2021年3月17日 · 1. TGFβ通路可以直接转录激活DACT1；DACT1可以抑制Wnt/β-catenin通路. 2. DACT1可以在细胞质中通过液-液相分离形成凝聚物并将CK2束缚在其中，进而抑制CK2 …

Wnt/β-catenin 途径调控着干细胞的多能分化、器官的发育和再生，在功能上与Hippo、Notch和TGF-β等类似，当然也与这些发育调控相关的信号通路有着不同程度的交联。

2012年3月13日 · TGF-β stimulates canonical Wnt signalling in a p38-dependent manner by decreasing the expression of the Wnt antagonist Dickkopf-1. Tissue samples from human fibrotic diseases show enhanced...

2022年1月3日 · TGF-β stimulates Wnt secretion and activates the Wnt/β-catenin signalling pathway through the TAK1 pathway to promote myofibroblast differentiation, which leads to myocardial fibrosis. 113,114

2021年3月9日 · The transforming growth factor beta (TGF-β) and canonical Wingless integration site (WNT)–β-catenin pathways are amongst the most well-studied cell signal transduction pathways in...

Wnt/β-catenin interacts with TGF-β signaling pathway during wound healing. The crosstalk between TGF-β and Wnt/β-catenin has been widely reported, however, the exact molecular cascade that leads to this interaction has not been fully described.

TGF-β and WNT ligands bind to different receptors and trigger various outputs. However, a growing body of evidence points to cross-regulation between these two pathways. It has been recognized that in cardiac pathologies TGF-β activates WNT/β-catenin signalling, which in turn stabilizes the TGF-β/Smad response.

2019年8月15日，来自美国Stowers研究所的Alejandro Sánchez Alvarado团队在Nature上发表文章Wnt and TGFβ coordinate growth and patterning to regulate size-dependent behavior，揭示了Wnt和TGFβ信号通路如何协调生长和模式化进而调控涡虫大小与横裂 生殖行为 的具体机制。

2012年3月13日 · The transforming growth factor-β (TGF-β) signalling pathway is a key mediator of fibroblast activation that drives the aberrant synthesis of extracellular matrix in fibrotic diseases. Here we demonstrate a novel link between transforming growth factor-β …

2021年9月17日 · TGF-β and WNT signaling have been implicated in pathogenesis of cardiac fibrosis, however, little is known about molecular cross-talk between these two pathways. The aim of this study was to examine the effect of exogenous canonical WNT3a and non-canonical WNT5a in TGF-β-activated human cardiac fibroblasts.