Deletion of Smad4 in fibroblasts leads to defective chondrocyte maturation and cartilage production in a TGFβ type II receptor independent manner
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چکیده
منابع مشابه
SMAD4 suppresses AURKA-induced metastatic phenotypes via degradation of AURKA in a TGFβ-independent manner.
UNLABELLED SMAD4 has been suggested to inhibit the activity of the WNT/β-catenin signaling pathway in cancer. However, the mechanism by which SMAD4 antagonizes WNT/β-catenin signaling in cancer remains largely unknown. Aurora A kinase (AURKA), which is frequently overexpressed in cancer, increases the transcriptional activity of β-catenin/T-cell factor (TCF) complex by stabilizing β-catenin thr...
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ژورنال
عنوان ژورنال: Biochemical and Biophysical Research Communications
سال: 2011
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2011.02.142