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Multi-Omics Profiling Reveals Distinct Microenvironment Characterization and Suggests Immune Escape Mechanisms of Triple-Negative Breast Cancer | Clinical Cancer Research
Purpose: The tumor microenvironment has a profound impact on prognosis and immunotherapy. However, the landscape of the triple-negative breast cancer (TNBC) microenvironment has not been fully understood.

Experimental Design: Using the largest original multi-omics dataset of TNBC (n = 386), we conducted an extensive immunogenomic analysis to explore the heterogeneity and prognostic significance of the TNBC microenvironment. We further analyzed the potential immune escape mechanisms of TNBC.

Results: The TNBC microenvironment phenotypes were classified into three heterogeneous clusters: cluster 1, the “immune-desert” cluster, with low microenvironment cell infiltration; cluster 2, the “innate immune-inactivated” cluster, with resting innate immune cells and nonimmune stromal cells infiltration; and cluster 3, the “immune-inflamed” cluster, with abundant adaptive and innate immune cells infiltration. The clustering result was validated internally with pathologic sections and externally with The Cancer Genome Atlas and METABRIC cohorts. The microenvironment clusters had significant prognostic efficacy. In terms of potential immune escape mechanisms, cluster 1 was characterized by an incapability to attract immune cells, and MYC amplification was correlated with low immune infiltration. In cluster 2, chemotaxis but inactivation of innate immunity and low tumor antigen burden might contribute to immune escape, and mutations in the PI3K-AKT pathway might be correlated with this effect. Cluster 3 featured high expression of immune checkpoint molecules.

Conclusions: Our study represents a step toward personalized immunotherapy for patients with TNBC. Immune checkpoint inhibitors might be effective for “immune-inflamed” cluster, and the transformation of “cold tumors” into “hot tumors” should be considered for “immune-desert” and “innate immune-inactivated” clusters.
TNBC  gene_expression  survival  mutations 
7 days ago by Segalllab
Oncotarget | Immunocompetent mouse allograft models for development of therapies to target breast cancer metastasis
Useful summary of the standard mouse breast cancer cell lines, including 4T1, Met1, EO771 and others - genetic mutation and gene expression analysis as well. Most are luminal. Metastasis data are in supplemental table 1 - MET1s are only metastatic by tail vein and they not high variability for them.

Effective drug development to combat metastatic disease in breast cancer would be aided by the availability of well-characterized preclinical animal models that (a) metastasize with high efficiency, (b) metastasize in a reasonable time-frame, (c) have an intact immune system, and (d) capture some of the heterogeneity of the human disease. To address these issues, we have assembled a panel of twelve mouse mammary cancer cell lines that can metastasize efficiently on implantation into syngeneic immunocompetent hosts. Genomic characterization shows that more than half of the 30 most commonly mutated genes in human breast cancer are represented within the panel. Transcriptomically, most of the models fall into the luminal A or B intrinsic molecular subtypes, despite the predominance of an aggressive, poorly-differentiated or spindled histopathology in all models. Patterns of immune cell infiltration, proliferation rates, apoptosis and angiogenesis differed significantly among models. Inherent within-model variability of the metastatic phenotype mandates large cohort sizes for intervention studies but may also capture some relevant non-genetic sources of variability. The varied molecular and phenotypic characteristics of this expanded panel of models should aid in model selection for development of antimetastatic therapies in vivo, and serve as a useful platform for predictive biomarker identification.
mouse_models  breast_cancer  mutations  gene_expression 
7 days ago by Segalllab
Lymph‐circulating tumor cells show distinct properties to blood‐circulating tumor cells and are efficient metastatic precursors
Study of MTLn3 and expression in lymph and blood ctc's (!) - use in vitro culture to expand before analysis I think. Also do some stemness/spheroid studies though not by facs. The leading cause of breast cancer‐associated death is metastasis. In 80% of solid tumors, metastasis via the lymphatic system precedes metastasis via the vascular system. However, the molecular properties of tumor cells as they exit the primary tumor into the afferent lymphatics en route to the sentinel lymph nodes (SLNs) are not yet known. Here, we developed an innovative technique that enables the collection of lymph and lymph‐circulating tumor cells (LCTCs) en route to the SLN in an immunocompetent animal model of breast cancer metastasis. We found that the gene and protein expression profiles of LCTCs and blood‐circulating tumor cells (BCTCs) as they exit the primary tumor are similar, but distinct from those of primary tumors and lymph node metastases (LNMs). LCTCs, but not BCTCs, exist in clusters, display a hybrid epithelial/mesenchymal phenotype and cancer stem cell‐like properties, and are efficient metastatic precursors. These results demonstrate that tumor cells that metastasize through the lymphatic system are different from those spread by blood circulation. Understanding the relative contribution of these cells to overall peripheral blood‐circulating tumor cells is important for cancer therapy. Whether these two types of cell occur in cancer patients remains to be determined.
MTLn3  CTCs  gene_expression  stemness  CD44  CD24  mammosphere 
7 days ago by Segalllab
DepMap: The Cancer Dependency Map Project at Broad Institute
Cancer Dependency Map
for cell lines - mutations, gene expression gene dependencies, etc
The mutations that cause cancer cells to grow also confer specific vulnerabilities that normal cells lack. Some of these acquired alterations represent compelling therapeutic targets. The challenge is that, for the overwhelming majority of cancers, we do not fully understand the relationship between the genetic alterations of cancer and the dependencies they cause. To solve this problem, we are creating a “cancer dependency map” by systematically identifying genetic dependencies and small molecule sensitivities and discovering the biomarkers that predict them.

