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抗Human YAP1 抗体:
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Human Polyclonal YAP1 Primary Antibody for ChIP, ICC - ABIN258559
Kapoor, Yao, Ying, Hua, Liewen, Wang, Zhong, Wu, Sadanandam, Hu, Chang, Chu, Al-Khalil, Jiang, Xia, Fletcher-Sananikone, Lim, Horwitz, Viale, Pettazzoni, Sanchez, Wang, Protopopov, Zhang, Heffernan et al.: Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. ... in Cell 2014
Show all 26 Pubmed References
Human Monoclonal YAP1 Primary Antibody for IF, IHC (p) - ABIN564526
Lau, Murray, Houshmandi, Xu, Gutmann, Yu: Merlin is a potent inhibitor of glioma growth. in Cancer research 2008
Show all 17 Pubmed References
Human Polyclonal YAP1 Primary Antibody for FACS, IHC - ABIN5663829
Zhang, Pei, Wang, Xiang, Sun, Cheng, Qi, Marchetti, Xu, Sun, Edgar, Yuan: A Balance of Yki/Sd Activator and E2F1/Sd Repressor Complexes Controls Cell Survival and Affects Organ Size. in Developmental cell 2018
Show all 4 Pubmed References
Human Polyclonal YAP1 Primary Antibody for FACS, IHC - ABIN6674128
Gao, Yang, Yuan, Huang, Xu, Mao, Yuan, Bi: TNFα-YAP/p65-HK2 axis mediates breast cancer cell migration. in Oncogenesis 2017
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Polyclonal YAP1 Primary Antibody for IHC (p), IP - ABIN540874
Dong, Loukinova, Chen, Gangi, Chanturita, Liu, Van Waes et al.: Molecular profiling of transformed and metastatic murine squamous carcinoma cells by differential display and cDNA microarray reveals altered expression of multiple genes related to growth, ... in Cancer research 2001
Show all 3 Pubmed References
Human Monoclonal YAP1 Primary Antibody for FACS, IHC - ABIN969574
Fernandez-L, Northcott, Dalton, Fraga, Ellison, Angers, Taylor, Kenney: YAP1 is amplified and up-regulated in hedgehog-associated medulloblastomas and mediates Sonic hedgehog-driven neural precursor proliferation. in Genes & development 2009
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Human Polyclonal YAP1 Primary Antibody for IF, IHC - ABIN6712420
Zhang, Wu, Xing: YAP accelerates Aβ(25-35)-induced apoptosis through upregulation of Bax expression by interaction with p73. in Apoptosis : an international journal on programmed cell death 2011
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Human Polyclonal YAP1 Primary Antibody for IHC, WB - ABIN6150315
Wang, Xiu, Chen, Sun, Chen, Wu, Liu, Zhao: The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression. in Tumour biology 2017
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Human Polyclonal YAP1 Primary Antibody for IHC, WB - ABIN6689882
Zhang, Gong, Sun, Huang, Fan: Enhanced osteogenic differentiation of MC3T3-E1 cells on grid-topographic surface and evidence for involvement of YAP mediator. in Journal of biomedical materials research. Part A 2016
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Human Polyclonal YAP1 Primary Antibody for IF (p), IHC (p) - ABIN701485
Li, Shang, Shu, Zhang, Ji, Sun, Li, Xie: gga-miR-375 plays a key role in tumorigenesis post subgroup J avian leukosis virus infection. in PLoS ONE 2014
Studies indicate that the transcriptional co-activators YAP and TAZ recently emerged as key mediators of the biological effects that are observed in response to extracellular matrix (ECM) elasticity and cell shape.
Study confirmed the increase of TAZ/YAP in skin biopsies from patients with diffuse systemic sclerosis.
The homologous proteins Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are the key regulators in the Hippo pathway.
Study provides evidence that YAP acts as a promoter of focal adhesion and tumour invasiveness via regulating FAK phosphorylation in breast cancer. Further experiments reveal that YAP could induce FAK phosphorylation through a TEAD-dependent manner.
