Ask about this productRelated genes to: YAP1 antibody
- 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 antibody
Related articles to: YAP1 antibody
- Orthodontic tooth movement (OTM) is frequently accompanied by inflammatory responses, including periodontitis, which may compromise treatment outcomes. This study investigated the protective role of quercetin, a natural flavonoid, in OTM-associated periodontitis and its underlying mechanism involving macrophage metabolic reprogramming via the IL-17/Hippo/YAP axis. - Source: PubMed
Yao FenSong ZhipingWu WuchaoLiu BingqianXia RongqiZhou YaoWang WenxiaChen YujieLiao Zhengyu - : Yes-associated protein 1 (YAP1) is a transcriptional cofactor that coordinates the complex interplay between cell proliferation, survival, differentiation, metabolism, biomechanics, and tissue regeneration. Previous studies have shown that YAP1 activity is reduced during aging, and replacing YAP1 function has been shown to rejuvenate old cells by mitigating senescence and its associated inflammation. : As YAP1 is now confirmed to exert a profound regenerative influence on multiple organs, we wanted to gain more insight into the molecular signature of YAP1 expression relevant to brain cells. Since proteomics is a very powerful tool for discoveries, we generated SH-SY5Y cells stably expressing GFP-YAP1 and screened 8000 human proteins using multiplex arrays that utilize biotin-label-based antibody arrays. : We found YAP1 expression in astrocytes, microglia, neuronal and neuroblastoma cell lines, as well as human neurons. Importantly, YAP1 protein levels were significantly reduced selectively in the nuclear fractions of the brains of patients with Alzheimer's disease (AD) relative to normal control (NC) subjects. The screen resulted in the identification of 283 differentially expressed proteins. In line with YAP1's known role in the regulation of actin and cytoskeleton, we found a 2.53-fold upregulated level of Rho guanine nucleotide exchange factor 1 (ARHGEF1), a guanine nucleotide exchange factor (GEF) for the RhoA GTPase, which is crucial for dendritic spine regulation. A 6.19-fold upregulated level of NECAP endocytosis-associated 2 (NECAP2), the highest known increase for any protein in this screen, plays an essential role in clathrin-mediated endocytosis. Most importantly, another upregulated protein was Neudesin Neurotrophic Factor (NENF) (3.07-fold increase), also known as Neudesin, which primarily acts as a neurotrophic factor, and it promotes neuronal survival, enhances cell proliferation, and neurogenesis in neural progenitor cells. Neural Precursor Cell Expressed, Developmentally Down-Regulated 9(NEDD9) levels were also upregulated by 2.46-fold, and it affects neuronal cell number and synaptic connections through its role in neurite formation. However, it should be noted that these proteomic results are preliminary in nature as they are derived from single-sample data. The upregulated levels of ARHGEF1 and NEDD9 were confirmed by immunoblots. We also found a drastic reduction in the levels of p16INK4a, a marker of senescence. : Thus, the anti-senescence effect of YAP1 may be mediated through p16INK4a, which in turn may be crucial for YAP1's regenerative functions through NENF and NEDD9. - Source: PubMed
Publication date: 2026/05/21
Devadoss DineshAkkaoui JulietVashist ArtiArias Adriana YndartNefzi AdelLakshmana Madepalli K - Advanced non-small cell lung cancer (NSCLC) harboring KRAS mutations can be treated with selective inhibitors, however progression-free survival remains limited. Resistance has been associated with co-mutations in TP53, STK11, and KEAP1, persistent plasma KRAS , and activation of the MRAS-SHOC2-PP1C pathway with downstream YAP1 signaling. We evaluated the expression of MRAS-SHOC2-PP1C and YAP1-related genes in KRAS mutant NSCLC. Messenger RNA levels of twenty genes were quantified using nCounter in tumor samples from 98 NSCLC patients, including KRAS (n=23), KRAS (n=24), and KRAS (n=51) cases. Longitudinal plasma samples from ten KRAS patients treated with selective inhibitors were analyzed at baseline, day 3, week 6, and week 12. Eight genes (NFE2L2, NRAS, KRAS, ENO1, SHOC2, VCP1, LIFR, and MRAS) were differentially expressed in KRAS compared with KRAS wild-type tumors (p<0.05). LIFR, KRAS, and MET were differentially expressed in KRAS tumors. Among 30 KRAS-mutant patients, high LIFR expression was associated with improved survival. In plasma, twelve genes were consistently detected, and SHOC2, YAP1, LZTR1, RGS3, and ZDHHC7 were significantly upregulated at week 6. Low tumor LIFR expression was associated with poorer survival, supporting its potential as a prognostic biomarker and highlighting the feasibility of plasma-based gene expression monitoring. - Source: PubMed
