In the control group,the relative expression levels of f1,f2,and f8 DNA fragments that bound the antiERα antibody were two-fold higher than the relative expression of the f9 fragment (P < 0.01).In the SAHA and leptin groups,the relative expression of f1 to f10 DNA fragment that bound anti-ERα antibody was significantly lower than that of the control.The binding affinity of ERα for the f8 fragment was the lowest (P < 0.01) in the SAHA group,and it was significantly lower than that in the leptin group (P < 0.01).Conclusion ERα could be recruited to the p21WAFI/CIP1 promoter via signaling pathways activated during the proliferation of breast cancer MCF-7 cells.Moreover,the DNA fragment ranging from-2 800 to-3 200 bp upstream of the p21 WAF1/CIP1 promoter is the target functional region for high-affinity binding with ERα.%目的 研究雌激素受体(ER)α募集于p21WAF1/CIP1启动子区调控其转录活性的具体作用位点,明确辛二酰苯胺异羟肟酸(SAHA)及瘦素(leptin)在调节p21WAF1/CIP1启动子功能中的分子机制.方法 将处于对数生长期的乳腺癌MCF-7细胞在无血清培养基中饥饿24 h后,分别用20μmol/L的SAHA 0.88 μL(SAHA组)、0.625 nmol/L的leptin 10 μL(leptin组)处理24 h,对照组在完全型RPMI-1640培养基中培养细胞.应用染色质免疫共沉淀技术将各组细胞裂解液与ERα抗体孵育,收集纯化结合ERα抗体的DNA片段,应用实时PCR法检测p21WAF1/CIP1启动子区从转录起始点到其上游(+ 2~-4 000 bp) f1 ~f10片段的DNA相对表达量并用2-△△Ct法分析.结果 对照组中,与ERα抗体结合的f1、f2、f8片段DNA相对表达量较f9片段高出2倍以上(P<0.01).与对照组比较,SAHA及leptin组f1~f10片段与ERα抗体结合能力均降低,其中SAHA组f8片段DNA相对表达量达最低值(P<0.01),且明显低于leptin组(P<0.01).SAHA组中以f8片段为对照,其他片段与ERα抗体结合能力均较其升高(P< 0.05或0.01).leptin组中以f8片段为对照,其他片段与ERα抗体结合能力均较其降低,除f1外均有统计学差异(P<0.01).结论 乳腺癌细胞增殖过程中细胞增殖信号招募ERα至p21WAF1/CIP1启动子区,且p21WAF1/CIP1启动子区-2 800bp~-3 200 bp区域存在与ERα高度结合的靶功能区.
    • 刘晓娟
    • 摘要: 目的 探讨地诺孕素治疗子宫内膜异位症的临床效果.方法 92例未接受剥除术晚期增殖期子宫内膜(异位囊肿组织)育龄期女性依据子宫内膜病变状况结合用药方式分为异位对照组(正常培养异位子宫内膜间质细胞)及异位地诺孕素组(以50 nmol,L-1地诺孕素对异位子宫内膜间质细胞进行处理)各组46例;92例无子宫内膜异位症子宫内膜组织正常并行子宫全切术者依据用药方式分为正常对照组(正常培养子宫内膜间质细胞)及正常地诺孕素组(以5092例nM地诺孕素对正常子宫内膜间质细胞进行处理)各46例.观察各组Bcl-2、NF-κB、Bcl-XL、p21Waf1/Cip1、p16INK4a等指标的mRNA表达水平及蛋白表达水平,分析细胞凋亡状况.结果 异位地诺孕素组Bcl-2、NF-κB、Bcl-XL、p21Waf1/Cip1、p16INK4a的mRNA表达水平及蛋白表达水平均低于正常地诺孕素组、异位对照组,且细胞凋亡率高于其他3组,差异有显著性(P<0.05).结论 地诺孕素治疗子宫内膜异位症,可经Bcl-2、NF-κB、Bcl-XL、p21 Waf1/Cip1、p16INK4a等有关因子及NF-κB通路途径促使异位子宫内膜间质细胞凋亡,抑制DNA合成,实现治疗目的,改善患者预后.
