کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8452006 | 1547699 | 2017 | 41 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of HC11 mouse breast epithelial cell differentiation by the E-cadherin/Rac axis
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
GFPPAKIL6ECLRPMIshRNAGEFGTPRACSH2WAPEGFSTAT3E-cadherin - E-CadherinGTPase Activating Protein - GTPase فعال کردن پروتئینSTAT - آمارImmunofluorescence - ایمونوفلورسانسinterleukin-6 - اینترلوکین ۶enhanced chemiluminescence - بهبود شیمیایی لومنDifferentiation - تفکیکGDP - تولید ناخالص ملیMammary epithelial cells - سلول های اپیتلیال پستانGAP - شکافepidermal growth factor - عامل رشد اپیدرمیguanine nucleotide exchange factor - فاکتور تبادل نوکلئوتید گوانینSignal transducer and activator of transcription - مبدل سیگنال و فعال کننده رونویسیHIP - مفصل ران یا مفصل هیپRoswell Park Memorial Institute medium - موسسه خاطرات Roswell Park mediumWhey acidic protein - پروتئین اسیدی آب پنیرgreen fluorescent protein - پروتئین فلورسنت سبزepithelial cadherin - کادرسین اپیتلیالp21-activated kinase - کیناز فعال p21CRIB - گهوارهguanosine 5′-triphosphate - گوانوزین 5'-تری فسفاتguanosine 5′-diphosphate - گوانوزین 5'-دی فسفات
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
It was previously demonstrated that differentiation of some established breast epithelial cell lines requires confluence and stimulation with hydrocortisone, insulin and prolactin inducers. We and others previously demonstrated that E-cadherin engagement, which is favored under conditions of confluence, increases the levels and activity of the Rac small GTPase. To investigate the functional relationship between the transforming ability of Rac and its role as an integral component of the differentiative E-cadherin signaling pathway, we introduced a mutationally activated form of Rac, RacV12, into the mouse breast epithelium-derived cell line, HC11. Our results demonstrate that the strength of the Rac signal is key for the outcome of the differentiation process; cRac1 is critically required for differentiation, and at low levels, mutationally activated RacV12 is able to increase differentiation, presumably reinforcing the E-cadherin/Rac differentiative signal. However, high RacV12 expression blocked differentiation concomitant with E-cadherin downregulation, while inducing neoplastic transformation. Therefore, the intensity of the Rac signal is a central determinant in the balance between cell proliferation vs differentiation, two fundamentally opposed processes, a finding which could also have important therapeutic implications.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 361, Issue 1, 1 December 2017, Pages 112-125
Journal: Experimental Cell Research - Volume 361, Issue 1, 1 December 2017, Pages 112-125
نویسندگان
Maximilian Niit, Rozanne Arulanandam, Jamaica Cass, Mulu Geletu, Victoria Hoskin, Graham Côté, Patrick Gunning, Bruce Elliott, Leda Raptis,