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Journal articles on the topic 'ChIP-Seq motifs finding'

Author: Grafiati

Published: 5 June 2025

Last updated: 1 August 2025

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1

Zhang, Yipu, and Ping Wang. "A Fast Cluster Motif Finding Algorithm for ChIP-Seq Data Sets." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/218068.

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New high-throughput technique ChIP-seq, coupling chromatin immunoprecipitation experiment with high-throughput sequencing technologies, has extended the identification of binding locations of a transcription factor to the genome-wide regions. However, the most existing motif discovery algorithms are time-consuming and limited to identify binding motifs in ChIP-seq data which normally has the significant characteristics of large scale data. In order to improve the efficiency, we propose a fast cluster motif finding algorithm, named as FCmotif, to identify the(l, d)motifs in large scale ChIP-seq

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Mukhin, A. M., V. G. Levitsky, and S. A. Lashin. "Developing of WebMCOT Web-Service for Finding Cooperative Site-Binding TF DNA-Motifs." Vestnik NSU. Series: Information Technologies 17, no. 4 (2019): 74–86. http://dx.doi.org/10.25205/1818-7900-2019-17-4-5-74-86.

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Regulation of eukaryotic gene transcription is controlled by specific proteins transcription factors. Transcription factors bind certain regions of genomic DNA (binding sites or motives). Common action of two or more transcription factors is widespread mechanism of transcription factor action. Hence, the term ‘composite element’ implied two closely located and frequently occurred in genomic DNA motives. Composite elements are partitioned onto those with two overlapped motifs, or with these two motifs separated with a spacer. Currently, the chromatin immunoprecipitation high throughput approach

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Ngo, Vu, Mengchi Wang, and Wei Wang. "Finding de novo methylated DNA motifs." Bioinformatics 35, no. 18 (2019): 3287–93. http://dx.doi.org/10.1093/bioinformatics/btz079.

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Abstract Motivation Increasing evidence has shown that nucleotide modifications such as methylation and hydroxymethylation on cytosine would greatly impact the binding of transcription factors (TFs). However, there is a lack of motif finding algorithms with the function to search for motifs with modified bases. In this study, we expand on our previous motif finding pipeline Epigram to provide systematic de novo motif discovery and performance evaluation on methylated DNA motifs. Results mEpigram outperforms both MEME and DREME on finding modified motifs in simulated data that mimics various mo

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Vishnevsky, Oleg V., Andrey V. Bocharnikov, and Nikolay A. Kolchanov. "Argo_CUDA: Exhaustive GPU based approach for motif discovery in large DNA datasets." Journal of Bioinformatics and Computational Biology 16, no. 01 (2018): 1740012. http://dx.doi.org/10.1142/s0219720017400121.

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The development of chromatin immunoprecipitation sequencing (ChIP-seq) technology has revolutionized the genetic analysis of the basic mechanisms underlying transcription regulation and led to accumulation of information about a huge amount of DNA sequences. There are a lot of web services which are currently available for de novo motif discovery in datasets containing information about DNA/protein binding. An enormous motif diversity makes their finding challenging. In order to avoid the difficulties, researchers use different stochastic approaches. Unfortunately, the efficiency of the motif

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Mahmoud, Hammad, Bani Baker Qanita, Al-Smadi Mohammed, and Alrashdan Wesam. "Towards enhancing the user experience of ChIP-Seq data analysis web tools." International Journal of Electrical and Computer Engineering (IJECE) 12, no. 5 (2022): 5236–47. https://doi.org/10.11591/ijece.v12i5.pp5236-5247.

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Deoxyribonucleic acid (DNA) sequencing is the process of locating the sequence of the main chemical bases in the DNA. Next-generation sequencing (NGS) is the state-of-the-art DNA sequencing technique. The NGS technique advanced the biological science in analyzing human DNA due to its scalability, high throughput, and speed. Analyzing human DNA is crucial to determine the ability of a person to develop certain diseases and his ability to respond to certain medications. ChIP-sequencing is a method that combines chromatin immunoprecipitation (ChIP) with NGS sequencing to analyze protein interacti

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Tran, Ngoc Tam L., and Chun-Hsi Huang. "A survey of motif finding Web tools for detecting binding site motifs in ChIP-Seq data." Biology Direct 9, no. 1 (2014): 4. http://dx.doi.org/10.1186/1745-6150-9-4.

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Li, Yang, Pengyu Ni, Shaoqiang Zhang, Guojun Li, and Zhengchang Su. "ProSampler: an ultrafast and accurate motif finder in large ChIP-seq datasets for combinatory motif discovery." Bioinformatics 35, no. 22 (2019): 4632–39. http://dx.doi.org/10.1093/bioinformatics/btz290.

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Abstract Motivation The availability of numerous ChIP-seq datasets for transcription factors (TF) has provided an unprecedented opportunity to identify all TF binding sites in genomes. However, the progress has been hindered by the lack of a highly efficient and accurate tool to find not only the target motifs, but also cooperative motifs in very big datasets. Results We herein present an ultrafast and accurate motif-finding algorithm, ProSampler, based on a novel numeration method and Gibbs sampler. ProSampler runs orders of magnitude faster than the fastest existing tools while often more ac

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Zambelli, Federico, Graziano Pesole, and Giulio Pavesi. "PscanChIP: finding over-represented transcription factor-binding site motifs and their correlations in sequences from ChIP-Seq experiments." Nucleic Acids Research 41, W1 (2013): W535—W543. http://dx.doi.org/10.1093/nar/gkt448.

