کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5511271 | 1539852 | 2017 | 27 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cellular senescence regulated by SWI/SNF complex subunits through p53/p21 and p16/pRB pathway
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کلمات کلیدی
stress induced premature senescencePVDFSWItch/Sucrose NonFermentableDDRSenescence associated-β-galactosidaseGFPMSP58MRTSAHFLC50SA-β-galDMSO - DMSOSWI/SNF - SWI / SNFSWI/SNF complex - SWI / SNF پیچیدهImmunoprecipitation - تخریب ایمنیmalignant rhabdoid tumor - تومور رابدوی بدخیمDimethyl sulfoxide - دیمتیل سولفواکسیدrat mesenchymal stem cells - سلول های بنیادی مزانشیمی موش صحراییSips - سیر می شودLethal concentration 50 - غلظت مرگبار 50non-specific - غیر اختصاصیDNA damage response - واکنش به آسیب DNA green fluorescent protein - پروتئین فلورسنت سبزPropidium iodide - پروتئین یدیدPolyvinylidene fluoride - پلی وینیلیدین فلورایدSenescence - پیریReplicative senescence - پیری تکراری
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
SWI/SNF complex is an evolutionarily well-conserved chromatin-remodeling complex, which is implicated in the nucleosomes removing or sliding, impacting on the DNA repair, replication and genes expression regulation. The SWI/SNF complex consists up to 12 protein subunits. The catalytic subunits are BRG1 or BRM, which are exclusive ATPase subunits. BRG1 has been reported to play an important role in cellular senescence. However, The function of non-catalytic subunits involved in cellular senescence is rarely investigated. Therefore, we focused on the senescence regulation roles of SWI/SNF non-catalytic subunits in cellular senescent model induced by H2O2. H2O2 treatment was used to induce cellular senescence models in vitro. Screening the candidate subunits involved in this process by comparing the expression levels of SWI/SNF subunits with/without H2O2 treatment. Over-expression and knockdown the candidate subunits were utilized to investigate the functions and mechanism of the subunits involved in senescence regulation. The expressions of BAF57, BAF60a and SNF5 were changed significantly after H2O2 treatment. Overexpression of the three subunits separately induced cell growth arrest in both HaCaT and GLL19 cells, while knockdown of the subunits separately eased the senescence induced by H2O2 treatment. Results further showed that BAF57, BAF60a and SNF5 regulated cellular senescence via both p53/p21 and p16/pRB pathways, and the three subunits all had a directly interaction with p53. These results indicated that BAF57, BAF60a and SNF5 might act as novel pro-senescence factors in both normal and tumor human skin cells. Therefore, inhibiting expression of the three factors might delay the cellular senescence process.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 90, September 2017, Pages 29-37
Journal: The International Journal of Biochemistry & Cell Biology - Volume 90, September 2017, Pages 29-37
نویسندگان
Ling He, Ying Chen, Jianguo Feng, Weichao Sun, Shun Li, Mengting Ou, Liling Tang,