DepMap scientists are profiling hundreds of cancer cell line models for genomic information and sensitivity to genetic and small molecule perturbations. By triangulating information from these and other large-scale datasets, the hope is to define a landscape of genetic targets for therapeutic development, identify patients who respond to these therapies, and develop a better understanding of the vulnerabilities of cancer.

The Cancer Dependency Map project is committed to open science. We make all the data generated by the project available to the public under a Creative Commons license. The datasets are released pre-publication on a quarterly basis and are accessible on the DepMap portal.
The DepMap project at the Broad Institute is part of a strategic collaboration with the Wellcome Sanger Institute (Hinxton, UK). By leveraging the expertise and infrastructure available at both organisations, we aim to more rapidly deliver a high-quality DepMap. We anticipate that this foundational dataset will catalyse a new wave of precision cancer medicines.
cell_lines  gene_expression  gene_dependencies 
8 days ago by Segalllab
Integrated analyses of murine breast cancer models reveal critical parallels with human disease | Nature Communications
Key molecular analysis of PyMT and Neu models
Mouse models have an essential role in cancer research, yet little is known about how various models resemble human cancer at a genomic level. Here, we complete whole genome sequencing and transcriptome profiling of two widely used mouse models of breast cancer, MMTV-Neu and MMTV-PyMT. Through integrative in vitro and in vivo studies, we identify copy number alterations in key extracellular matrix proteins including collagen 1 type 1 alpha 1 (COL1A1) and chondroadherin (CHAD) that drive metastasis in these mouse models. In addition to copy number alterations, we observe a propensity of the tumors to modulate tyrosine kinase-mediated signaling through mutation of phosphatases such as PTPRH in the MMTV-PyMT mouse model. Mutation in PTPRH leads to increased phospho-EGFR levels and decreased latency. These findings underscore the importance of understanding the complete genomic landscape of a mouse model and illustrate the utility this has in understanding human cancers.
MMTV-pymt  MMTV-Neu  genomic  copy_number  gene_expression  mutations 
28 days ago by Segalllab
Transcriptional profiling of macrophage and tumor cell interactions in vitro
Macrophages are important mediators of tumor progression and their function is broadly influenced by different microenvironmental stimuli. To understand the molecular basis of the tumor-supporting role of macrophages in aggressive breast cancer we co-cultured human peripheral monocytes with two breast cancer cell lines representing distinct aggressive cellular phenotype and transcriptionally profiled the changes occurring in both cells during in vitro activated crosstalk. Here we provide a detailed description of the experimental design, sample identity and analysis of the Illumina RNA-Seq data, which have been deposited into Gene Expression Omnibus (GEO): GSE75130.
Keywords: Breast cancer, Co-culture, RNA-Seq, Illumina
T47D  231_cells  coculture  Macrophages  gene_expression 
4 weeks ago by Segalllab
Integrated Transcriptomic and Proteomic Analysis of Primary Human Umbilical Vein Endothelial Cells - Madugundu - - PROTEOMICS - Wiley Online Library