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Korbolina, Elena E., Leonid O. Bryzgalov, Diana Z. Ustrokhanova, et al. "A Panel of rSNPs Demonstrating Allelic Asymmetry in Both ChIP-seq and RNA-seq Data and the Search for Their Phenotypic Outcomes through Analysis of DEGs." International Journal of Molecular Sciences 22, no. 14 (2021): 7240. http://dx.doi.org/10.3390/ijms22147240.

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Currently, the detection of the allele asymmetry of gene expression from RNA-seq data or the transcription factor binding from ChIP-seq data is one of the approaches used to identify the functional genetic variants that can affect gene expression (regulatory SNPs or rSNPs). In this study, we searched for rSNPs using the data for human pulmonary arterial endothelial cells (PAECs) available from the Sequence Read Archive (SRA). Allele-asymmetric binding and expression events are analyzed in paired ChIP-seq data for H3K4me3 mark and RNA-seq data obtained for 19 individuals. Two statistical approa

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Martin-Trujillo, Alejandro, Nihir Patel, Felix Richter, et al. "Rare genetic variation at transcription factor binding sites modulates local DNA methylation profiles." PLOS Genetics 16, no. 11 (2020): e1009189. http://dx.doi.org/10.1371/journal.pgen.1009189.

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Although DNA methylation is the best characterized epigenetic mark, the mechanism by which it is targeted to specific regions in the genome remains unclear. Recent studies have revealed that local DNA methylation profiles might be dictated by cis-regulatory DNA sequences that mainly operate via DNA-binding factors. Consistent with this finding, we have recently shown that disruption of CTCF-binding sites by rare single nucleotide variants (SNVs) can underlie cis-linked DNA methylation changes in patients with congenital anomalies. These data raise the hypothesis that rare genetic variation at

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Lee, Young Koung, Sunita Kumari, Andrew Olson, Felix Hauser, and Doreen Ware. "Role of a ZF-HD Transcription Factor in miR157-Mediated Feed-Forward Regulatory Module That Determines Plant Architecture in Arabidopsis." International Journal of Molecular Sciences 23, no. 15 (2022): 8665. http://dx.doi.org/10.3390/ijms23158665.

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In plants, vegetative and reproductive development are associated with agronomically important traits that contribute to grain yield and biomass. Zinc finger homeodomain (ZF-HD) transcription factors (TFs) constitute a relatively small gene family that has been studied in several model plants, including Arabidopsis thaliana L. and Oryza sativa L. The ZF-HD family members play important roles in plant growth and development, but their contribution to the regulation of plant architecture remains largely unknown due to their functional redundancy. To understand the gene regulatory network control

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Rai, Shinya, Gerben Duns, Fabian Frontzek, et al. "Multiomic Profiling Reveals Pleiotropic Effects of Somatic IRF4-C99R Mutations in Primary Mediastinal Large B-Cell Lymphomas." Blood 144, Supplement 1 (2024): 2966. https://doi.org/10.1182/blood-2024-199227.

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Introduction: Interferon Regulatory Factor 4 (IRF4) is a transcription factor that plays a critical role in the regulation of pre-B-cell development, the germinal center reaction as well as plasma cell differentiation. IRF4 has emerged as a master regulator of cancer-specific gene expression programs in various lymphoid malignancies. Prior studies uncovered a hotspot missense mutation in the DNA-binding domain of IRF4 (C99R) that alters the affinity of binding to specific DNA motifs and leads to disease-specific changes in classic Hodgkin lymphoma (Schleussner et al, 2023). The C99R mutations

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De Gobbi, Marco, Jim R. Hughes, Karen M. Lower, et al. "Discovering Regulatory SNPs by Genome-Wide Analysis of Differential Scl/TAL-1 Occupancy in Human Primary Erythroid Cells,." Blood 118, no. 21 (2011): 3381. http://dx.doi.org/10.1182/blood.v118.21.3381.3381.

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Abstract Abstract 3381 It is well established that the level of gene expression can vary significantly between normal individuals, and that the majority of this variation is due to naturally occurring genomic variability caused by single nucleotide polymorphisms (SNPs). Therefore, identifying functional cis-regulatory polymorphisms and understanding how they influence gene expression is an important new task in many areas of medical research, including molecular hematology. We have previously shown that an entirely new form of alpha-thalassemia is caused by a gain of function regulatory SNP in

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Neri, Paola, Ines Tagoug, Justin Simms, et al. "Ikaros-Dependent Downregulation of MYC with IMiDs in Myeloma (MM) Cells Is Mediated through the Depletion of the Acetylated Chromatin Reader BRD4 at Super-Enhancer Loci." Blood 126, no. 23 (2015): 4175. http://dx.doi.org/10.1182/blood.v126.23.4175.4175.

