Ask about this productRelated genes to: YAP1 Blocking Peptide
- Gene:
- YAP1 NIH gene
- Name:
- Yes associated protein 1
- Previous symbol:
- -
- Synonyms:
- YAP65
- Chromosome:
- 11q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-10-05
Related products to: YAP1 Blocking Peptide
Related articles to: YAP1 Blocking Peptide
- Thoracic and head and neck NUT carcinoma is a rare, highly aggressive NUTM1-rearranged malignancy with substantial diagnostic difficulty, marked phenotypic heterogeneity, and no established biomarker framework for immunotherapy stratification. Although fusion partners may contribute to clinicopathologic diversity, their relationship to phenotype and immune biomarkers remains insufficiently defined. - Source: PubMed
Publication date: 2026/05/28
Xiang ShuangYe ZhuomiaoDai YifanShang ShipengYang DanCheng TaoDeng ChaoZhang MinghuiYin Mingzhu - Tumor matrix stiffness, a pivotal physical attribute of the tumor microenvironment, has evolved from a passive physical barrier to an active immunoregulatory platform, profoundly impacting the initiation and effector phases of anti-tumor immune responses. This review systematically elaborates on the dual mechanisms that drive immunosuppression. Directly, stiffness attenuates T-cell and natural killer (NK) cell functions by activating pathways such as Yes-associated protein (YAP)/Transcriptional co-activator with PDZ-binding motif (TAZ) and Piezo-type mechanosensitive ion channel component 1 (Piezo1). It also drives the polarization of macrophages and dendritic cells towards immunosuppressive phenotypes. Indirectly, stiffness fosters an immune escape ecosystem by persistently activating cancer-associated fibroblasts, inducing tumor cell epithelial-mesenchymal transition, and upregulating immune checkpoints. Consequently, strategies such as enzymatic degradation, targeting mechanotransduction pathways, employing anti-fibrotic drugs, and developing intelligent combination therapies have emerged, aiming to soften tumors and reverse immunosuppression. Clinical studies confirm that high expression of the mechanosignaling hub Yes-associated protein 1 (YAP1) is associated with resistance to immunotherapy. In the future, integrating mechanobiology, immunometabolism, and smart materials to develop precise multimodal combination strategies holds promise for reversing the "cold tumor" microenvironment and opening new avenues to overcome immunotherapy resistance in solid tumors. - Source: PubMed
Publication date: 2026/05/29
Wu FeiZhang PoWu WeichiHou TianJiang XiaobingHuang Tao - Recent transcriptome analysis has demonstrated increased expression of Vascular Endothelial Growth Factor receptor-1 (VEGFR-1/FLT1) and in AD brain. Increased expression of VEGFR1 and its ligand VEGFB were associated with a more rapid rate of cognitive decline, providing evidence of a potential link between increased VEGFR-1 expression in AD pathogenesis. In this study, we explored the potential role of VEGFR-1 expression in neurons on AD pathology. - Source: PubMed
Publication date: 2026/05/29
Mukhopadhyay DebabrataDas PritamAngom Ramcharan SinghDutta ShamitLi ZonghuaCastanedes-Casey MonicaKulkarni TanmayChakravarty TrishaWang EnfengDickson DennisRachamala Hari Krishnareddy - Glaucoma is the second leading cause of blindness, and intraocular pressure (IOP) is the principal and only modifiable risk factor. The trabecular meshwork (TM) remains the most important target for IOP regulation; although it is highly mechanosensitive, TM responses to high IOP remain unclear. This study suggested that human TM cells are susceptible to mechanical stimuli using single-cell sequencing; further, and models of acute ocular hypertension were established. TM cells underwent significant cell death and cytoskeletal rearrangement after acute IOP elevation. Expression of classic fibrotic biomarkers was significantly upregulated in both mice and human TM cells, whereas levels of phosphorylated YAP1 and Rap1 were reduced. Notably, Rap1b knockin mice exhibited no significant TM death, extracellular matrix disruption, or upregulation of YAP1 following acute IOP elevation. Accordingly, Rap1-YAP1 mechanosignaling might be a novel therapeutic target for TM protection following glaucoma-associated acute IOP elevation. - Source: PubMed
Publication date: 2026/06/05
Zhang YupengLi XueHu QiumeiLuo LinlinLuo QianGuan XiangbinZhu Jingyi - Stem cell-based dental pulp regeneration is a promising treatment for pulp necrosis, wherein vascularization is critical. Dental pulp cells (DPCs) are mechanosensitive; however, the mechanism by which compressive stress regulates their angiogenic activity remains unclear. This study investigated the underlying mechanotransductive mechanisms and optimal loading parameters. - Source: PubMed
Publication date: 2026/06/04
Zhang NingningHuang QianShen ShuhuiTu JingxuanYang WenjieHuang ChupengAn XiaoliSi Qingzong