Novel kindlin-2 signaling axis that senses the mechanical cues of cell microenvironment and controls mesenchymal stem cell fate decision through YAP1/TAZ.
A novel 1 bp deletion in YAP1 was identified in a boy with bilateral microphthalmia and bilateral chorioretinal coloboma.
metformin depresses YAP promoter by interfering with the binding of the transcription factor IRF-1. Importantly, verteporfin sensitizes metformin-induced the depression of YAP and inhibition of cell growth and invasion in lung cancer cells.
Increased USP9X expression correlates with increased YAP1 protein in human breast cancer cell lines and patient samples. Moreover, depletion of USP9X increases YAP1 polyubiquitination, which in turn elevates YAP1 turnover and cell sensitivity to chemotherapy.
The crosstalk between the Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) transcription factors and Notch signaling influences cell self-renewal, stem cell differentiation, cell fate decisions, epithelial-stromal interactions, inflammation, morphogenesis, and large-scale gene oscillations.
Nuclear YAP expression correlates with increased collagen abundance in melanoma.
VEGF-A interacts with NRP-1 and GIPC1 to regulate alpha6/beta4-integrin, FAK, Src, PI3K/PDK1, LATS1 signaling to increase YAP1/Np63alpha accumulation.
Heterozygous IDH1(R132H/WT) created by "single base editing" inhibits human astroglial cell growth by downregulating YAP
YAP1 expression was associated with early relapse in tissue samples of patients with TNBC taxol chemoresistance (P < .001).
LOX nuclear localization was significantly associated with poor survival in patients with Colorectal cancer (CRC). Nuclear LOX expression was correlated with synchronous or postoperative lung/hepatic metastasis. LOX may prove to be a potential target gene of YAP and TEAD4.
Knockdown of YAP/TAZ using siRNA significantly reduced the expression of the leukocyte adhesion molecule VCAM1 induced by TNF-alpha.
This study indicates that YAP/TAZ couples cell proliferation with a metabolism suited for DNA replication and facilitates escape from oncogene-induced senescence. We speculate that this activity might be relevant during the initial phases of tumour progression or during experimental stem cell reprogramming induced by YAP.
Yap is an autophagy substrate and mediator of tissue remodeling and hepatocarcinogenesis independent of the p62/Sqstm1-Nrf2 axis.
aberrant promoter methylation of YAP and significant association with its downregulation in Indian breast cancer patients.
YAP1-TEAD1 signaling induces mitochondrial biogenesis in endothelial cells and stimulates angiogenesis through PGC1alpha.
TAZ/YAP is highly expressed in malignant melanoma tumor tissues; high expression of TAZ/YAP promotes the progression of malignant melanoma and affects the postoperative survival of patients.
Yap1 has a crucial role in controlling the limb regenerative capacity in Xenopus
targeting mTORC2 retards fibroblast activation and kidney fibrosis through suppressing Yap/Taz activation.
Turnover through YAP1 recruitment.
Hippo pathway is inactivated after hepatic ischemia-reperfusion injury and Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) activation is detected in hepatic stellate cells, promoting cell proliferation and liver regeneration.
CREB and YAP form a positive feedback loop that is critical to maintain the stability of phosphorylated CREB and promote neurite outgrowth.
Yap is not essential for achieving proper liver size during development or in the perinatal period but is required to mount an effective regenerative response following hepatectomy.
The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.
These data demonstrate that YAP and TAZ combinatorially promote bone development through regulation of osteoblast activity, matrix quality, and osteoclastic remodeling.
Shavenbaby and Yorkie mediate Hippo signaling to protect adult stem cells from apoptosis
Expression of mutant GNAS caused phosphorylated YAP1 to be sequestered in the cytoplasm, altering tumor progression.
Using liver cancer as a model, NUAK2 was identified as an essential mediator of YAP-driven hepatomegaly and tumorigenesis in vivo.
