cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1402048.v28
title: Revealing Missing Human Protein Isoforms Based on Ab Initio Prediction, RNA-seq and Proteomics

description: In this project, we design a methods to detect novel transcripts integrating ab initio prediction on genomic sequences and filtration with various RNA-seq data. 100 splice sites were selected and RT-PCR on 48 human tissues and cell lines (including a blank negative control) were conducted. The product of the same tissue or cell line were mixed and sequenced with Illumina Mi-seq.
DOI: 10.6084/m9.figshare.1402048.v29
title: Revealing Missing Human Protein Isoforms Based on Ab Initio Prediction, RNA-seq and Proteomics

description: In this project, we design a methods to detect novel transcripts integrating ab initio prediction on genomic sequences and filtration with various RNA-seq data. 100 splice sites were selected and RT-PCR on 48 human tissues and cell lines (including a blank negative control) were conducted. The product of the same tissue or cell line were mixed and sequenced with Illumina Mi-seq.
DOI: 10.6084/m9.figshare.1402048.v31
title: Revealing Missing Human Protein Isoforms Based on Ab Initio Prediction, RNA-seq and Proteomics

description: In this project, we design a methods to detect novel transcripts integrating ab initio prediction on genomic sequences and filtration with various RNA-seq data. 100 splice sites were selected and RT-PCR on 48 human tissues and cell lines (including a blank negative control) were conducted. The product of the same tissue or cell line were mixed and sequenced with Illumina Mi-seq.
DOI: 10.6084/m9.figshare.1402048.v30
title: Revealing Missing Human Protein Isoforms Based on Ab Initio Prediction, RNA-seq and Proteomics

description: In this project, we design a methods to detect novel transcripts integrating ab initio prediction on genomic sequences and filtration with various RNA-seq data. 100 splice sites were selected and RT-PCR on 48 human tissues and cell lines (including a blank negative control) were conducted. The product of the same tissue or cell line were mixed and sequenced with Illumina Mi-seq.
DOI: 10.6084/m9.figshare.1404169
title: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes

description: Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized. Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling. Trichostatin A (TSA) regulates cardiac gene expression and attenuates transverse aortic constriction (TAC) induced hypertrophy. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) to map, for the first time, genome-wide histone acetylation changes in a preclinical model of pathological cardiac hypertrophy and attenuation of pathogenesis with TSA. Pressure overload-induced cardiac hypertrophy was associated with histone acetylation of genes implicated in cardiac contraction, collagen deposition, inflammation, and extracellular matrix identified by ChIP-seq. Gene set enrichment analysis identified NF-kappa B (NF-κB) transcription factor activation with load induced hypertrophy. Increased histone acetylation was observed on the promoters of NFκB target genes (<i>Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10</i>) consistent with gene activation in the hypertrophied heart. Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation. Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition. The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
DOI: 10.6084/m9.figshare.1404169.v1
title: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes

description: Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized. Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling. Trichostatin A (TSA) regulates cardiac gene expression and attenuates transverse aortic constriction (TAC) induced hypertrophy. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) to map, for the first time, genome-wide histone acetylation changes in a preclinical model of pathological cardiac hypertrophy and attenuation of pathogenesis with TSA. Pressure overload-induced cardiac hypertrophy was associated with histone acetylation of genes implicated in cardiac contraction, collagen deposition, inflammation, and extracellular matrix identified by ChIP-seq. Gene set enrichment analysis identified NF-kappa B (NF-κB) transcription factor activation with load induced hypertrophy. Increased histone acetylation was observed on the promoters of NFκB target genes (<i>Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10</i>) consistent with gene activation in the hypertrophied heart. Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation. Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition. The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
DOI: 10.6084/m9.figshare.1404169.v2
title: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes

description: Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized. Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling. Trichostatin A (TSA) regulates cardiac gene expression and attenuates transverse aortic constriction (TAC) induced hypertrophy. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) to map, for the first time, genome-wide histone acetylation changes in a preclinical model of pathological cardiac hypertrophy and attenuation of pathogenesis with TSA. Pressure overload-induced cardiac hypertrophy was associated with histone acetylation of genes implicated in cardiac contraction, collagen deposition, inflammation, and extracellular matrix identified by ChIP-seq. Gene set enrichment analysis identified NF-kappa B (NF-κB) transcription factor activation with load induced hypertrophy. Increased histone acetylation was observed on the promoters of NFκB target genes (<i>Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10</i>) consistent with gene activation in the hypertrophied heart. Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation. Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition. The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
DOI: 10.6084/m9.figshare.1404169.v3
title: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes

description: Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized. Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling. Trichostatin A (TSA) regulates cardiac gene expression and attenuates transverse aortic constriction (TAC) induced hypertrophy. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) to map, for the first time, genome-wide histone acetylation changes in a preclinical model of pathological cardiac hypertrophy and attenuation of pathogenesis with TSA. Pressure overload-induced cardiac hypertrophy was associated with histone acetylation of genes implicated in cardiac contraction, collagen deposition, inflammation, and extracellular matrix identified by ChIP-seq. Gene set enrichment analysis identified NF-kappa B (NF-κB) transcription factor activation with load induced hypertrophy. Increased histone acetylation was observed on the promoters of NFκB target genes (<i>Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10</i>) consistent with gene activation in the hypertrophied heart. Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation. Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition. The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
DOI: 10.6084/m9.figshare.1404169.v4
title: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes

description: Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized. Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling. Trichostatin A (TSA) regulates cardiac gene expression and attenuates transverse aortic constriction (TAC) induced hypertrophy. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) to map, for the first time, genome-wide histone acetylation changes in a preclinical model of pathological cardiac hypertrophy and attenuation of pathogenesis with TSA. Pressure overload-induced cardiac hypertrophy was associated with histone acetylation of genes implicated in cardiac contraction, collagen deposition, inflammation, and extracellular matrix identified by ChIP-seq. Gene set enrichment analysis identified NF-kappa B (NF-κB) transcription factor activation with load induced hypertrophy. Increased histone acetylation was observed on the promoters of NFκB target genes (<i>Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10</i>) consistent with gene activation in the hypertrophied heart. Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation. Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition. The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
DOI: 10.6084/m9.figshare.1404170
title: Disruption of BRD4 at H3K27Ac-enriched enhancer region correlates with decreased c-Myc expression in Merkel cell carcinoma

description: Pathologic c-Myc expression is frequently detected in human cancers, including Merkel cell carcinoma (MCC), an aggressive skin cancer with no cure for metastatic disease. Bromodomain protein 4 (BRD4) regulates gene transcription by binding to acetylated histone H3 lysine 27 (H3K27Ac) on the chromatin. Super-enhancers of transcription are identified by enrichment of H3K27Ac. BET inhibitor JQ1 disrupts BRD4 association with super-enhancers, downregulates proto-oncogenes, such as <i>c-Myc</i>, and displays antitumor activity in preclinical animal models of human cancers. Here we show that an enhancer proximal to the <i>c-Myc</i> promoter is enriched in H3K27Ac and associated with high occupancy of BRD4, and coincides with a putative <i>c-Myc</i> super-enhancer in MCC cells. This observation is mirrored in tumors from MCC patients. Importantly, depleted BRD4 occupancy at the putative <i>c-Myc</i> super-enhancer region by JQ1 correlates with decreased c-Myc expression. Thus, our study provides initial evidence that super-enhancers regulate c-Myc expression in MCC.
DOI: 10.6084/m9.figshare.1404170.v1
title: Disruption of BRD4 at H3K27Ac-enriched enhancer region correlates with decreased c-Myc expression in Merkel cell carcinoma

description: Pathologic c-Myc expression is frequently detected in human cancers, including Merkel cell carcinoma (MCC), an aggressive skin cancer with no cure for metastatic disease. Bromodomain protein 4 (BRD4) regulates gene transcription by binding to acetylated histone H3 lysine 27 (H3K27Ac) on the chromatin. Super-enhancers of transcription are identified by enrichment of H3K27Ac. BET inhibitor JQ1 disrupts BRD4 association with super-enhancers, downregulates proto-oncogenes, such as <i>c-Myc</i>, and displays antitumor activity in preclinical animal models of human cancers. Here we show that an enhancer proximal to the <i>c-Myc</i> promoter is enriched in H3K27Ac and associated with high occupancy of BRD4, and coincides with a putative <i>c-Myc</i> super-enhancer in MCC cells. This observation is mirrored in tumors from MCC patients. Importantly, depleted BRD4 occupancy at the putative <i>c-Myc</i> super-enhancer region by JQ1 correlates with decreased c-Myc expression. Thus, our study provides initial evidence that super-enhancers regulate c-Myc expression in MCC.
DOI: 10.6084/m9.figshare.1404170.v2
title: Disruption of BRD4 at H3K27Ac-enriched enhancer region correlates with decreased c-Myc expression in Merkel cell carcinoma

description: Pathologic c-Myc expression is frequently detected in human cancers, including Merkel cell carcinoma (MCC), an aggressive skin cancer with no cure for metastatic disease. Bromodomain protein 4 (BRD4) regulates gene transcription by binding to acetylated histone H3 lysine 27 (H3K27Ac) on the chromatin. Super-enhancers of transcription are identified by enrichment of H3K27Ac. BET inhibitor JQ1 disrupts BRD4 association with super-enhancers, downregulates proto-oncogenes, such as <i>c-Myc</i>, and displays antitumor activity in preclinical animal models of human cancers. Here we show that an enhancer proximal to the <i>c-Myc</i> promoter is enriched in H3K27Ac and associated with high occupancy of BRD4, and coincides with a putative <i>c-Myc</i> super-enhancer in MCC cells. This observation is mirrored in tumors from MCC patients. Importantly, depleted BRD4 occupancy at the putative <i>c-Myc</i> super-enhancer region by JQ1 correlates with decreased c-Myc expression. Thus, our study provides initial evidence that super-enhancers regulate c-Myc expression in MCC.
DOI: 10.17876/plate/dr.3/plates/204_43498
title: Digital object identifier (DOI) for the plate 43498 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43499
title: Digital object identifier (DOI) for the plate 43499 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43500
title: Digital object identifier (DOI) for the plate 43500 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43501
title: Digital object identifier (DOI) for the plate 43501 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43502
title: Digital object identifier (DOI) for the plate 43502 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43503
title: Digital object identifier (DOI) for the plate 43503 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43504
title: Digital object identifier (DOI) for the plate 43504 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43505
title: Digital object identifier (DOI) for the plate 43505 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43506
title: Digital object identifier (DOI) for the plate 43506 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43507
title: Digital object identifier (DOI) for the plate 43507 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43508
title: Digital object identifier (DOI) for the plate 43508 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43509
title: Digital object identifier (DOI) for the plate 43509 in archive 204 from the APPLAUSE DR3
DOI: 10.5281/zenodo.8256827
title: Liste, travaux et publications des Groupes thématiques numériques (2020-2023)