    • 毋磊; 董斌; 李广帅; 刘林嶓
    • 摘要: Objective To examine the expression of HDAC6,p21WAF1/CIP1and CyclinD1 in the skin squamous cell carcinoma(SCC)tissue. Methods SP immunohistochemieal staining was used to investigate the expression of HDAC6,p21WAF1/CIP1and CyclinD1 in 40 cases of SCC and 15 cases of normal skin. Results The expression rates of HDAC6(70.0%),CyclinD1(72.5%)in SCC tissue were higher than those of the normal skin(33.3%,40.0%).The expression rate of p21WAF1/CIP1(32.5%)in SCC lower than the normal skin(66.7%) (P<0.05).The expression rate of HDAC6 was correlated with the CyclinD1 expression rate1(r=0.330,P=0.038),The expression rate of HDAC6 was negative correlated with the p21WAF1/CIP1expression rate(r=-0.594,P=0.000). Conclusion HDAC6 can affect the tumor cell's proliferation and differentiation by influencing p21WAF1/CIP1and CyclinD1,and provide the theory basis of HDAC6 inhibitors used in the treatment of skin squamous cell carcinoma.%目的:检测皮肤鳞状细胞癌(SCC)组织中HDAC6、p21WAF1/CIP1及CyclinD1的表达。方法:采用免疫组织化学SP法检测40例SCC及15例正常皮肤组织中HDAC6、p21WAF1/CIP1及CyclinD1的表达。结果:SCC组织中HDAC6及CyclinD1阳性表达率(70.0%、72.5%)均高于正常皮肤组织(33.3%、40.0%),p21WAF1/CIP1阳性表达率(32.5%)低于正常皮肤组织(66.7%),差异均有统计学意义(P<0.05)。SCC组织中HDAC6与p21WAF1/CIP1表达呈负相关(r=-0.594, P=0.000),HDAC6与CyclinD1表达呈正相关(r=0.330,P=0.038)。结论:HDAC6在SCC中可能通过影响p21WAF1/CIP1及CyclinD1对肿瘤细胞的增殖分化产生影响,为HDAC6抑制剂应用于SCC的治疗提供理论依据。
    • 张爱红; 郑全辉; 郑茗予; 郑爱华
    • 摘要: Objective To explore the effect of p21Waf1/Cip1 methylation changes on the process of cellular senescence .Methods Bisulfite sequencing was used to analyze the methylation changes of p21Waf1/Cip1 in the process of cellular senescence;p21Waf1/Cip1 ex‐pression was detected by RT‐PCR and Western‐blot ;Middle‐aged 2BS cells was treated by 5‐aza‐CdR and cellular senescence was detected by MTT and SA‐β‐Gal staining .Results Bisulfite sequencing analysis of p21Waf1/Cip1 promoter showed that CpGs were methylated by 1 .25% in the young 2BS cells ,by 27 .27% in the middle‐aged 2BS cells ,while only by 0 .64% in the senescent cells . The expression of p21Waf1/Cip1 was low in the young(28 PD) 2BS cells ,it increased first(35 PD) but decreased later in the middle‐aged(42 PD) cells .In the senescent 2BS cells ,p21Waf1/Cip1 expression was further increased .5‐aza‐CdR treatment resulted in de‐creased growth rate but increasedβ‐Gal staining of middle‐aged 2BS cells .Conclusion The process of cellular senescence is regula‐ted by the status of p21Waf1/Cip1 methylation ,and p21Waf1/Cip1 demethylation accelerates cellular senescence .%目的:探讨 p21Waf1/Cip1启动子甲基化改变对细胞衰老进程的影响。方法采用克隆、测序的方法定量检测p21Waf1/Cip1启动子在人胚肺二倍体成纤维细胞(2BS)衰老过程中的甲基化改变;RT‐PCR和Western blot检测p21Waf1/Cip1的表达;采用5‐氮杂‐2‐脱氧胞苷去甲基化处理2BS细胞,通过M T T和β‐半乳糖苷酶染色检测细胞衰老。结果 p21Waf1/Cip1启动子在年轻2BS中,CpG甲基化的发生率为1.25%;在中年细胞中为27.27%;在衰老2BS细胞中为0.64%;p21Waf1/Cip1的表达在细胞衰老过程中呈波动性变化,先增加,后降低,到细胞开始衰老时,表达又显著增加;中年2BS细胞经5‐氮杂‐2‐脱氧胞苷处理后,p21Waf1/Cip1表达增加,细胞增殖速率较正常中年细胞显著降低,同时细胞β‐半乳糖苷酶染色阳性率增加。结论 p21Waf1/Cip1去甲基化加速细胞衰老。
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