GATA Transcription Factor

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Yuzhi Wang - One of the best experts on this subject based on the ideXlab platform.

  • Atypical GATA Transcription Factor TRPS1 represses gene expression by recruiting CHD4/NuRD(MTA2) and suppresses cell migration and invasion by repressing TP63 expression
    Oncogenesis, 2018
    Co-Authors: Yuzhi Wang, Lele Wu, Weiguang Liu, Xue Gong, Jian Li, Xue Lin, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • atypical GATA Transcription Factor trps1 represses gene expression by recruiting chd4 nurd mta2 and suppresses cell migration and invasion by repressing tp63 expression
    Oncogenesis, 2018
    Co-Authors: Weiguang Liu, Xue Gong, Xue Lin, Yuzhi Wang, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • tricho rhino phalangeal syndrome 1 protein functions as a scaffold required for ubiquitin specific protease 4 directed histone deacetylase 2 de ubiquitination and tumor growth
    Breast Cancer Research, 2018
    Co-Authors: Lele Wu, Xue Gong, Yuzhi Wang, Jun Zhang, Jean Paul Thiery, Liming Chen
    Abstract:

    Background Although numerous studies have reported that tricho-rhino-phalangeal syndrome type I (TRPS1) protein, the only reported atypical GATA Transcription Factor, is overexpressed in various carcinomas, the underlying mechanism(s) by which it contributes to cancer remain unknown.

Liming Chen - One of the best experts on this subject based on the ideXlab platform.

  • Atypical GATA Transcription Factor TRPS1 represses gene expression by recruiting CHD4/NuRD(MTA2) and suppresses cell migration and invasion by repressing TP63 expression
    Oncogenesis, 2018
    Co-Authors: Yuzhi Wang, Lele Wu, Weiguang Liu, Xue Gong, Jian Li, Xue Lin, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • atypical GATA Transcription Factor trps1 represses gene expression by recruiting chd4 nurd mta2 and suppresses cell migration and invasion by repressing tp63 expression
    Oncogenesis, 2018
    Co-Authors: Weiguang Liu, Xue Gong, Xue Lin, Yuzhi Wang, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • tricho rhino phalangeal syndrome 1 protein functions as a scaffold required for ubiquitin specific protease 4 directed histone deacetylase 2 de ubiquitination and tumor growth
    Breast Cancer Research, 2018
    Co-Authors: Lele Wu, Xue Gong, Yuzhi Wang, Jun Zhang, Jean Paul Thiery, Liming Chen
    Abstract:

    Background Although numerous studies have reported that tricho-rhino-phalangeal syndrome type I (TRPS1) protein, the only reported atypical GATA Transcription Factor, is overexpressed in various carcinomas, the underlying mechanism(s) by which it contributes to cancer remain unknown.

Xue Gong - One of the best experts on this subject based on the ideXlab platform.

  • Atypical GATA Transcription Factor TRPS1 represses gene expression by recruiting CHD4/NuRD(MTA2) and suppresses cell migration and invasion by repressing TP63 expression
    Oncogenesis, 2018
    Co-Authors: Yuzhi Wang, Lele Wu, Weiguang Liu, Xue Gong, Jian Li, Xue Lin, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • atypical GATA Transcription Factor trps1 represses gene expression by recruiting chd4 nurd mta2 and suppresses cell migration and invasion by repressing tp63 expression
    Oncogenesis, 2018
    Co-Authors: Weiguang Liu, Xue Gong, Xue Lin, Yuzhi Wang, Jun Zhang, Liming Chen
    Abstract:

    Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA Transcription Factor, functions as a Transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal Transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 Transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided Transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the Transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.

  • tricho rhino phalangeal syndrome 1 protein functions as a scaffold required for ubiquitin specific protease 4 directed histone deacetylase 2 de ubiquitination and tumor growth
    Breast Cancer Research, 2018
    Co-Authors: Lele Wu, Xue Gong, Yuzhi Wang, Jun Zhang, Jean Paul Thiery, Liming Chen
    Abstract:

    Background Although numerous studies have reported that tricho-rhino-phalangeal syndrome type I (TRPS1) protein, the only reported atypical GATA Transcription Factor, is overexpressed in various carcinomas, the underlying mechanism(s) by which it contributes to cancer remain unknown.

Charalampos Rallis - One of the best experts on this subject based on the ideXlab platform.

  • the GATA Transcription Factor gaf1 represses trnas inhibits growth and extends chronological lifespan downstream of fission yeast torc1
    Cell Reports, 2020
    Co-Authors: Maria Rodriguezlopez, Olivia Hillson, Suam Gonzalez, Edward Tunnacliffe, Sandra Codlin, Victor A. Tallada, Jürg Bähler, Charalampos Rallis
    Abstract:

    Target of Rapamycin Complex 1 (TORC1) signaling promotes growth and aging. Inhibition of TORC1 leads to reduced protein translation, which promotes longevity. TORC1-dependent post-Transcriptional regulation of protein translation has been well studied, while analogous Transcriptional regulation is less understood. Here we screen fission yeast mutants for resistance to Torin1, which inhibits TORC1 and cell growth. Cells lacking the GATA Factor Gaf1 (gaf1Δ) grow normally even in high doses of Torin1. The gaf1Δ mutation shortens the chronological lifespan of non-dividing cells and diminishes Torin1-mediated longevity. Expression profiling and genome-wide binding experiments show that upon TORC1 inhibition, Gaf1 directly upregulates genes for small-molecule metabolic pathways and indirectly represses genes for protein translation. Surprisingly, Gaf1 binds to and downregulates the tRNA genes, so it also functions as a Transcription Factor for RNA polymerase III. Thus, Gaf1 controls the Transcription of both protein-coding and tRNA genes to inhibit translation and growth downstream of TORC1.

  • The GATA Transcription Factor Gaf1 represses tRNA genes, inhibits growth, and extends chronological lifespan downstream of fission yeast TORC1
    2019
    Co-Authors: María Rodríguez-lópez, Olivia Hillson, Suam Gonzalez, Edward Tunnacliffe, Sandra Codlin, Victor A. Tallada, Jürg Bähler, Charalampos Rallis
    Abstract:

    Abstract Target of Rapamycin Complex 1 (TORC1) signaling promotes growth and ageing. Inhibition of TORC1 leads to a down-regulation of Factors that stimulate protein translation, including RNA polymerase III, which in turn contributes to longevity. TORC1-mediated post-Transcriptional regulation of protein translation has been well studied, while analogous Transcriptional regulation is less well understood. Here we screened fission yeast deletion mutants for resistance to Torin1, which inhibits TORC1 and cell growth. Mutants lacking the GATA Transcription Factor Gaf1 (gaf1Δ) grew normally even in high doses of Torin1. The gaf1Δ mutants shortened the chronological lifespan of non-dividing cells and diminished the lifespan extension triggered by Torin1 treatment. Expression profiling and genome-wide binding experiments showed that, after TORC1 inhibition, Gaf1 directly up-regulated genes for small-molecule metabolic pathways and indirectly repressed genes for protein translation. Surprisingly, Gaf1 also bound to the tRNA genes and down-regulated them, so functions as a Transcription Factor for genes transcribed by RNA polymerase III. We conclude that Gaf1 controls the Transcription of both coding and tRNA genes to inhibit translation and growth downstream of TORC1.

Lele Wu - One of the best experts on this subject based on the ideXlab platform.