Name: Analysis of YAP1 phosphorylation sites induced by TAK1
Keywords: Human

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Analysis of YAP1 phosphorylation sites induced by TAK1

ABSTRACT: This study aims at determining which YAP residues are phosphorylated by TAK1.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Wounds And Injuries

SUBMITTER: Yujie Deng

LAB HEAD: Hai Song

PROVIDER: PXD011256 | Pride | 2018-11-04

REPOSITORIES: Pride

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			Action	DRS
	Gel.jpg	Other
	Rawdata-FL-YAPwithHA-TAK1-KD.raw	Raw
	Rawdata-FL-YAPwithHA-TAK1.raw	Raw
	Resultdata-FL-YAPwithHA-TAK1-KD.xlsx	Xlsx
	Resultdata-FL-YAPwithHA-TAK1.xlsx	Xlsx

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Publications

Reciprocal inhibition of YAP/TAZ and NF-κB regulates osteoarthritic cartilage degradation.

Deng Yujie Y Lu Jinqiu J Li Wenling W Wu Ailing A Zhang Xu X Tong Wenxue W Ho Kiwai Kevin KK Qin Ling L Song Hai H Mak Kinglun Kingston KK

Nature communications 20181101 1

Osteoarthritis is one of the leading causes of pain and disability in the aged population due to articular cartilage damage. This warrants investigation of signaling mechanisms that could protect cartilage from degeneration and degradation. Here we show in a murine model of experimental osteoarthritis that YAP activation by transgenic overexpression or by deletion of its upstream inhibitory kinases Mst1/2 preserves articular cartilage integrity, whereas deletion of YAP in chondrocytes promotes c ...[more]

PMID: 30385786

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YAP1 exerts its transcriptional control via TEAD mediated activation of enhancers

Project description:YAP is the principle effector of the Hippo signaling pathway; a key regulator of tissue homeostasis whose dysregulation is linked to cancer development. YAP regulation of gene expression is thought to involve the TEAD transcription factor family. Here we show that YAP and TEAD1 binding always co-occurs and is mediated by single as well as double TEAD1 motifs with a particular 3bp spacer (CATTCCNNNCATTCC). This suggests that YAP activity appears exclusively mediated by TEAD1. Despite being characterized as a promoter-binding factor YAP/TEAD actually binds predominantly to enhancers. Moreover we show that YAP is necessary for activity of the linked gene and proper chromatin state of regulated enhancers. These results establish mode of binding and activation of YAP mediated nuclear response of the Hippo pathway by TEAD1 and provide a comprehensive list and a novel class of direct target genes that are regulated distally and could be exploited for cancer therapeutics. Sequencing of ChIP and input samples for YAP1 and TEAD1 transcription factors and H3K27ac histone modification in SF268 glioblastoma cells and for YAP1 transcription factor in NCI-H2052 mesothelioma cells.

2015-08-25 | E-GEOD-61852 | biostudies-arrayexpress

Analysis of Liver Progenitor Cells Generated from Yap Expression [Set 1]

Project description:Hippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype. Organoid cells derived from mouse livers under various conditions, wild-type, Yap ON (Plus Dox), and Yap ON then OFF (Minus Dox) was examined. Comparison between freshly isolated hepatocytes; Uninduced_YPF-#.cel against Organoids grown in wild-type conditions (WT), Yap On (in vivo) off (in vitro) - YapOrganoidDoxMinus , and Yap On continuously - YapOrganoidDoxPlus. Organoids grown in culture or YFP+ sorted liver cells after the indicated time of Yap expression were collected. These were amplified using Nugene technology and hybridized to Affymetrix MoGene1.0 st arrays.

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Transcription profiling of human YAP wild-type or mutants overexpressing MCF10A cells

Project description:This study compares gene expression change upon expression of Yes-associated protein (YAP) wild-type or mutants in order to establish the importance of TEAD binding and WW domains in the gene-induction function of YAP. The results indicate that gene-induction is seriously comprised in YAP-S94A (TEAD binding domain mutant) expressing cells. And mutantion of WW domains (YAP-W1W2) also affect a fraction of YAP induced genes. Therefore both TEAD binding domain and WW domains are required for the full function of YAP in gene-induction. Experiment Overall Design: Four samples are included: 1. pQCXIH vector control; 2 YAP-WT expression; 3. YAP-S94A expression; 4. YAP-W1W2 expression. Gene expression profiles of YAP wild-type or mutants expressing cells were compared to that of vector control. Experiments were done in MCF10A mammary epithelial cells.

