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Journal articles on the topic 'Remodelled genes'

Author: Grafiati

Published: 14 December 2024

Last updated: 31 July 2025

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1

Germain, Adeline, Jeanne-Marie Perotin, Gonzague Delepine, Myriam Polette, Gaëtan Deslée, and Valérian Dormoy. "Whole-Exome Sequencing of Bronchial Epithelial Cells Reveals a Genetic Print of Airway Remodelling in COPD." Biomedicines 10, no. 7 (2022): 1714. http://dx.doi.org/10.3390/biomedicines10071714.

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The remodelling of the airways is a hallmark of chronic obstructive pulmonary disease, but it is highly heterogeneous and erratically distributed in the airways. To assess the genetic print of remodelling in chronic obstructive pulmonary disease (COPD), we performed a comparative whole-exome sequencing analysis on microdissected bronchial epithelia. Lung resections from four non-COPD and three COPD subjects (ex-smokers and current smokers) were formalin-fixed paraffin-embedded (FFPE). Non-remodelled and remodelled bronchial epithelia were isolated by laser microdissection. Genomic DNA was capt

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Li, Mengyao, Su Mon Aye, Maizbha Uddin Ahmed, et al. "Pan-transcriptomic analysis identified common differentially expressed genes of Acinetobacter baumannii in response to polymyxin treatments." Molecular Omics 16, no. 4 (2020): 327–38. http://dx.doi.org/10.1039/d0mo00015a.

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Our pan-transcriptomic study for polymyxin-treated A. baumannii identified that the remodelled outer membrane, up-regulated efflux pumps and down-regulated fatty acid biosynthesis might be essential for early responses to polymyxins in A. baumannii.

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Ou, Yaqing, and James O. McInerney. "Eukaryote Genes Are More Likely than Prokaryote Genes to Be Composites." Genes 10, no. 9 (2019): 648. http://dx.doi.org/10.3390/genes10090648.

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The formation of new genes by combining parts of existing genes is an important evolutionary process. Remodelled genes, which we call composites, have been investigated in many species, however, their distribution across all of life is still unknown. We set out to examine the extent to which genomes from cells and mobile genetic elements contain composite genes. We identify composite genes as those that show partial homology to at least two unrelated component genes. In order to identify composite and component genes, we constructed sequence similarity networks (SSNs) of more than one million

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Kuleesha, Yadav, Wee Choo Puah, and Martin Wasser. "A model of muscle atrophy based on live microscopy of muscle remodelling in Drosophila metamorphosis." Royal Society Open Science 3, no. 2 (2016): 150517. http://dx.doi.org/10.1098/rsos.150517.

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Genes controlling muscle size and survival play important roles in muscle wasting diseases. In Drosophila melanogaster metamorphosis, larval abdominal muscles undergo two developmental fates. While a doomed population is eliminated by cell death, another persistent group is remodelled and survives into adulthood. To identify and characterize genes involved in the development of remodelled muscles, we devised a workflow consisting of in vivo imaging, targeted gene perturbation and quantitative image analysis. We show that inhibition of TOR signalling and activation of autophagy promote developm

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Wang, Yuzhe, Shiyu Li, Mengge Liu, et al. "Rhodosporidium toruloides sir2-like genes remodelled the mitochondrial network to improve the phenotypes of ageing cells." Free Radical Biology and Medicine 134 (April 2019): 64–75. http://dx.doi.org/10.1016/j.freeradbiomed.2018.12.036.

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Ahmedien, Diaa Ahmed Mohamed. "Bio-pixels: A stem cell-based interactive–generative interface designed to redefine technologies of self-making in new media arts." Convergence: The International Journal of Research into New Media Technologies 26, no. 5-6 (2019): 1367–90. http://dx.doi.org/10.1177/1354856519890096.

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Bio-pixels is a stem cell-based interactive–generative interface designed to investigate the concept of ‘self-making’. The project uses stem cells as a biological prototype of an identity-free substance and defines in vivo stem cell differentiation processes as nature’s self-making technology. It therefore considers in vitro-induced differentiation processes as artificial self-making technologies that were recontextualized through the interactions between the world of genes and the world of bits. The project’s system was functionally built based on three operational principles derived from con

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Vora, Hemangini Hasit. "Identification of Extra Cellular Matrix (ECM) Genes in Triple Negative Breast Cancer." Asian Pacific Journal of Cancer Biology 10, no. 2 (2025): 301–7. https://doi.org/10.31557/apjcb.2025.10.2.301-307.

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Introduction: Extracellular Matrix (ECM) is often abnormally produced, degraded, and remodelled, which creates a pro-tumorigenic environment in cancer and leads to tumor growth, angiogenesis, invasion and metastasis. This study aimed to investigate ECM genes by microarray-based transcriptome analysis and miRNA that target ECM genes in triple-negative breast cancer (TNBC). Materials and Methods: The current study evaluated 682 TME-related genes using Array Comparative Genomic Hybridization (aCGH) in 55 patients with TNBC. Results: 266 ECM genes were studied by transcriptome analysis, and it was

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Dalla Torre, Marco, Daniele Pittari, Alessandra Boletta, Laura Cassina, Roberto Sitia, and Tiziana Anelli. "Mitochondria remodeling during endometrial stromal cell decidualization." Life Science Alliance 7, no. 12 (2024): e202402627. http://dx.doi.org/10.26508/lsa.202402627.

