کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815050 | 1058444 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Downregulation of PEA-15 reverses G1 arrest, and nuclear and chromatin changes of senescence phenotype via pErk1/2 translocation to nuclei
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
We previously showed that senescent cells respond to TPA with translocation of senescence associated-pErk1/2 (SA-pErk1/2) into nuclei along with reversal of senescence morphology. Here, we describe that the reversal of senescence phenotype was manifested by knockdown of cytoplasmic PEA-15 expression, a sequestrator of cytoplasmic pErk1/2. Transfection of short-interfering RNA to PEA-15 (siPEA-15) significantly induced nuclear translocation of SA-pErk1/2, and siPEA-15 with TPA co-treatment further increased the translocation. Moreover, the reversal of senescence phenotype, such as expressions of SA-β-galactosidase, p53, p21WAF1, PML body, 53BP1 and H3K9me2, was modified by either knockdown of PEA-15 or TPA treatment, indicating that nuclear translocation of SA-pErk1/2 might inhibit senescence progression. Indeed, knockdown of PEA-15 or TPA treatment significantly induced progression of G1 arrested cells to S-phase in human diploid fibroblast (HDF) senescent cells, examined by immunocytochemistry, FACS and immunoblot analyses. In conclusion, downregulation of PEA-15 expression reverses senescence phenotypes via nuclear translocation of SA-pErk1/2, which suggests in vivo maintenance of senescence phenotype by sequestration of pErk1/2 in cytoplasm.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 27, Issue 6, June 2015, Pages 1102-1109
Journal: Cellular Signalling - Volume 27, Issue 6, June 2015, Pages 1102-1109
نویسندگان
Yun Yeong Lee, Hong Seok Kim, In Kyoung Lim,