کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8293683 | 1536747 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HDAC8 regulates neural differentiation through embryoid body formation in P19â¯cells
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کلمات کلیدی
CRISPR-Cas9Smc3CdLSHDAC8FGF8HDACall-trans retinoic acid - آل – ترانس رتینوئیک اسیدneurodevelopment - توسعه عصبیembryoid body - جنین جنینES cells - سلول ESEmbryonic stem cells - سلولهای بنیادی جنینیCornelia de Lange Syndrome - سندرم کرنلیا د لانگهFibroblast growth factor 8 - عامل رشد فیبروبلاست 8knockout - ناکاوتwild-type - نوع وحشیhistone deacetylase - هیستون داستیلازCell cycle - چرخه سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Histone acetylation and deacetylation correlate with diverse biological phenomena through gene transcription. Histone deacetylases (HDACs) regulate deacetylation of histones and other proteins. However, as a member of the HDAC family, HDAC8 function during neurodevelopment is currently unknown. Therefore, we investigated HDAC8 function during neurodevelopment by examining embryoid body (EB) formation in P19â¯cells. HDAC8-selective inhibitor (NCC-149) (HDAC8i)-treated cells showed smaller EBs than non-treated cells, as well as reduced expression levels of the neuronal marker, NeuN. Additionally, HDAC8i treatment led to inhibition of cellular proliferation by G2/M phase accumulation and downregulated cyclin A2 and cyclin B1 gene expression. Furthermore, two independent HDAC8 knockout cell lines were established by CRISPR-Cas9, which resulted in smaller EBs, similar to HDAC8i-treated cells. These results suggest that HDAC8 regulates neural differentiation by exerting control of EB formation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 498, Issue 1, 25 March 2018, Pages 45-51
Journal: Biochemical and Biophysical Research Communications - Volume 498, Issue 1, 25 March 2018, Pages 45-51
نویسندگان
Syouichi Katayama, Atsushi Morii, Juliet O. Makanga, Takayoshi Suzuki, Naoki Miyata, Tetsuya Inazu,