2010-01-19 | E-GEOD-13218 | biostudies-arrayexpress

Pi3kcb links Hippo-YAP and PI3K-AKT signaling pathways to promote cardiomyocyte proliferation and survival [microarray]

Project description:Background—YAP, the nuclear effector of Hippo signaling, regulates cellular growth and survival in multiple organs, including the heart, by interacting with TEAD sequence specific DNA-binding proteins. Recent studies showed that YAP stimulates cardiomyocyte proliferation and survival. However, the direct transcriptional targets through which YAP exerts its effects are poorly defined. Methods and Results—To identify genes directly regulated by YAP in cardiomyocytes, we combined differential gene expression analysis in YAP gain- and loss-of-function with genome-wide identification of YAP bound loci using chromatin immunoprecipitation and high throughput sequencing. This screen identified Pik3cb, encoding p110β, a catalytic subunit of phosphoinositol-3-kinase (PI3K), as a candidate YAP effector that promotes cardiomyocyte proliferation and survival. We validated YAP and TEAD occupancy of a conserved enhancer within the first intron of Pik3cb, and show that this enhancer drives YAP-dependent reporter gene expression. Yap gain- and loss-of-function studies indicated that YAP is necessary and sufficient to activate the PI3K-Akt pathway. Like Yap, Pik3cb gain-of-function stimulated cardiomyocyte proliferation, and Pik3cb knockdown dampened the YAP mitogenic activity. Reciprocally, Yap loss-of-function impaired heart function and reduced cardiomyocyte proliferation and survival, all of which were significantly rescued by AAV-mediated Pik3cb expression. Conclusion—Pik3cb is a crucial direct target of YAP, through which the YAP activates PI3K-AKT pathway and regulates cardiomyocyte proliferation and survival. Two groups were involved in this study:TNTcreYapfl_het group and TNTcreYapfl_KO group. Each group contained three biological replicates. Embryo hearts were collected at E12.5 and dissociated. Cardiomyocytes were collected by FACS. The total RNA of cardiomyocytes were isolated for microarray analysis.

2015-02-20 | E-GEOD-57718 | biostudies-arrayexpress

Gene expression data from livers of Yap+/+ and Yap+/- mice at postnatal day 30

Project description:Liver undergoes both size increase and differentiation during postnatal period, which in mice is approximately first 30 days. The mechanisms of simultaneous postnatal liver cell proliferation and maturation are not clear. In these experiments, role of yes associated protein (Yap), the downstream effector of Hippo Kinase signaling pathway was investigated. Total RNA isolated from livers of Yap+/+ and Yap+/- mice at Postnatal day 30. Pooled livers from 5 mice per genotype were used.

2012-04-04 | E-GEOD-31281 | biostudies-arrayexpress

YAP mediates crosstalk between the Hippo and PI3K-TOR pathway by suppressing PTEN via miR-29

Project description:We aimed to identify microRNAs that are regulated by YAP in human mammary epithelial cells. We utilized deep sequencing technology to identify microRNAs that are induced by YAP overexpression and repressed by YAP knockdown.

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Analysis of Liver Progenitor Cells Generated from Yap Expression [Set 2]

Project description:Hippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype. Rosa26-lsl-YFP mice had recombination induced and cells were FACS sorted using YFP as a marker at either 1 week or 6 weeks after recombination. YFP expression is a surrogate for Yap expression (our protein of interest) and time was varied in vivo. RNA was immediately extracted after sorting and labeled to be hybridized to the array. FACS sorted Yap expressing liver cells were sorted one or six weeks after induction and compared to fetal liver samples as controls The control data from fetal liver samples have been previously published and is available in the GEO database as GSE12117 (GSM305568, GSM305569, GSM305570). The complete dataset representing: Yap Expressiong Liver samples and the fetal liver control Samples from Series GSE12117 (re-processed in this study), is linked below as a supplementary file.

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Identification of Yap-interacting proteins in Xenopus egg extracts by co-immunoprecipitation coupled to LC/MS/MS

Project description:Yap (Yes-associated protein 1) is a downstream effector of the Hippo signaling pathway and known as a transcriptional co-activator. We previously identified Yap1 as a novel factor implicated in the control of the temporal DNA replication program in Xenopus retinal stem cells. However, whether Yap is directly involved in DNA replication dynamics and whether it could regulate DNA replication during early embryonic divisions in the absence of transcription remained to be investigated. We now found that in Yap depleted Xenopus laevis egg extracts the activation of replication origins was increased. In order to understand by which mechanism Yap could regulate the initiation of DNA replication in the absence of transcription we searched for new interacting factors. We immunoprecipitated Yap from Xenopus laevis egg extracts using anti-Yap, compared to control antibodies, and analyzed co-immunoprecipitating proteins by nanoLC/MS/MS.

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The effect of YAP/TAZ knockdown on the intestinal epithelium

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