Ask about this productRelated genes to: SAV1 antibody
- Gene:
- SAV1 NIH gene
- Name:
- salvador family WW domain containing protein 1
- Previous symbol:
- -
- Synonyms:
- WW45, WWP4, salvador
- Chromosome:
- 14q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-15
- Date modifiied:
- 2016-10-05
Related products to: SAV1 antibody
Related articles to: SAV1 antibody
- The Hippo pathway is an evolutionarily conserved signaling cascade whose dysregulation is implicated in a wide range of diseases. While many RNA-binding proteins (RBPs) regulate this pathway through canonical functions such as modulating mRNA stability and translation, the potential for RBP-mediated regulation via non-canonical, RNA-binding-independent mechanisms remains poorly defined. Here, we report that the RBP TIAL1 exhibits oncogenic properties in hepatocellular carcinoma, promoting cancer cell proliferation, migration, and invasion. Mechanistically, TIAL1 directly interacts with the core Hippo component SAV1, disrupting the MST1-SAV1 interaction and thereby suppressing Hippo signaling and activating YAP. Notably, this regulatory function is independent of the RNA-binding activity of TIAL1. Furthermore, extracellular stimuli such as energy surplus and EGF significantly upregulate TIAL1 expression, linking microenvironmental cues to Hippo pathway dysregulation. Together, our results reveal a previously unrecognized, RNA-binding-independent mode of RBP-mediated regulation, in which TIAL1 serves as a molecular integrator that conveys extracellular signals to the Hippo pathway to drive hepatocellular carcinoma progression, providing potential avenues for therapeutic intervention. - Source: PubMed
Publication date: 2026/04/24
Dai QianlongLou LeiZhu XiaojieZhao HaotianCai ZixinWei PengchengZhong YaxianPeng ShuchangHu XinyueSun RuohanTang XiaotianPeng KaiHe YanwenGu FengDeng XiyunZhou YingqunZhou JunhuaWang YirongXue LeiGuo Xiaowei - Extensive extracellular matrix (ECM) remodeling is a hallmark of clear-cell renal cell carcinoma (ccRCC), and collagen I has been widely implicated in ccRCC progression through multiple oncogenic pathways. However, the receptor-level mechanisms by which collagen I engages specific signaling and metabolic programs remain incompletely understood. Here, we demonstrate that collagen I is highly expressed in ccRCC and predicts poor prognosis. We further uncover OSCAR as its key functional receptor, mediating tumor progression and metabolic reprogramming through Hippo signaling modulation. Mechanistically, collagen I binding induces OSCAR internalization and its interaction with the Hippo regulator SAV1. This disrupts SAV1 membrane localization, allowing YAP to enter the nucleus and activate downstream genes, which enhances proliferation, metastasis, and de novo fatty acid synthesis. Furthermore, we designed a lipid nanoparticle (CCP-LNP) that blocks the collagen I-OSCAR interaction and effectively suppresses tumor progression in vitro and in vivo. These findings reveal a collagen I-OSCAR-Hippo axis that links ECM signaling to metabolic reprogramming and suggest a potential therapeutic strategy for ccRCC. - Source: PubMed
Publication date: 2026/04/08
Shi HengyuShi JianDong XuejiaoWu SongmingLv QingyangHuang QiangqiangMiao DaojiaLu FeiyiWang ChengtaoZhang XiaopingLiang Huageng - Hongwu mixture (HWM) consists of Taxus chinensis, Marsdenia tenacissima, Rhizoma Curcumae, and Semen coicis. The objective of this study was to ascertain the potential role of the Hongwu mixture (HWM) in the treatment of triple-negative breast cancer (TNBC). TNBC cells were treated with low, medium, and high doses of HWM, and CCK-8 assays were conducted to evaluate the impact of different doses of HWM on TNBC cell viability. The target molecules of HWM were predicted using RNA-sequencing, and molecular docking models between HWM components and target proteins were developed. As the dose of HWM increased, TNBC cell viability gradually decreased. HWM inhibited the proliferation and mobility of TNBC cells, slowed the tumor growth, and upregulated the apoptosis of TNBC cells. HWM promoted Zinc finger protein 143 (ZNF143)-mediated transcriptional activation of salvador family WW domain-containing protein 1 (SAV1) by stabilizing ZNF143 protein expression, leading to phosphorylation of large tumor suppressor homolog 1 (LATS1) and Yes-associated protein 1 (YAP1). Knockdown of ZNF143/SAV1 signaling impaired the therapeutic effect of HWM, and treatment with verteporfin, pharmacological inhibition of YAP/TAZ, reversed the effects of knockdown of SAV1. Therefore, HWM might offer a potent strategy for managing TNBC effectively. - Source: PubMed
Publication date: 2026/03/27
Wu AipingMa JunWang QiongChen AifeiLv WenlingZhang YuZhang Hongying - Lung fibrosis is a severe disease with limited therapeutic options. The vascular niche is critical for lung function and fibrotic diseases, but the mechanisms by which endothelial cells (ECs) are regulated during lung injury and fibrosis remain largely unknown. As a critical regulatory pathway in lung development, regeneration, and fibrosis, the role of Hippo/YAP1 in the endothelial niche remains elusive. Here, we provide evidence that endothelial Hippo facilitates lung fibrosis via regulating the neutrophil niche. The YAP1 is activated in ECs of fibrotic lungs in mice and humans. Activating YAP1 via depleting the upstream repressor SAV1 in ECs promotes bleomycin-induced lung fibrosis, while endothelial YAP1 deficiency reverses lung fibrosis. Mechanism study reveals that endothelial YAP1 regulates the expression of CXCL1, which recruits CXCR2 neutrophil in injured lungs. Blocking neutrophil recruitment via CXCR2 antagonist reduces lung fibrosis and blocks the effects of endothelial YAP1 activation. Therapeutically, inhibition of YAP1 with verteporfin reduces endothelial CXCL1 expression, neutrophil recruitment and lung fibrosis. Collectively, these findings demonstrate the roles of Hippo/YAP1 in regulating endothelial-neutrophil niche to participate in lung fibrosis. - Source: PubMed
Publication date: 2026/03/21
Wu ChuanChen XiangqiZhou JingyueWang HanHuang XiaojuanTang XiaoqiangCao ZhongweiDing Bi-Sen - Clear cell renal cell carcinoma (ccRCC) represents 70% of kidney cancers, with 20-50% recurrence risk after surgery. Despite therapeutic advances, no reliable biomarkers have been identified for patient stratification or treatment response prediction. While VHL gene alterations are well-established in ccRCC pathogenesis, the role of the Hippo pathway remains underexplored despite ample evidence of its involvement. - Source: PubMed
Publication date: 2026/02/28
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