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Abstract Background: IMiDs are now recognized to promote the proteasomal degradation of IKZF1/3 and the transcriptional repression of MYC and IRF4. MYC locus rearrangement is a recurrent somatic event in MM and results in MYC repositioning near superenhancers (such as IGH@, IGL@ and others). The mechanisms of IMiDs-mediated downregulation of MYC in MM cells is not well understood, in particular it is unclear how IMiDs alter the activity of the super-enhancers driving MYC transcription. Methods and results: Transcriptome analysis (RNAseq) of MM cells (OPM2 and MM1S) treated with lenalidomide or

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Loh, Christopher, Sung-ho Park, Angela Lee, Ruoxi Yuan, Lionel B. Ivashkiv, and George D. Kalliolias. "TNF-induced inflammatory genes escape repression in fibroblast-like synoviocytes: transcriptomic and epigenomic analysis." Annals of the Rheumatic Diseases 78, no. 9 (2019): 1205–14. http://dx.doi.org/10.1136/annrheumdis-2018-214783.

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ObjectiveWe investigated genome-wide changes in gene expression and chromatin remodelling induced by tumour necrosis factor (TNF) in fibroblast-like synoviocytes (FLS) and macrophages to better understand the contribution of FLS to the pathogenesis of rheumatoid arthritis (RA).MethodsFLS were purified from patients with RA and CD14+ human monocyte-derived macrophages were obtained from healthy donors. RNA-sequencing, histone 3 lysine 27 acetylation (H3K27ac), chromatin immunoprecipitation-sequencing (ChIP-seq) and assay for transposable accessible chromatin by high throughput sequencing (ATAC-

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Schulz, Vincent P., Kimberly Lezon-Geyda, Yelena Maksimova, and Patrick G. Gallagher. "Enhancers and Super Enhancers Are Associated With Genes That Control Phenotypic Traits In Primary Human Erythroid Cells." Blood 122, no. 21 (2013): 1200. http://dx.doi.org/10.1182/blood.v122.21.1200.1200.

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Abstract Identification of cell-type specific enhancers is important for understanding the regulation of programs controlling cellular development and differentiation. Recent studies have shown that enhancers are frequently associated with biologically relevant and disease-associated genetic variants. We hypothesized that unique sets of enhancers and super enhancers regulate gene expression in erythroid cells, a specialized cell type evolved to carry oxygen, and associated variants influence erythroid phenotypic variability. Active enhancers are part of a chromatin landscape marked by histone

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Patterson, Shaun David, Matthew E. Massett, Helen Wheadon, Xu Huang, Heather G. Jørgensen, and Alison M. Michie. "NFATC2 regulates Targets of MYC Signaling in MLL-AF9 AML." Blood 138, Supplement 1 (2021): 3301. http://dx.doi.org/10.1182/blood-2021-151388.

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Abstract Background: Acute myeloid leukemia (AML) arises due to an accumulation of genetic lesions within myeloid progenitors and oncogenic transformation is often characterised by disordered transcription. Recently the histone lysine demethylase KDM4A was shown to be essential for AML blast survival and self-renewal. shRNA knockdown (KD) of KDM4A led to downregulated expression of the transcription factor NFATC2 an MLL-AF9 AML model, suggesting that it is a key target of KDM4A oncogenic function. The Nuclear Factor of Activated T Cells (NFAT) family of transcription factors control cell cycle

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Huang, Tinghua, Hong Xiao, Qi Tian, et al. "Identification of upstream transcription factor binding sites in orthologous genes using mixed Student’s t-test statistics." PLOS Computational Biology 18, no. 6 (2022): e1009773. http://dx.doi.org/10.1371/journal.pcbi.1009773.

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Background Transcription factor (TF) regulates the transcription of DNA to messenger RNA by binding to upstream sequence motifs. Identifying the locations of known motifs in whole genomes is computationally intensive. Methodology/Principal findings This study presents a computational tool, named “Grit”, for screening TF-binding sites (TFBS) by coordinating transcription factors to their promoter sequences in orthologous genes. This tool employs a newly developed mixed Student’s t-test statistical method that detects high-scoring binding sites utilizing conservation information among species. T

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Lin, Karena Hsijan, Annie Wang, Kailey Lashbrook, et al. "Crispri Essentiality Screen Reveals the Essential Enhancers and Oncogenes Comprising the “Regulome” of the Notch-Collaborating Transcription Factor ETS1 in Human T-ALL." Blood 144, Supplement 1 (2024): 4131. https://doi.org/10.1182/blood-2024-210398.

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive lymphoid malignancy derived from immature T cells. No targeted therapies are currently available. Although over 60% of T-ALL samples carry activating mutations in the Notch signaling pathway, this finding has been difficult to translate clinically as pan-Notch inhibitors have significant toxicities. We previously showed that ETS1 is an important Notch co-binding transcription factor in T-ALL and could represent a safer therapeutic target. ETS motifs are the top-ranked motif next to Notch-RBPJ sites in T-ALL, suggesting a strong colla

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Eapen, Amy A., Sreeja Parameswaran, Carmy Forney, et al. "Epigenetic and transcriptional dysregulation in CD4+ T cells in patients with atopic dermatitis." PLOS Genetics 18, no. 5 (2022): e1009973. http://dx.doi.org/10.1371/journal.pgen.1009973.

