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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 24 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
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
Show all 2 Pubmed References
Dog (Canine) Polyclonal YAP1 Primary Antibody for ELISA, WB - ABIN4219868
Zender, Spector, Xue, Flemming, Cordon-Cardo, Silke, Fan, Luk, Wigler, Hannon, Mu, Lucito, Powers, Lowe: Identification and validation of oncogenes in liver cancer using an integrative oncogenomic approach. in Cell 2006
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
Human Monoclonal YAP1 Primary Antibody for IF, IHC - ABIN395579
Rose, Behm, Drgon, Johnson, Uhl: Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. in Molecular medicine (Cambridge, Mass.) 2010
Show all 6 Pubmed References
that lncRNA B4GALT1-AS1 promotes OS cells stemness and migration via recruiting HuR to enhance YAP activity
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.
The miR-590-5p/YAP axis may be an important novel mechanism in the pathogenesis of CD and colorectal cancer.
The observed decrease in total YAP levels in endothelial cells exposed to pulsatile flow is due to degradation via a proteasome-independent mechanism.
disruption of TAZ/YAP activity alleviates tumor burden in Lats1/2-deficient mice and inhibits human malignant peripheral nerve sheath tumors cell proliferation
Molecular mechanisms of YAP protein in the lung physiological conditions and lung diseases.[review]
Report that YAP is subject to non-proteolytic, K63-linked polyubiquitination by the SCF(SKP2) E3 ligase complex (SKP2), which is reversed by the deubiquitinase OTUD1. The non-proteolytic ubiquitination of YAP enhances its interaction with its nuclear binding partner TEAD, thereby inducing YAP's nuclear localization, transcriptional activity, and growth-promoting function.
Dual governing of YAP and COX-2 may lead to the discovery of promising therapeutic strategies for HCC patients.
YAP messenger RNA (mRNA) and protein expression levels were less in preeclamptic placentas. Yes-associated protein enhanced cell invasion, reduced the cellular apoptotic response, and had no effect on proliferation.
Study indicated that lncRNAATB functions as a ceRNA to promote MM proliferation and invasion by enhancing Yes associated protein 1 expression by competitively sponging microRNA miR5905p.
O-GlcNAcylation of YAP was required for high-glucose-induced liver tumorigenesis.
These results unveil a novel mechanism of YAP activation in cancer and open the possibility to target GR to prevent cancer stem cells self-renewal and chemoresistance.
High YAP1 expression is associated with the pathogenesis of gastric cancer.
YAP1 as a fluid mechanosensor that functions to regulate genes that promote metastasis.
These observations revealed the importance of YAP in promoting TKI-resistance and combined YAP inhibition can be a potential therapy delaying the occurrence of TKI-resistance in lung adenocarcinoma.
High Yap expression is associated with resistance to EGFR inhibitors in colorectal cancer.
High YAP1 expression is associated with malignant melanoma.
Data (including data from studies in knockout mice) suggest that KIBRA plays important role in regulating HPO activity, YAP signaling, and actin cytoskeletal dynamics in podocytes; expression of KIBRA and YAP plus phosphorylation of YAP are up-regulated in glomeruli of patients with focal segmental glomerulosclerosis. (KIBRA = kidney/brain protein-KIBRA; HPO = hepatopoietin protein; YAP = Yes associated protein-1)
YAP/TAZ mechanotransduction integrates with cell-cell communication pathways for fine-grained orchestration of stem cell decisions.
YAP1 regulates the SOX2 expression in urothelial carcinoma of the bladder.COX2 and YAP1 signaling pathways are connected with each other to induce SOX2 expression, cancer stem cell enrichment, and acquired resistance to chemotherapy in urothelial carcinoma of the bladder.
Yap1 has a crucial role in controlling the limb regenerative capacity in Xenopus
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.
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.
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.
Functional impairment of YAP/YAPdeltaC by mutant Atxn1 during development determines the adult pathology of spinocerebellar ataxia type 1 by suppressing RORalpha-mediated transcription.
Low YAP expression is associated with low liver regeneration.
these observations suggest that Zyxin promotes colon cancer tumorigenesis in a mitotic-phosphorylation-dependent manner and through CDK8-mediated YAP activation.
During and after liver development, the activation of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epithelial cell lineage.
YAP promotes myelin and non-myelin genes transcription while the polarity protein Crb3, localized at the tips of the myelin sheath, activates the Hippo pathway to temper YAP activity, therefore allowing for optimal myelin growth.
The YAP/TEAD1 complex binds to DNA element and regulates the expression of genes involved in cell growth..our data demonstrate an important role of TEAD1 in early development in mice, and the floxed TEAD1 mouse model will be a valuable genetic tool to determine the temporal and tissue-specific functions of TEAD1.
RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ntestinal stem cells (ISCs) marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function.
YAP promotes the neurite outgrowth via targeting the promoter of miR-29a, and it may be an effective therapeutic medicine for the neural disease.
Plk2 acts as coordinator of cell proliferation and early lineage commitment in cardiac progenitor cells downstream of Yes-associated protein 1.
Physiologically, steroid sex hormones stimulate follicle growth by activating YAP1; however, the preovulatory inhibition of YAP1 activity in granulosa cells is a prerequisite of LH actions.
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