Publication date: 2026/05/25
Giménez-Capitán AnaOlmo-Gónzalez DanielMartínez-Pérez ElizabethAguilar-Hernández AndrésGonzález-Cao MaríaReyes RoxanaMoya IreneAlbarrán VíctorSullivan IvanaValarezo JoselynGarcía BeatrizRomán RuthDe Las Casas Clara MayoMolina-Vila Miguel ÁngelRosell Rafael - Fumonisin B1 (FB1) and Ochratoxin A (OTA) are two nephrotoxic mycotoxins that frequently co-occur in feed and food. Ferroptosis, an iron-dependent form of programmed cell death, is involved in kidney injury. Hippo/YAP signalling pathway is involved in cell proliferation and ferroptosis. This study aims to investigate the role of the Hippo/YAP signalling pathway and ferroptosis in the nephrotoxicity induced by co-exposure to FB1 and OTA in mice and PK-15 cells. Results showed that co-exposure to FB1 and OTA significantly induced kidney injury as demonstrated by increasing histopathological lesions, kidney index, serum BUN, CRE and UA levels, decreasing PK-15 cell viabilities, increasing PK-15 cell LDH release and kidney injury molecule and inflammatory cytokine expression levels of kidney and PK-15 cells. RNA-seq analysis of PK-15 cells revealed that OTA and FB1 co-exposure identified 664 DEGs and enriched ferroptosis and Hippo signalling pathway of KEGG. FB1 and OTA co-exposure induced ROS production, decreased GSH content, increased MDA level, iron content, and 4-HNE expression, and increased ACSL4, LPCAT3 and HO-1 expressions, and decreased GPX4, SLC7A11 and FTH expressions. FB1 and OTA co-exposure increased YAP1, TEAD1, and LAST1 expressions, while concurrently reduced YAP1 and LAST1 phosphorylation levels. Knock-down ASCL4 attenuated nephrotoxicity induced by OTA and FB1 co-exposure. Knock-down YAP1 rescued the MDA and iron accumulation and GSH decreasing, inhibited ferroptosis, and alleviated OTA and FB1-induced nephrotoxicity. This study elucidates that YAP1 played a key role in OTA and FB1 co-exposure induced nephrotoxicity through regulating ferroptosis, providing targets against combination of OTA and FB1 exposure-induced nephrotoxicity. - Source: PubMed
Publication date: 2026/05/25
Wang QiQuan LiTang JiangyuZeng JunyaWang MengmengHuang KeheChen XingxiangGan Fang - High-grade neuroendocrine carcinoma (NEC) can be difficult to diagnose, particularly when conventional neuroendocrine (NE) markers are weakly expressed or absent. This challenge is particularly pronounced in NE-low tumors with lineage-defining transcription factor profiles (e.g., POU2F3 and/or YAP1), which may exhibit squamoid (basal-like) morphology and reduced or absent expression of synaptophysin (Syn), chromogranin A (CgA), and CD56, thereby phenotypically overlapping with non-small cell lung cancer (NSCLC) and increasing the risk of misclassification. In this case, needle biopsies from the lung and liver both showed a poorly differentiated carcinoma with squamoid morphology and squamoid/basal-like immunohistochemical features. Syn, CgA, and CD56 were negative in both specimens, leading to an initial diagnosis of poorly differentiated squamous cell carcinoma. However, the subsequent clinical course revealed discordant clinicobiologic features, including rapid progression of the liver metastases, markedly elevated NSE levels, and a high Ki-67 labeling index (60-80%). These discrepancies prompted further molecular evaluation, and 90-gene expression profiling (90-GEP) supported a neuroendocrine lineage assignment. Retrospective immunohistochemistry further demonstrated positivity for POU2F3 and YAP1, whereas INSM1 was negative in both specimens, supporting classification as an NE-marker-negative high-grade NEC with an NE-low NEC/SCLC-like lineage profile. The patient subsequently showed a marked response to etoposide plus carboplatin, consistent with the known chemosensitivity of high-grade NEC/SCLC to platinum-based chemotherapy. This case highlights an underrecognized diagnostic pitfall of NE-marker-negative high-grade NEC with squamoid mimicry. When morphology, immunophenotype, and clinical behavior are discordant, integration of expanded immunohistochemistry (including lineage-defining transcription factors), molecular lineage assays (e.g., GEP), and treatment response may help avoid misdiagnosis and guide appropriate therapy. - Source: PubMed
Publication date: 2026/05/08
He WenTang YingLi YanZhang JianfengYou XuyangWu Qiaozhen