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Atopic dermatitis (AD) is one of the most common skin disorders among children. Disease etiology involves genetic and environmental factors, with 29 independent AD risk loci enriched for risk allele-dependent gene expression in the skin and CD4+ T cell compartments. We investigated the potential epigenetic mechanisms responsible for the genetic susceptibility of CD4+ T cells. To understand the differences in gene regulatory activity in peripheral blood T cells in AD, we measured chromatin accessibility (an assay based on transposase-accessible chromatin sequencing, ATAC-seq), nuclear factor ka

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Gao, Ang, Parth Khatri, Gui Ma, et al. "Abstract 4308: BRD8 is a therapeutic vulnerability for overcoming resistance to dual ER/HER2 blockade therapy in HR+/HER2+ breast cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 4308. https://doi.org/10.1158/1538-7445.am2025-4308.

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Abstract Hormone receptor (HR)-positive, HER2-positive breast cancers often develop resistance to endocrine and anti-HER2 therapies due to the heterogeneous expression of estrogen receptor (ER) and HER2 and the crosstalk of these growth-promoting pathways. However, how anti-HER2 agents activate ER and other growth-promoting pathways remains unknown. Single-cell RNA sequencing of BT474 breast cancer cells identified Bromodomain Containing Protein 8 (BRD8), an acetyl-lysine reader protein in the histone acetylase EP400 complex, as a pivotal mediator to activate ER in response to neratinib treatm

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Liu, Bingqiang, Jinyu Yang, Yang Li, Adam McDermaid, and Qin Ma. "An algorithmic perspective of de novo cis-regulatory motif finding based on ChIP-seq data." Briefings in Bioinformatics 19, no. 5 (2017): 1069–81. http://dx.doi.org/10.1093/bib/bbx026.

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Hogart, Amber, Jens Lichtenberg, Subramanian Ajay, Elliott Margulies, and David M. Bodine. "Genome-Wide DNA Methylation Profiling of Hematopoietic Stem and Progenitor Cells Reveals Over-Representation of ETS Transcrition Factor Binding Sites." Blood 118, no. 21 (2011): 211. http://dx.doi.org/10.1182/blood.v118.21.211.211.

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Abstract Abstract 211 The hematopoietic system is ideal for the study of epigenetic changes in primary cells because hematopoietic cells representing distinct stages of hematopoiesis can be enriched and isolated by differences in surface marker expression. DNA methylation is an essential epigenetic mark that is required for normal development. Conditional knockout of the DNA methyltransferase enzymes in the mouse hematopoietic compartment have revealed that methylation is critical for long-term renewal and lineage differentiation of hematopoietic stem cells (Broske et al 2009, Trowbridge el al

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Kong, Qing, Perng-Kuang Chang, Chunjuan Li, et al. "Identification of AflR Binding Sites in the Genome of Aspergillus flavus by ChIP-Seq." Journal of Fungi 6, no. 2 (2020): 52. http://dx.doi.org/10.3390/jof6020052.

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We report here the AflR binding motif of Aspergillus flavus for the first time with the aid of ChIP-seq analysis. Of the 540 peak sequences associated with AflR binding events, 66.8% were located within 2 kb upstream (promoter region) of translational start sites. The identified 18-bp binding motif was a perfect palindromic sequence, 5′-CSSGGGWTCGAWCCCSSG’3′ with S representing G or C and W representing A or T. On closer examination, we hypothesized that the 18-bp motif sequence identified contained two identical parts (here called motif A and motif B). Motif A was in positions 8–18 on the upp

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Schulz, Vincent P., Kimberly Lezon-Geyda, Peiying Shan, et al. "Identification of a Novel Gene Regulatory Element in Human Erythroid Progenitor Cells." Blood 142, Supplement 1 (2023): 9. http://dx.doi.org/10.1182/blood-2023-186046.

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Early erythropoiesis involves commitment of multi-lineage progenitors to erythroid progenitor cells and differentiation into erythroid burst-forming unit (BFU-E) cells, then erythroid colony-forming unit (CFU-E) cells. In contrast to terminal erythroid differentiation, regulation of gene expression in early erythropoiesis is poorly defined. To address this knowledge gap, we identified active enhancers in erythroid progenitor cells linked to known disease genes and genes associated with erythrocyte traits in genome wide association studies. Human CD34+ hematopoietic stem and progenitor cells (H

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Kurita, Daisuke, Jun-ichirou Yasunaga, Azusa Tanaka, Mahgoub Mohamed, and Masao Matsuoka. "Dynamic Changes of Chromatin Structure and Transcriptome By Transient Expression of HTLV-1 Tax in ATL Cells." Blood 132, Supplement 1 (2018): 4094. http://dx.doi.org/10.1182/blood-2018-99-111125.

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Abstract Adult T-cell leukemia-lymphoma (ATL) is a fatal malignancy of CD4+ T cells, which is caused by human T-cell leukemia virus type 1 (HTLV-1). HTLV-1 encodes two oncogenic viral factors, Tax and HTLV-1 bZIP factor (HBZ) in the sense and antisense of the provirus respectively. HBZ is constitutively expressed in infected cells and plays critical roles for cell proliferation. Tax potently promotes viral replication and activates various oncogenic signaling pathways in HTLV-1 infected cells; however, Tax expression is generally suppressed in infected cells owing to its high immunogenicity. T

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Taing, Len, Gali Bai, Clara Cousins, et al. "CHIPS: A Snakemake pipeline for quality control and reproducible processing of chromatin profiling data." F1000Research 10 (June 30, 2021): 517. http://dx.doi.org/10.12688/f1000research.52878.1.