Understanding the molecular profile of every human cell type is essential for understanding its role in normal physiology and disease. Technological advancements in DNA sequencing, mass spectrometry, and computational methods allow us to carry out multiomics analyses although such approaches are not routine yet. Human umbilical vein endothelial cells (HUVECs) are a widely used model system to study pathological and physiological processes associated with the cardiovascular system. In this study, next‐generation sequencing and high‐resolution mass spectrometry to profile the transcriptome and proteome of primary HUVECs is employed. Analysis of 145 million paired‐end reads from next‐generation sequencing confirmed expression of 12 186 protein‐coding genes (FPKM ≥0.1), 439 novel long non‐coding RNAs, and revealed 6089 novel isoforms that were not annotated in GENCODE. Proteomics analysis identifies 6477 proteins including confirmation of N‐termini for 1091 proteins, isoforms for 149 proteins, and 1034 phosphosites. A database search to specifically identify other post‐translational modifications provide evidence for a number of modification sites on 117 proteins which include ubiquitylation, lysine acetylation, and mono‐, di‐ and tri‐methylation events. Evidence for 11 “missing proteins,” which are proteins for which there was insufficient or no protein level evidence, is provided. Peptides supporting missing protein and novel events are validated by comparison of MS/MS fragmentation patterns with synthetic peptides. Finally, 245 variant peptides derived from 207 expressed proteins in addition to alternate translational start sites for seven proteins and evidence for novel proteoforms for five proteins resulting from alternative splicing are identified. Overall, it is believed that the integrated approach employed in this study is widely applicable to study any primary cell type for deeper molecular characterization.
HUVECs  gene_expression  proteomics  rnaseq 
4 weeks ago by Segalllab
Accelerated evolution of oligodendrocytes in human brain | bioRxiv
> Recent discussions of human brain evolution have largely focused on increased neuron numbers and changes in their connectivity and expression. However, it is increasingly appreciated that oligodendrocytes play important roles in cognitive function and disease. Whether both cell-types follow similar or distinctive evolutionary trajectories is not known. We examined the transcriptomes of neurons and oligodendrocytes in the frontal cortex of humans, chimpanzees, and rhesus macaques. We identified human-specific trajectories of gene expression in neurons and oligodendrocytes and show that both cell-types exhibit human-specific upregulation. Moreover, oligodendrocytes have undergone accelerated gene expression evolution in the human lineage compared to neurons. The signature of acceleration is enriched for cell type-specific expression alterations in schizophrenia
oligodendrocytes  schizophrenia  evolution  gene_expression 
april 2019 by porejide
Genomic and Transcriptomic Analysis Reveals Incremental Disruption of Key Signaling Pathways during Melanoma Evolution: Cancer Cell
This study further delineates the sequential order in which signaling pathways become disrupted as benign and intermediate precursors evolve to melanoma in situ, invasive melanoma, and metastases. Activation of the MAPK pathway induces a benign nevus, constrained by replicative senescence, G1/S arrest, and chromatin organization. These barriers are incrementally overrun during melanoma formation, and melanomas continue to accumulate genetic alterations that ramp-up MAPK pathway signaling output and perturb the p53 and PI3K pathways. No mutations were specifically associated with metastatic dissemination to regional sites. Overall, we identify crucial steps in the development of melanoma, which can be subject to future treatments and can guide biomarker strategies to improve diagnosis and staging.
gene_expression  progression  tumorigenesis  melanoma 
march 2019 by Segalllab
The genomic landscape of UM-SCC oral cavity squamous cell carcinoma cell lines - ScienceDirect
Hmm - maybe only has deletions but they do not provide the RNAseq data??

