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Homo sapiens

ABSTRACT: Role of BET proteins in YAP/TAZ-dependent transcription [ChIP-seq]

PROVIDER: PRJNA397708 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5919400.fastq.gz	Fastqsanger.gz
	SRR5919410.fastq.gz	Fastqsanger.gz
	SRR5919420.fastq.gz	Fastqsanger.gz
	SRR5919401.fastq.gz	Fastqsanger.gz
	SRR5919411.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:Role of BET proteins in YAP/TAZ-dependent transcription [RNA-seq 1]

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Role of BET proteins in YAP/TAZ-dependent transcription

Project description:Role of BET proteins in YAP/TAZ-dependent transcription

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Role of BET proteins in YAP/TAZ-dependent transcription [ChIP-seq]

Project description:We performed ChIP-seq experiments to investigate the role of BET proteins in YAP/TAZ transcriptional activity.

2018-09-15 | GSE102406 | GEO

Role of BET proteins in YAP/TAZ-dependent transcription [RNA-seq 1]

Project description:We performed RNA-seq experiments to identify YAP/TAZ target genes in triple negative breast cancer cells, and evaluate the relevance of BET proteins for their expression.

2018-09-15 | GSE102407 | GEO

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [ChIP-Seq]

Project description:The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. ChIP-seq analysis of YAP, TAZ, TEAD4 and JUN in MDA-MB-231 cells. Two independent replicates were analysed for each TF, as well as for negative controls.

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Muscle stems cell LC-MS - Common and Distinctive Functions of the Hippo Effectors Taz and Yap in Skeletal Muscle Stem Cell Function

Project description:Abstract Hippo pathway downstream effectors Yap and Taz play key roles in cell proliferation and regeneration, regulating gene expression especially via interaction with Tead transcription factors. To investigate their role in skeletal muscle stem cells, we analysed Taz in vivo and ex vivo in comparison to Yap. Taz was expressed in activated satellite cells. siRNA knockdown or constitutive expression of wildtype or constitutively active TAZ mutants showed that TAZ promoted proliferation, a function that was shared with YAP. However, at later stages of myogenesis, TAZ also enhanced myogenic differentiation of myoblasts, whereas YAP inhibits such differentiation. Functionally, while muscle growth was mildly affected in Taz (gene symbol Wwtr1-/-) knockout mice, there were no overt effect on regeneration. However, conditional knockout of Yap in satellite cells of Pax7Cre-ERT2/+ : Yapflox/flox : Rosa26Lacz mice produced a marked regeneration deficit. To identify potential mechanisms, microarray analysis showed many common Taz/Yap targets, but Taz also regulates some genes independently of Yap, including myogenic genes such as Pax7, Myf5 and Myod1. Proteomic analysis of Yap/Taz revealed many common binding partners, but Taz also interacts with proteins distinct from Yap, that are mainly involved in myogenesis and aspects of cytoskeleton organization. Neither TAZ nor YAP bind members of the Wnt destruction complex but both extensively changed expression of Wnt and Wnt-cross talking genes with known roles in myogenesis. Finally, TAZ operates through Tead4 to enhance myogenic differentiation. In summary, Taz and Yap have overlapping functions in promoting myoblast proliferation but Taz then switches to promote myogenic differentiation.

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A YAP/TAZ-TEAD signaling module links endothelial nutrient acquisition to angiogenic growth

Project description:Angiogenesis, the process by which endothelial cells (ECs) form new blood vessels from existing ones, is intimately linked to the tissue's metabolic milieu and often occurs at nutrient-deficient sites. However, ECs rely on sufficient metabolic resources to support growth and proliferation. How endothelial nutrient acquisition and usage are regulated is unknown. Here we show that these processes are dictated by YAP/TAZ-TEAD – a transcriptional module whose function is highly responsive to changes in the tissue environment. ECs lacking YAP/TAZ or their transcriptional partners, TEAD1, 2, and 4 fail to divide, resulting in stunted vascular growth in mice. Conversely, activation of TAZ, the more abundant paralogue in ECs, boosts proliferation, leading to vascular hyperplasia. We find that YAP/TAZ promote angiogenesis by fueling nutrient mTORC1 signaling. By orchestrating the transcription of a repertoire of cell-surface transporters, YAP/TAZ-TEAD stimulate the import of amino acids and other essential nutrients, thereby enabling mTORC1 pathway activation. Dissociating mTORC1 from these nutrient inputs – elicited by the loss of Rag GTPases – inhibits mTORC1 activity and prevents YAP/TAZ-dependent vascular growth. These findings define a pivotal role for YAP/TAZ-TEAD in steering endothelial mTORC1 and illustrate the essentiality of coordinated nutrient fluxes in the vasculature.

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The TAZ-CAMTA1 and YAP-TFE3 fusion proteins modulate the basal TAZ/YAP transcriptional program by recruiting the Ada2a-containing histone acetyltransferase complex [atacseq]

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The TAZ-CAMTA1 and YAP-TFE3 fusion proteins modulate the basal TAZ/YAP transcriptional program by recruiting the Ada2a-containing histone acetyltransferase complex [chipseq]

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