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Motivation: The chromatin profile measured by ATAC-seq, ChIP-seq, or DNase-seq experiments can identify genomic regions critical in regulating gene expression and provide insights on biological processes such as diseases and development. However, quality control and processing chromatin profiling data involves many steps, and different bioinformatics tools are used at each step. It can be challenging to manage the analysis. Results: We developed a Snakemake pipeline called CHIPS (CHromatin enrIchment ProcesSor) to streamline the processing of ChIP-seq, ATAC-seq, and DNase-seq data. The pipelin

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Lien, Yu-Chin, Paul Zhiping Wang, Xueqing Maggie Lu, and Rebecca A. Simmons. "Altered Transcription Factor Binding and Gene Bivalency in Islets of Intrauterine Growth Retarded Rats." Cells 9, no. 6 (2020): 1435. http://dx.doi.org/10.3390/cells9061435.

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Intrauterine growth retardation (IUGR), which induces epigenetic modifications and permanent changes in gene expression, has been associated with the development of type 2 diabetes. Using a rat model of IUGR, we performed ChIP-Seq to identify and map genome-wide histone modifications and gene dysregulation in islets from 2- and 10-week rats. IUGR induced significant changes in the enrichment of H3K4me3, H3K27me3, and H3K27Ac marks in both 2-wk and 10-wk islets, which were correlated with expression changes of multiple genes critical for islet function in IUGR islets. ChIP-Seq analysis showed t

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Zhang, Yipu, Ping Wang, and Maode Yan. "An Entropy-Based Position Projection Algorithm for Motif Discovery." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9127474.

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Motif discovery problem is crucial for understanding the structure and function of gene expression. Over the past decades, many attempts using consensus and probability training model for motif finding are successful. However, the most existing motif discovery algorithms are still time-consuming or easily trapped in a local optimum. To overcome these shortcomings, in this paper, we propose an entropy-based position projection algorithm, called EPP, which designs a projection process to divide the dataset and explores the best local optimal solution. The experimental results on real DNA sequenc

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Behera, Vivek, Perry Evans, Carolyne J. Face, Laavanya Sankaranarayanan, and Gerd A. Blobel. "Deep Mining of Natural Genetic Variation in Erythroid Cells Reveals New Insights about In Vivo Transcription Factor Binding and Chromatin Accessibility." Blood 128, no. 22 (2016): 3879. http://dx.doi.org/10.1182/blood.v128.22.3879.3879.

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Abstract Erythroid transcription factors (TFs) control gene expression programs, lineage decisions, and disease outcomes. How transcription factors contact DNA has been studied extensively in vitro, but in vivo binding characteristics are less well understood as they are influenced in a reciprocal manner by chromatin accessibility and neighboring transcription factors. Here, we present a comparative analysis approach that takes advantage of non-coding sequence variation between functionally equivalent erythroid cell lines to conduct an in-depth analysis of erythroid TF binding profiles and chr

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Weigel, Christoph, Yassen Assenov, Charles Imbusch, et al. "Recurrent Mutations in EGR2 Direct Specific Epigenetic Reconfiguration in Chronic Lymphocytic Leukemia." Blood 132, Supplement 1 (2018): 650. http://dx.doi.org/10.1182/blood-2018-99-119070.

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Abstract Epigenetic alterations are universal in cancer and are important in establishing the malignant phenotype. Dissection of the factors that shape the tumor-specific epigenome may reveal insight into key aspects of tumorigenesis and therapeutic resistance. In chronic lymphocytic leukemia (CLL), we have previously found that broad changes in epigenetic patterns co-occur with the evolution of genetic alterations. We have also uncovered that aberrant patterning of DNA methylation in CLL involves excessive activity of a defined group of transcription factors (TFs), including the early growth

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Zhu, Heqing, Yingying Li, He Xu, et al. "Role of Csdc2 in Regulating Secondary Hair Follicle Growth in Cashmere Goats." International Journal of Molecular Sciences 25, no. 15 (2024): 8349. http://dx.doi.org/10.3390/ijms25158349.

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Cashmere goats possess two types of hair follicles, with the secondary hair follicles producing valuable cashmere fiber used for textiles. The growth of cashmere exhibits a seasonal pattern arising from photoperiod change. Transcription factors play crucial roles during this process. The transcription factor, cold-shock domain, containing C2 (Csdc2) plays a crucial role in modulating cell proliferation and differentiation. Our preceding research indicated that the expression of Csdc2 changes periodically during anagen to telogen. However, the mechanisms of Csdc2 in regulating SHF growth remain

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Stender, Joshua D., Kyuri Kim, Tze Howe Charn та ін. "Genome-Wide Analysis of Estrogen Receptor α DNA Binding and Tethering Mechanisms Identifies Runx1 as a Novel Tethering Factor in Receptor-Mediated Transcriptional Activation". Molecular and Cellular Biology 30, № 16 (2010): 3943–55. http://dx.doi.org/10.1128/mcb.00118-10.