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Upon hormonal stimulation, uterine endometrial stromal cells undergo a dramatic morpho-functional metamorphosis that allows them to secrete large amounts of matrix proteins, cytokines, and growth factors. This step, known as decidualization, is crucial for embryo implantation. We previously demonstrated how the secretory pathway is remodelled during this process. Here we show that hormonal stimulation rapidly induces the expression of many mitochondrial genes, encoded in both the mitochondrial and the nuclear genomes. Altogether, the mitochondrial network quadruples its size and establishes mo

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Reik, Wolf, Fatima Santos, Kohzoh Mitsuya, Hugh Morgan, and Wendy Dean. "Epigenetic asymmetry in the mammalian zygote and early embryo: relationship to lineage commitment?" Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1436 (2003): 1403–9. http://dx.doi.org/10.1098/rstb.2003.1326.

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Epigenetic asymmetry between parental genomes and embryonic lineages exists at the earliest stages of mammalian development. The maternal genome in the zygote is highly methylated in both its DNA and its histones and most imprinted genes have maternal germline methylation imprints. The paternal genome is rapidly remodelled with protamine removal, addition of acetylated histones, and rapid demethylation of DNA before replication. A minority of imprinted genes have paternal germline methylation imprints. Methylation and chromatin reprogramming continues during cleavage divisions, but at the blas

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Chen, Xinxin, Jun Wang, Donna Woltring, Steve Gerondakis, and M. Frances Shannon. "Histone Dynamics on the Interleukin-2 Gene in Response to T-Cell Activation." Molecular and Cellular Biology 25, no. 8 (2005): 3209–19. http://dx.doi.org/10.1128/mcb.25.8.3209-3219.2005.

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ABSTRACT Several models have been proposed for the mechanism of chromatin remodelling across the promoters of inducible genes in mammalian cells. The most commonly held model is one of cooccupation where histone proteins are modified by acetylation or phosphorylation and nucleosomes are remodelled, allowing the assembly of transcription factor complexes. Using chromatin immunoprecipitation, we observed an apparent decrease of histone acetylation and phosphorylation signals at the proximal promoter region of the inducible interleukin-2 and granulocyte-macrophage colony-stimulating factor genes

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PRAJAPATI, SURENDRA K., RICHARD CULLETON, and OM P. SINGH. "Protein trafficking in Plasmodium falciparum-infected red cells and impact of the expansion of exported protein families." Parasitology 141, no. 12 (2014): 1533–43. http://dx.doi.org/10.1017/s0031182014000948.

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SUMMARYErythrocytes are extensively remodelled by the malaria parasite following invasion of the cell. Plasmodium falciparum encodes numerous virulence-associated and host-cell remodelling proteins that are trafficked to the cytoplasm, the cell membrane and the surface of the infected erythrocyte. The export of soluble proteins relies on a sequence directing entry into the secretory pathways in addition to an export signal. The export signal consisting of five amino acids is termed the Plasmodium export element (PEXEL) or the vacuole transport signal (VTS). Genome mining studies have revealed

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Boudin, Eveline, and Wim Van Hul. "MECHANISMS IN ENDOCRINOLOGY: Genetics of human bone formation." European Journal of Endocrinology 177, no. 2 (2017): R69—R83. http://dx.doi.org/10.1530/eje-16-0990.

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Throughout life, bone is continuously remodelled to be able to fulfil its multiple functions. The importance of strictly regulating the bone remodelling process, which is defined by the sequential actions of osteoclasts and osteoblasts, is shown by a variety of disorders with abnormalities in bone mass and strength. The best known and most common example of such a disorder is osteoporosis, which is marked by a decreased bone mass and strength that consequently results in an increased fracture risk. As osteoporosis is a serious health problem, a large number of studies focus on elucidating the

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Wood, W., M. Turmaine, R. Weber, et al. "Mesenchymal cells engulf and clear apoptotic footplate cells in macrophageless PU.1 null mouse embryos." Development 127, no. 24 (2000): 5245–52. http://dx.doi.org/10.1242/dev.127.24.5245.

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Apoptosis is one of the key tools used by an embryo to regulate cell numbers and sculpt body shape. Although massive numbers of cells die during development, they are so rapidly phagocytosed that very few corpses are ever seen in most embryonic tissues. In this paper, we focus on the catastrophic cell death that occurs as the developing footplate is remodelled to transform webbed regions into free interdigital spaces. In the wild-type embryo, these dead cells are rapidly engulfed and cleared by macrophages. We show that in a macrophageless mouse embryo, null for the haemopoetic-lineage-specifi

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Farrell, K., K. Uh, and K. Lee. "45 Expression patterns of PRDM family genes in porcine pre-implantation embryos." Reproduction, Fertility and Development 32, no. 2 (2020): 148. http://dx.doi.org/10.1071/rdv32n2ab45.