Objectives

We sought to describe the genetic complexity of 14 UM-SCC oral cavity cancer cell lines that have remained uncharacterized despite being used as model systems for decades.
Materials and Methods

We performed exome sequencing on 14 oral cavity UM-SCC cell lines and denote the mutational profile of each line. We used a SNP array to profile the multiple copy number variations of each cell line and use immunoblotting to compare alterations to protein expression of commonly amplified genes (EGFR, PIK3CA, etc.). RNA sequencing was performed to characterize the expression of genes with copy number alterations.
Results

The cell lines displayed a highly complex network of genetic aberrations that was consistent with alterations identified in the HNSCC TCGA project including PIK3CA amplification, CDKN2A deletion, as well as TP53 and CASP8 mutations, enabling genetic stratification of each cell line in the panel. Copy number FISH and spectral karyotyping analysis demonstrate that cell lines retain chromosomal heterogeneity.
Conclusions

Collectively, we developed an important resource for future oral cavity HNSCC cell line studies and highlight the complexity of genomic aberrations in cell lines.
umscc1  umscc47  mutations  gene_expression  rnaseq 
february 2019 by Segalllab
Mammary molecular portraits reveal lineage-specific features and progenitor cell vulnerabilities | JCB
Data are in excel files as supplementary data.

Here, we build a multimodal resource for the adult gland through comprehensive profiling of primary cell epigenomes, transcriptomes, and proteomes. We define systems-level relationships between chromatin–DNA–RNA–protein states, identify lineage-specific DNA methylation of transcription factor binding sites, and pinpoint proteins underlying progesterone responsiveness. Comparative proteomics of estrogen and progesterone receptor–positive and –negative cell populations, extensive target validation, and drug testing lead to discovery of stem and progenitor cell vulnerabilities. Top epigenetic drugs exert cytostatic effects; prevent adult mammary cell expansion, clonogenicity, and mammopoiesis; and deplete stem cell frequency. Select drugs also abrogate human breast progenitor cell activity in normal and high-risk patient samples. This integrative computational and functional study provides fundamental insight into mammary lineage and stem cell biology.
mammary_development  gene_expression  proteomics  epigenetics 
february 2019 by Segalllab
CANCERTOOL: A Visualization and Representation Interface to Exploit Cancer Datasets | Cancer Research
could be useful?

With the advent of OMICs technologies, both individual research groups and consortia have spear-headed the characterization of human samples of multiple pathophysiologic origins, resulting in thousands of archived genomes and transcriptomes. Although a variety of web tools are now available to extract information from OMICs data, their utility has been limited by the capacity of nonbioinformatician researchers to exploit the information. To address this problem, we have developed CANCERTOOL, a web-based interface that aims to overcome the major limitations of public transcriptomics dataset analysis for highly prevalent types of cancer (breast, prostate, lung, and colorectal). CANCERTOOL provides rapid and comprehensive visualization of gene expression data for the gene(s) of interest in well-annotated cancer datasets. This visualization is accompanied by generation of reports customized to the interest of the researcher (e.g., editable figures, detailed statistical analyses, and access to raw data for reanalysis). It also carries out gene-to-gene correlations in multiple datasets at the same time or using preset patient groups. Finally, this new tool solves the time-consuming task of performing functional enrichment analysis with gene sets of interest using up to 11 different databases at the same time. Collectively, CANCERTOOL represents a simple and freely accessible interface to interrogate well-annotated datasets and obtain publishable representations that can contribute to refinement and guidance of cancer-related investigations at all levels of hypotheses and design.

Significance: In order to facilitate access of research groups without bioinformatics support to public transcriptomics data, we have developed a free online tool with an easy-to-use interface that allows researchers to obtain quality information in a readily publishable format. Cancer Res; 78(21);
gene_expression  omics_analysis 
february 2019 by Segalllab
The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel | Cancer Research
Could be useful....

The intracellular effects and overall efficacies of anticancer therapies can vary significantly by tumor type. To identify patterns of drug-induced gene modulation that occur in different cancer cell types, we measured gene-expression changes across the NCI-60 cell line panel after exposure to 15 anticancer agents. The results were integrated into a combined database and set of interactive analysis tools, designated the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), that allows exploration of gene-expression modulation by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across agents and cell types and uncovered gene-expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses and identifying candidate biomarkers of drug activity. The NCI TPW, publicly available at https://tpwb.nci.nih.gov, provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to commonly used anticancer drugs.