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ABSTRACT Nuclear receptor estrogen receptor alpha (ERα) controls the expression of hundreds of genes responsible for target cell phenotypic properties, but the relative importance of direct versus tethering mechanisms of DNA binding has not been established. In this first report, we examine the genome-wide chromatin localization of an altered-specificity mutant ER with a DNA binding domain deficient in binding to estrogen response element (ERE)-containing DNA (DBDmut ER) versus wild-type ERα. Using high-throughput sequencing of ER chromatin immunoprecipitations (ChIP-Seq) and mRNA transcriptio

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Tu, Ting-Hui Clair, Jennifer Knapp, Laura Harmacek, et al. "Altered CD4+ T cell Transcriptional and Epigenetic Programming Define Changes in Sarcoidosis Disease Phenotypes." Journal of Immunology 204, no. 1_Supplement (2020): 224.42. http://dx.doi.org/10.4049/jimmunol.204.supp.224.42.

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Abstract Sarcoidosis is an inflammatory disease, which is characterized by granulomas in the lungs, extrapulmonary inflammation, and can cause death by lung fibrosis. It is known that CD4+ T cell lung population increases in Sarcoidosis. However, the immunopathology remains unclear and no biomarker has been identified. Here we use RNA-seq to examine gene expression in CD4+ T cells of differential Sarcoidosis phenotypes and healthy donors. Our data showed that BATF, a Tfh inducer/key factor in Th17 differentiation was up-regulated while BCL6, a Th17 repressor is down-regulated in RNA-seq. IRF4

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Zhu, Dandan, Jian Tu, Zijun Huo, et al. "Abstract 1616: Dissecting the biology and therapeutic vulnerabilities of RB1-mutant osteosarcoma using hereditary retinoblastoma iPSCs." Cancer Research 82, no. 12_Supplement (2022): 1616. http://dx.doi.org/10.1158/1538-7445.am2022-1616.

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Abstract Patients with hereditary retinoblastoma (RB), an inherited autosomal dominant cancer disordercaused by germline mutations/deletions in the RB1 gene, have a &gt;400 fold increased incidenceof osteosarcoma (OS), suggesting a strong mechanistic link between RB1 loss andosteosarcomagenesis. Although mice offer many advantages when conducting cancer research,unlike humans, Rb1 knockout mice do not develop OS, suggesting the urgent requirement foralternative disease models to understand how RB1 mutation leads to osteosarcomagenesis.Here, we generated patient-derived induced pluripotent

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Connelly, John C., Justyna Cholewa-Waclaw, Shaun Webb, Verdiana Steccanella, Bartlomiej Waclaw, and Adrian Bird. "Absence of MeCP2 binding to non-methylated GT-rich sequences in vivo." Nucleic Acids Research 48, no. 7 (2020): 3542–52. http://dx.doi.org/10.1093/nar/gkaa102.

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Abstract MeCP2 is a nuclear protein that binds to sites of cytosine methylation in the genome. While most evidence confirms this epigenetic mark as the primary determinant of DNA binding, MeCP2 is also reported to have an affinity for non-methylated DNA sequences. Here we investigated the molecular basis and in vivo significance of its reported affinity for non-methylated GT-rich sequences. We confirmed this interaction with isolated domains of MeCP2 in vitro and defined a minimal target DNA sequence. Binding depends on pyrimidine 5′ methyl groups provided by thymine and requires adjacent guan

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Stephens, Kimberly E., Weiqiang Zhou, Zhicheng Ji, Hongkai Ji, Yun Guan, and Sean D. Taverna. "63438 Differential chromatin accessibility at dorsal root ganglia enhancers is associated with nerve injury." Journal of Clinical and Translational Science 5, s1 (2021): 5. http://dx.doi.org/10.1017/cts.2021.414.

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ABSTRACT IMPACT: Our improved understanding of the changes in chromatin accessibility that occur in persistent pain states may identify regulatory genomic elements that play essential roles in modulating gene expression in the DRG. OBJECTIVES/GOALS: Efforts to understand genetic variability involved in an individual’s susceptibility to persistent pain support a role for upstream regulation by epigenetic mechanisms. Our objective was to examine the transcriptomic and epigenetic basis of persistent pain following nerve injury. METHODS/STUDY POPULATION: We used a multiomic approach to identify no

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El Zarif, Talal, Karl Semaan, Marc Eid, et al. "Epigenomic profiling nominates master transcription factors (TFs) driving sarcomatoid differentiation (SD) of renal cell carcinoma (RCC)." Oncologist 28, Supplement_1 (2023): S8. http://dx.doi.org/10.1093/oncolo/oyad216.012.

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Abstract Background Sarcomatoid differentiation of RCC (sRCC) is associated with poor survival. Recent studies showed marked response of sRCC to immune checkpoint blockade (ICB). While distinctive patterns of gene expression in sRCC have been identified, the gene regulatory programs and TFs that drive SD remain unknown. The aim of this study is to nominate TFs responsible for SD and to investigate their association with the clinical outcomes of patients with RCC. Methods Chromatin immunoprecipitation and sequencing (ChIP-seq) for H3K27ac – a histone modification associated with active regulato

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Arabzade, Amir, Yanhua Zhao, Srinidhi Varadharajan, et al. "EPEN-30. C11ORF95-RELA FUSION PROTEIN ENGAGES NOVEL GENOMIC LOCI TO DRIVE MURINE EPENDYMOMA GROWTH." Neuro-Oncology 22, Supplement_3 (2020): iii314. http://dx.doi.org/10.1093/neuonc/noaa222.166.