description: Les groupes thématiques numériques (GTnum) sont coordonnés par la Direction du numérique pour l'éducation du Ministère de l'Education nationale et de la Jeunesse. Les GTnum ont pour objectif de mettre à disposition des équipes éducatives, de façon accessible et ouverte, un état de la recherche sur quelques grandes thématiques relatives au numérique dans l'éducation. Financeur du projet : « Ministère de l'Éducation nationale et de la Jeunesse ». Accès aux publications : https://edunumrech.hypotheses.org/ https://hal.science/GTNUM/browse/latest-publications
DOI: 10.17876/plate/dr.3/plates/204_43510
title: Digital object identifier (DOI) for the plate 43510 in archive 204 from the APPLAUSE DR3
DOI: 10.5281/zenodo.8256826
title: Liste, travaux et publications des Groupes thématiques numériques (2020-2023)

description: Les groupes thématiques numériques (GTnum) sont coordonnés par la Direction du numérique pour l'éducation du Ministère de l'Education nationale et de la Jeunesse. Les GTnum ont pour objectif de mettre à disposition des équipes éducatives, de façon accessible et ouverte, un état de la recherche sur quelques grandes thématiques relatives au numérique dans l'éducation. Financeur du projet : « Ministère de l'Éducation nationale et de la Jeunesse ». Accès aux publications : https://edunumrech.hypotheses.org/ https://hal.science/GTNUM/browse/latest-publications
DOI: 10.17876/plate/dr.3/plates/204_43511
title: Digital object identifier (DOI) for the plate 43511 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43512
title: Digital object identifier (DOI) for the plate 43512 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43513
title: Digital object identifier (DOI) for the plate 43513 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43514
title: Digital object identifier (DOI) for the plate 43514 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43515
title: Digital object identifier (DOI) for the plate 43515 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43516
title: Digital object identifier (DOI) for the plate 43516 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43517
title: Digital object identifier (DOI) for the plate 43517 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43518
title: Digital object identifier (DOI) for the plate 43518 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43519
title: Digital object identifier (DOI) for the plate 43519 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43520
title: Digital object identifier (DOI) for the plate 43520 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43521
title: Digital object identifier (DOI) for the plate 43521 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43522
title: Digital object identifier (DOI) for the plate 43522 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43523
title: Digital object identifier (DOI) for the plate 43523 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43524
title: Digital object identifier (DOI) for the plate 43524 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43525
title: Digital object identifier (DOI) for the plate 43525 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43526
title: Digital object identifier (DOI) for the plate 43526 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43527
title: Digital object identifier (DOI) for the plate 43527 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43528
title: Digital object identifier (DOI) for the plate 43528 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43529
title: Digital object identifier (DOI) for the plate 43529 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43530
title: Digital object identifier (DOI) for the plate 43530 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43531
title: Digital object identifier (DOI) for the plate 43531 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43532
title: Digital object identifier (DOI) for the plate 43532 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43533
title: Digital object identifier (DOI) for the plate 43533 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43534
title: Digital object identifier (DOI) for the plate 43534 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43535
title: Digital object identifier (DOI) for the plate 43535 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43536
title: Digital object identifier (DOI) for the plate 43536 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43537
title: Digital object identifier (DOI) for the plate 43537 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43538
title: Digital object identifier (DOI) for the plate 43538 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43539
title: Digital object identifier (DOI) for the plate 43539 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43540
title: Digital object identifier (DOI) for the plate 43540 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43541
title: Digital object identifier (DOI) for the plate 43541 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43542
title: Digital object identifier (DOI) for the plate 43542 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43543
title: Digital object identifier (DOI) for the plate 43543 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43544
title: Digital object identifier (DOI) for the plate 43544 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43545
title: Digital object identifier (DOI) for the plate 43545 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43546
title: Digital object identifier (DOI) for the plate 43546 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43547
title: Digital object identifier (DOI) for the plate 43547 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43548
title: Digital object identifier (DOI) for the plate 43548 in archive 204 from the APPLAUSE DR3
DOI: 10.17876/plate/dr.3/plates/204_43549
title: Digital object identifier (DOI) for the plate 43549 in archive 204 from the APPLAUSE DR3