Significance: The NCI Transcriptional Pharmacodynamics Workbench represents the most extensive compilation to date of directly measured longitudinal transcriptional responses to anticancer agents across a thoroughly characterized ensemble of cancer cell lines.
drug_sensitivity  gene_expression 
february 2019 by Segalllab
Cryptic DNA sequences may help cells survive starvation
> The team concluded that in normal cells with introns, those introns repress ribosomal-protein genes when food is in short supply to conserve energy.

Abou Elela says that “70 to 80% of the introns have the same effect. We have found an entirely new way for the cell to regulate itself when nutrients are depleted.”
RNA  gene_expression 
january 2019 by porejide
Vav3-induced cytoskeletal dynamics contribute to heterotypic properties of endothelial barriers | JCB
Partial characterizaiton of multiple types of endothelium that was purchased using nanostring for 283 genes. Also single cell RNAseq for lung so lung endothelium at greater depth

Through multiple cell–cell and cell–matrix interactions, epithelial and endothelial sheets form tight barriers. Modulators of the cytoskeleton contribute to barrier stability and act as rheostats of vascular permeability. In this study, we sought to identify cytoskeletal regulators that underlie barrier diversity across vessels. To achieve this, we correlated functional and structural barrier features to gene expression of endothelial cells (ECs) derived from different vascular beds. Within a subset of identified candidates, we found that the guanosine nucleotide exchange factor Vav3 was exclusively expressed by microvascular ECs and was closely associated with a high-resistance barrier phenotype. Ectopic expression of Vav3 in large artery and brain ECs significantly enhanced barrier resistance and cortical rearrangement of the actin cytoskeleton. Mechanistically, we found that the barrier effect of Vav3 is dependent on its Dbl homology domain and downstream activation of Rap1. Importantly, inactivation of Vav3 in vivo resulted in increased vascular leakage, highlighting its function as a key regulator of barrier stability.
endothelium  gene_expression  single_cell_rnaseq  lung 
january 2019 by Segalllab
RNA-Seq of Circulating Tumor Cells in Stage II–III Breast Cancer | SpringerLink
PIK3CB was increased in CTCs over PTs.


Background

We characterized the whole transcriptome of circulating tumor cells (CTCs) in stage II–III breast cancer to evaluate correlations with primary tumor biology.
Methods

CTCs were isolated from peripheral blood (PB) via immunomagnetic enrichment followed by fluorescence-activated cell sorting (IE/FACS). CTCs, PB, and fresh tumors were profiled using RNA-seq. Formalin-fixed, paraffin-embedded (FFPE) tumors were subjected to RNA-seq and NanoString PAM50 assays with risk of recurrence (ROR) scores.
Results

CTCs were detected in 29/33 (88%) patients. We selected 21 cases to attempt RNA-seq (median number of CTCs = 9). Sixteen CTC samples yielded results that passed quality-control metrics, and these samples had a median of 4,311,255 uniquely mapped reads (less than PB or tumors). Intrinsic subtype predicted by comparing estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) versus PAM50 for FFPE tumors was 85% concordant. However, CTC RNA-seq subtype assessed by the PAM50 classification genes was highly discordant, both with the subtype predicted by ER/PR/HER2 and by PAM50 tumors. Two patients died of metastatic disease, both of whom had high ROR scores and high CTC counts. We identified significant genes, canonical pathways, upstream regulators, and molecular interaction networks comparing CTCs by various clinical factors. We also identified a 75-gene signature with highest expression in CTCs and tumors taken together that was prognostic in The Cancer Genome Atlas and Molecular Taxonomy of Breast Cancer International Consortium datasets.
Conclusion

It is feasible to use RNA-seq of CTCs in non-metastatic patients to discover novel tumor biology characteristics.
CTCs  rna-seq  gene_expression  pik3cb 
january 2019 by Segalllab
Human brain samples yield a genomic trove | Science
> Neurogeneticist Kevin Mitchell of Trinity College Dublin echoes some of Graur's concerns. “I'm not fully convinced that we know more today than we did yesterday,” he says. He doubts that a profile of gene expression can define disorders as heterogeneous as schizophrenia or autism—or give new insights into how to treat them. “It's a huge amount of work, very well intended and very well done,” he says, “but there are some limits to what you can do with genomics.”