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Abstract RATIONALE Over 70% of supratentorial (ST) ependymoma are characterized by an oncogenic fusion between C11ORF95 and RELA. C11ORF95-RELA fusion is frequently the sole genetic driver detected in ST ependymoma, thus ranking this genomic event as a lead target for therapeutic investigation. RELA is a transcription factor (TF) central to mediating NF-kB pathway activation in processes such as inflammation, cellular metabolism, and chemotaxis. HYPOTHESIS: We posited that C11ORF95-RELA acts as an oncogenic TF that aberrantly shapes the tumor epigenome to drive aberrant transcription. Approach

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Hall, Duane D., Kathryn M. Spitler, and Chad E. Grueter. "Disruption of cardiac Med1 inhibits RNA polymerase II promoter occupancy and promotes chromatin remodeling." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 2 (2019): H314—H325. http://dx.doi.org/10.1152/ajpheart.00580.2018.

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The Mediator coactivator complex directs gene-specific expression by binding distal enhancer-bound transcription factors through its Med1 subunit while bridging to RNA polymerase II (Pol II) at gene promoters. In addition, Mediator scaffolds epigenetic modifying enzymes that determine local DNA accessibility. Previously, we found that deletion of Med1 in cardiomyocytes deregulates more than 5,000 genes and promotes acute heart failure. Therefore, we hypothesized that Med1 deficiency disrupts enhancer-promoter coupling. Using chromatin immunoprecipitation-coupled deep sequencing (ChIP-seq; n =

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Lucky, Amuza Byaruhanga, Ahmad Rushdi Shakri, Xiaoying Liang, et al. "GCN5 Is a Master Regulator of Gene Expression in the Malaria Parasite Plasmodium falciparum." Cells 14, no. 12 (2025): 876. https://doi.org/10.3390/cells14120876.

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GCN5-containing SAGA complex is evolutionarily conserved across yeast, plants, and humans and acts as a general transcription coactivator in the genome-wide regulation of genes. In Plasmodium falciparum, PfGCN5 forms a divergent complex, and the mis-localization of this complex by deleting the PfGCN5 bromodomain (ΔBrd) causes a plethora of growth defects. To directly test the PfGCN5 function, we performed conditional knockdown (KD) of PfGCN5. Whereas PfGCN5 KD phenotypically recapitulated the ΔBrd growth defects, it caused fewer transcriptional alterations compared to ΔBrd. To decipher the mec

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Tempera, Italo, Alessandra De Leo, Andrew V. Kossenkov, et al. "Identification ofMEF2B,EBF1, andIL6Ras Direct Gene Targets of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Critical for EBV-Infected B-Lymphocyte Survival." Journal of Virology 90, no. 1 (2015): 345–55. http://dx.doi.org/10.1128/jvi.02318-15.

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ABSTRACTEpstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is the EBV-encoded nuclear antigen and sequence-specific DNA binding protein required for viral origin binding and episome maintenance during latency. EBNA1 can also bind to numerous sites in the cellular genome and can provide a host cell survival function, but it is not yet known how EBNA1 sequence-specific binding is responsible for host cell survival. Here, we integrate EBNA1 chromatin immunoprecipitation sequencing (ChIP-Seq) with transcriptome sequencing (RNA-Seq) after EBNA1 depletion to identify cellular genes directly regulate

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Gong, Han, Bin Hu, Wenwen Xu, et al. "HLTF Regulates Erythroid Differentiation through Transcription Factors and Chromatin Landscape Modulation." Blood 144, Supplement 1 (2024): 3845. https://doi.org/10.1182/blood-2024-207540.

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Erythroid development is a critical process in which multipotent hematopoietic stem cells differentiate into mature red blood cells. This process is tightly regulated by transcription factors (TF), with GATA1 playing a central role as a master TF. While previous studies have demonstrated that GATA1 expression changes dynamically during erythroid development, the precise mechanisms regulating GATA1 in erythroid cells remain incompletely understood. To identify regulators of GATA1 in erythroid differentiation, we conducted DNA pull-down experiments coupled with mass spectrometry at different tim

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Götz, Silvia, Satyaprakash Pandey, Sabrina Bartsch, Stefan Juranek, and Katrin Paeschke. "A Novel G-Quadruplex Binding Protein in Yeast—Slx9." Molecules 24, no. 9 (2019): 1774. http://dx.doi.org/10.3390/molecules24091774.

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G-quadruplex (G4) structures are highly stable four-stranded DNA and RNA secondary structures held together by non-canonical guanine base pairs. G4 sequence motifs are enriched at specific sites in eukaryotic genomes, suggesting regulatory functions of G4 structures during different biological processes. Considering the high thermodynamic stability of G4 structures, various proteins are necessary for G4 structure formation and unwinding. In a yeast one-hybrid screen, we identified Slx9 as a novel G4-binding protein. We confirmed that Slx9 binds to G4 DNA structures in vitro. Despite these find

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Zhang, Na, Rongbin Zheng, and Myles Brown. "Abstract 3894: The role of ELF3 in acquired resistance to endocrine therapy in ER-positive breast cancer." Cancer Research 83, no. 7_Supplement (2023): 3894. http://dx.doi.org/10.1158/1538-7445.am2023-3894.