YAP determines the cell fate of injured mouse hepatocytes in vivo.
disruption of TAZ/YAP activity alleviates tumor burden in Lats1/2-deficient mice and inhibits human malignant peripheral nerve sheath tumors cell proliferation
YAP1 and the YAP1-TEADs complex have roles in regulating osteoclastogenesis and related gene expression
Inhibition of YAP ameliorates choroidal neovascularization via inhibiting endothelial cell proliferation.
YAP/TAZ mechanotransduction integrates with cell-cell communication pathways for fine-grained orchestration of stem cell decisions.
Nuclear expression of YAP1 is detected in a small subset of hepatic cells starting at embryonic day (E) 13.5 when the hepatoblasts begin to differentiate into hepatocytes and cholangiocytes. At E18.5, nuclear YAP1 is undetectable in hepatoblasts & hepatocytes, but enriched within the nuclei of cholangiocytes. These levels remain postnatally, consistent with the role of YAP1 in cholangiocyte specification and maintenance.
The results indicate that EGFR and its activation are critical for YAP-mediated suppression of TGF-beta1-induced apoptosis. This study provides a new understanding of the regulatory mechanism underlying the determination of cell fate in response to TGF-beta1-mediated simultaneous apoptosis and epithelial mesenchymal transformation.
Fat4 is not required for the canonical activation of Hippo kinases but it sequesters a partner of Yap1, Amotl1, out of the nucleus.
Disrupted gene function in yap1(-/-); taz(+/-) embryos did not disturb liver bud formation, but instead impaired cell proliferation in liver and movement of the neighboring lateral plate mesoderm (LPM). Overexpression of wild type yap1 or taz could rescue the defective liver phenotypes in yap1(-/-); taz(+/-) embryos.
The authors show that the Hippo pathway transcriptional coactivators Yap1 and Wwtr1 are specifically localized to the presumptive epidermis and notochord, and play a critical and unexpected role in posterior body extension by regulating Fibronectin assembly underneath the presumptive epidermis and surrounding the notochord.
YAP activation is a hallmark of malignant brain tumours.
During vascular regression, Yap/Taz is activated by blood circulation in the endothelial cells. This leads to induction of Ctgf and actin polymerization. Interference with Yap/Taz activation decreased Ctgf production, which decreased actin polymerization and vascular regression.
that Yap1 entered the nucleus and promoted transcription in response to blood flow.
that Yap1 integrates the anabolic demands of tissue growth during development and tumorigenesis by reprogramming nitrogen metabolism to stimulate nucleotide biosynthesis
Amotl2a function in the control of lateral line primordium cell proliferation is mediated together by the Hippo pathway effector Yap1 and the Wnt/beta-catenin effector Lef1.
data reveals that Yap is required for pronephric duct integrity, maintenance of baso-lateral cell polarity, and ciliogenesis during zebrafish kidney development
Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt retinal pigment epithelium identity in zebrafish.
Yap is essential for fin regeneration and that its function is dependent on mechanical tension, conferred by a balancing act of cell density and cytoskeleton activity.
When transcriptional coactivators Yap and Taz were restricted from interacting with Tead transcription factors through expression of a dominant negative transgene, cardiac precursors failed to migrate completely to the midline.
Yap coordinately regulates cell proliferation and apoptosis and is required for dorsoventral axis formation, gastrulation, cardiogenesis, hematopoiesis, and somitogenesis.
zebrafish yap is required for the development of the brain, eyes, and neural crest during embryogenesis.
The data suggest that TEAD relocation and/or YAP degradation following its phosphorylation down-regulates IFNT gene transcription after conceptus attachment to the uterine endometrium.
This gene encodes the human ortholog of chicken YAP protein which binds to the SH3 domain of the Yes proto-oncogene product. This protein contains a WW domain that is found in various structural, regulatory and signaling molecules in yeast, nematode, and mammals, and may be involved in protein-protein interaction.
65 kDa Yes-associated protein
, yes-associated protein 2
, yorkie homolog
, Yes-associated protein 1, 65kDa
, Yes-associated protein 1, 65 kD
, yes-associated protein, 65 kDa