Notch signaling is required for normal prostatic epithelial cell proliferation and differentiation

تُعد إشارات نوتش (Notch) ضرورية للتكاثر والتمايز الطبيعيين للخلايا الظهارية البروستاتية.

Clicks: 476
ID: 271697
2006
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Abstract
Notch pathway is crucial for stem/progenitor cell maintenance, growth and differentiation in a variety of tissues. Using a transgenic cell ablation approach, we found in our previous study that cells expressing Notch1 are crucial for prostate early development and re-growth. Here, we further define …
يُعد مسار نوتش (Notch pathway) حاسمًا للحفاظ على الخلايا الجذعية/السلفية ونموها وتمايزها في مجموعة متنوعة من الأنسجة. وباستخدام نهج استئصال الخلايا المُحوّرة وراثيًا، توصّلنا في دراستنا السابقة إلى أن الخلايا المُعبِّرة عن Notch1 بالغة الأهمية للتطور المبكر للبروستاتا وإعادة نموها. وهنا، نحدد بمزيد من التفصيل …
Reference Key
xd2006developmentalnotch Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Wang XD;Leow CC;Zha J;Tang Z;Modrusan Z;Radtke F;Aguet M;de Sauvage FJ;Gao WQ;;
Journal Developmental biology
Year 2006
DOI
DOI not found
URL
http://www.ncbi.nlm.nih.gov/pubmed/16360140
Keywords
National Center for Biotechnology Information NCBI NLM MEDLINE Mice animals humans pubmed abstract nih national institutes of health national library of medicine male newborn Cells Cultured Knockout cell proliferation* oligonucleotide array sequence analysis stem cells / cytology stem cells / metabolism* cell transformation neoplastic down-regulation receptor epithelial cells / cytology Prostate / metabolism* cell cycle proteins / metabolism epithelial cells / metabolism* cell differentiation* morphogenesis prostate / growth & development pmid:16360140 doi:10.1016/j.ydbio.2005.11.009 xi-de wang ching ching leow wei-qiang gao amyloid precursor protein secretases aspartic acid endopeptidases basic helix-loop-helix transcription factors / metabolism endopeptidases / metabolism keratins / metabolism protease inhibitors / pharmacology notch1 / genetics notch1 / metabolism*

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