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Abstract Endocrine therapies targeting the estrogen receptor (ER) are the major treatments of ER+ breast cancer, however acquired resistance to endocrine therapy is almost unavoidable and is the main cause of death with breast cancer. The only FDA-approved selective estrogen receptor degrader (SERD) fulvestrant has been used in the second line treatment to overcome aromatase inhibitor- or tamoxifen-resistance. However, fulvestrant has poor pharmacokinetic properties, which has inspired the development of a new generation of oral SERDs including amcenestrant and giredestrant. To understand the

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Semaan, Karl, Talal El Zarif, Marc Eid, et al. "Abstract A029: Epigenomic profiling nominates master transcription factors (TFs) driving sarcomatoid differentiation of renal cell carcinoma (RCC)." Cancer Research 83, no. 16_Supplement (2023): A029. http://dx.doi.org/10.1158/1538-7445.kidney23-a029.

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Abstract Introduction Sarcomatoid RCC (sRCC) is associated with poor prognosis. Recent studies showed promising response rates of sRCC to immune checkpoint blockade (ICB). Although distinct patterns of gene expression in sRCC have been reported, the gene regulatory programs that drive SD remain unknown. This study aims to nominate TFs driving SD and to evaluate their impact on the clinical outcomes of patients (pts) with RCC. Methods Chromatin immunoprecipitation and sequencing (ChIP-seq) for H3K27ac was performed on histologically annotated areas of sRCC and non-sRCC fresh frozen tissue sampl

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Aster, Jon C., Hongfang Wang, James Zou, et al. "Genome-Wide Analysis Reveals Conserved and Divergent Features of Notch1/RBPJ Binding in Human and Murine T Lymphoblastic Leukemia Cells." Blood 118, no. 21 (2011): 5236. http://dx.doi.org/10.1182/blood.v118.21.5236.5236.

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Abstract Abstract 5236 Activated Notch1 regulates gene expression by associating with the DNA-binding factor RBPJ and is an important oncoprotein in murine and human T cell acute lymphoblastic leukemia/lymphoma (T-ALL), yet the interplay between Notch1 and other factors that regulate the transcriptional output of T-ALL cells is poorly understood. Using ChIP-Seq and starting with Notch1-dependent human and murine T-ALL cell lines, we find that Notch1 binds preferentially to promoters, to RBPJ binding sites, and near sites for ZNF143, as well as Ets and Runx factors. By ChIP-Seq, ZNF143 binds to

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Barski, Artem, Masashi Yukawa, Sajjeev Jagannathan, Andrey V. Kartashov, Xiaoting Chen, and Mathew T. Weirauch. "Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation." Journal of Immunology 202, no. 1_Supplement (2019): 125.13. http://dx.doi.org/10.4049/jimmunol.202.supp.125.13.

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Abstract Activation of T cells is dependent on organized and timely opening and closing of chromatin. Herein, we identify AP-1 as the transcription factor that directs most of this remodeling. Chromatin accessibility profiling showed quick opening of closed chromatin in naïve T cells within 5 hours of activation. These newly open regions were strongly enriched for the AP-1 motif, and indeed, ChIP-seq demonstrated AP-1 binding at more than 70% of them. Broad inhibition of AP-1 activity prevented chromatin opening at AP-1 sites and reduced expression of nearby genes. Similarly, induction of aner

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Khader, Nawrah, Anna Dorogin, Oksana Shynlova, and Jennifer A. Mitchell. "JUND plays a genome-wide role in the quiescent to contractile switch in the pregnant human myometrium." PLOS Genetics 21, no. 6 (2025): e1011261. https://doi.org/10.1371/journal.pgen.1011261.

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The myometrium, the muscular layer of the uterus, undergoes crucial transitions during pregnancy, maintaining quiescence throughout gestation, and generating coordinated contractions during labor. Dysregulation of this transition can lead to premature labor with serious complications for the infant. Despite extensive gene expression data available for varying myometrial states, the molecular mechanisms governing the increase in contraction-associated gene expression at labor onset remain unclear. Transcription factors, such as JUND and progesterone receptor (PR), play essential roles in regula

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Peng, Shurui, Liangbin Hu, Wei Ge, et al. "ChIP-Seq Analysis of AtfA Interactions in Aspergillus flavus Reveals Its Involvement in Aflatoxin Metabolism and Virulence Under Oxidative Stress." International Journal of Molecular Sciences 25, no. 22 (2024): 12213. http://dx.doi.org/10.3390/ijms252212213.

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The risk of Aspergillus flavus contamination is expanding with global warming. Targeting the pathogenicity of A. flavus at its source and diminishing its colonization within the host may be a potential control strategy. Oxidative stress transcription factor AtfA plays a pivotal role in A. flavus pathogenicity by combating reactive oxygen species (ROS) generated by host immune cells. This study employed chromatin immunoprecipitation sequencing to elucidate the binding sites and epigenetic mechanisms of AtfA under oxidative stress. Among the total 1022 identified potential AtfA-binding peaks, a

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