But many researchers defend the project's value. “I'm sure there are researchers out there who will look at these first papers and say, … ‘Where is our paradigm-shifting finding?’” says Alexander Nord, a neurogeneticist at UC Davis who was not in the consortium. “That's a bit of a straw man, expecting us to find that in one set of analyses.” The data set will grow richer as researchers work to interpret it, he says. “It's not going to go out of style.”
gene_expression  kevin_mitchell  psychiatry 
december 2018 by porejide
In Search for Reliable Markers of Glioma-Induced Polarization of Microglia
Expression analysis of immortalized (?) microglial lines cocultured with U87 or LN18 - need to ch



"Immune cells accumulating in the microenvironment of malignant tumors are tumor educated and contribute to its growth, progression, and evasion of antitumor immune responses. Glioblastoma (GBM), the common and most malignant primary brain tumor in adults, shows considerable accumulation of resident microglia and peripheral macrophages, and their polarization into tumor-supporting cells. There are controversies regarding a functional phenotype of glioma-associated microglia/macrophages (GAMs) due to a lack of consistent markers. Previous categorization of GAM polarization toward the M2 phenotype has been found inaccurate because of oversimplification of highly complex and heterogeneous responses. In this study, we characterized functional responses and gene expression in mouse and human microglial cultures exposed to fresh conditioned media [glioma-conditioned medium (GCM)] from human U87 and LN18 glioma cells. Functional analyses revealed mutual communication reflected by strong stimulation of glioma invasion by microglial cells and increased microglial phagocytosis after GCM treatment. To define transcriptomic markers of GCM-activated microglia, we performed selected and global gene expression analyses of stimulated microglial cells. We found activated pathways associated with immune evasion and TGF signaling. We performed computational comparison of the expression patterns of GAMs from human GBMs and rodent experimental gliomas to select genes consistently changed in different datasets. The analyses of marker genes in GAMs from different experimental models and clinical samples revealed only a small set of common genes, which reflects variegated responses in clinical and experimental settings. Tgm2 and Gpnmb were the only two genes common in the analyzed data sets. We discuss potential sources of the observed differences and stress a great need for definitive elucidation of a functional state of GAMs.
microglia  Glioblastoma  coculture  U87  ln18  gene_expression  macrophage_polarization  polarization 
november 2018 by Segalllab
JCI - Integrated RNA and DNA sequencing reveals early drivers of metastatic breast cancer
Strikingly, only p53 mutations in primary tumor were strongly correlated. Also could not develop a metastasis signature that predicted outcome, though unclear if they did this in a subtype specific manner.

"In summary, this study validates and further expands upon the compelling evidence of multiclonal seeding across multiple subtypes of breast cancer, especially for TNBC/basal-like tumors. Additionally, we show that most genetic drivers arise from CNAs. The mechanisms underlying the generation of genetic diversity are becoming known, including the consistency we observed across our patient cohort and previous literature suggesting that TP53 dysfunction is an early and critical event in the development of aggressive breast cancers. Despite the high degree of heterogeneity in primary breast cancers and metastases, our results also show that the majority of genetic drivers are established in the primary breast cancer and maintained throughout metastasis. This study provides hope that the therapeutic targeting of founding events driving the primary and metastatic tumor phenotype might both prevent and inhibit the progression of metastasis.
Metastasis  breast_cancer  gene_expression  rna-seq  p53 
july 2018 by Segalllab
VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis | Nature Communications
ERK phosphorylation of ETS1 leads to CBP acetylation of ETS1 for increased transcription.


RNAPII pausing and pausing-release is the rate-limiting step for productive transcription of many genes7, 8. Here we show that regulation of RNAPII pause release is critical for angiogenesis, and we delineate a molecular pathway that links VEGF to broad induction of EC gene transcription through RNAPII pause release (Fig. 7d). VEGF activates ERK, which phosphorylates ETS1 at T38 and S41. CBP is recruited to phosphorylated ETS1, inducing acetylation of ETS1 and likely other local chromatin elements such as histones. Acetylated ETS1 recruits BRD4 and the active P-TEFb pause release complex, thereby rapidly and widely increasing gene expression. In addition, VEGF increases ETS1 chromatin occupancy, which contributes to upregulation of late response genes, likely through both increased RNAPII recruitment and pause release (Fig. 7d).
ERK  ets1  acetylation  brd4  cbp  gene_expression 
may 2018 by Segalllab

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