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Establishing proper levels of pluripotency is essential for normal development. The genome of gametes is remodelled upon fertilisation and pluripotency-related genes are expressed in blastocysts. Multiple pluripotency-related genes are involved in the well-orchestrated process; however, detailed mechanistic actions remain elusive. The PRDM family genes are reported to be closely related to the pluripotency. A previous report noted that PRDM14 plays an important role in the maintenance of pluripotency in human embryonic stem cells (ESCs) and potentially murine ESCs; loss of PRDM14 was found to

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Paino, Francesca, Marcella La Noce, Alessandra Giuliani, et al. "Human DPSCs fabricate vascularized woven bone tissue: a new tool in bone tissue engineering." Clinical Science 131, no. 8 (2017): 699–713. http://dx.doi.org/10.1042/cs20170047.

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Human dental pulp stem cells (hDPSCs) are mesenchymal stem cells that have been successfully used in human bone tissue engineering. To establish whether these cells can lead to a bone tissue ready to be grafted, we checked DPSCs for their osteogenic and angiogenic differentiation capabilities with the specific aim of obtaining a new tool for bone transplantation. Therefore, hDPSCs were specifically selected from the stromal–vascular dental pulp fraction, using appropriate markers, and cultured. Growth curves, expression of bone-related markers, calcification and angiogenesis as well as an in v

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Ben-Aicha, Soumaya, Rafael Escate, Laura Casaní та ін. "High-density lipoprotein remodelled in hypercholesterolaemic blood induce epigenetically driven down-regulation of endothelial HIF-1α expression in a preclinical animal model". Cardiovascular Research 116, № 7 (2019): 1288–99. http://dx.doi.org/10.1093/cvr/cvz239.

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Abstract Aims High-density lipoproteins (HDLs) are circulating micelles that transport proteins, lipids, and miRNAs. HDL-transported miRNAs (HDL-miRNAs) have lately received attention but their effects on vascular cells are not fully understood. Additionally, whether cardiovascular risk factors affect HDL-miRNAs levels and miRNA transfer to recipient cells remains equally poorly known. Here, we have investigated the changes induced by hypercholesterolaemia on HDL-miRNA levels and its effect on recipient endothelial cells (ECs). Methods and results Pigs were kept on a high-fat diet (HC; n = 10)

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VINCENTI, Matthew P., Charles I. COON, J. Andrew MENGSHOL, Sue YOCUM, Peter MITCHELL, and Constance E. BRINCKERHOFF. "Cloning of the gene for interstitial collagenase-3 (matrix metalloproteinase-13) from rabbit synovial fibroblasts: differential expression with collagenase-1 (matrix metalloproteinase-1)." Biochemical Journal 331, no. 1 (1998): 341–46. http://dx.doi.org/10.1042/bj3310341.

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Cartilage, bone and the interstitial stroma, composed largely of the interstitial collagens, types I, II and III, are remodelled by three members of the metalloproteinase (MMP) family, collagenase-1 (MMP-1), collagenase-2 (MMP-8) and collagenase-3 (MMP-13). MMP-1 and MMP-13 may contribute directly to disease progression, since they are induced in patients with rheumatoid arthritis and osteoarthritis. The study of MMP-1 and MMP-13 gene regulation in models of arthritic disease has been problematic because mice and rats, which are typically used, only possess a homologue of MMP-13. Here we show

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18

Koenning, Matthias, Xianlong Wang, Menuka Karki, et al. "Neuronal SETD2 activity links microtubule methylation to an anxiety-like phenotype in mice." Brain 144, no. 8 (2021): 2527–40. http://dx.doi.org/10.1093/brain/awab200.

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Abstract Gene discovery efforts in autism spectrum disorder have identified heterozygous defects in chromatin remodeller genes, the ‘readers, writers and erasers’ of methyl marks on chromatin, as major contributors to this disease. Despite this advance, a convergent aetiology between these defects and aberrant chromatin architecture or gene expression has remained elusive. Recently, data have begun to emerge that chromatin remodellers also function directly on the cytoskeleton. Strongly associated with autism spectrum disorder, the SETD2 histone methyltransferase for example, has now been show

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Farrell, Jeffrey A., and Patrick H. O'Farrell. "From Egg to Gastrula: How the Cell Cycle Is Remodeled During theDrosophilaMid-Blastula Transition." Annual Review of Genetics 48, no. 1 (2014): 269–94. http://dx.doi.org/10.1146/annurev-genet-111212-133531.

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20

Ciciarello, Marilena, Francesca Girotti, Darina Ocadlikova, et al. "Interferon-Gamma Production By Dysplastic Cells Supports an Immune-Tolerant Bone Marrow Microenvironment in Myelodysplastic Syndrome Patients." Blood 144, Supplement 1 (2024): 6687. https://doi.org/10.1182/blood-2024-203447.

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Background: Myelodysplastic syndromes (MDS) are a heterogeneous group of haematological malignancies with a poor prognosis and a risk of evolving into acute myeloid leukaemia (AML). Besides intrinsic cellular defects, extrinsic microenvironmental factors, particularly inflammatory signals in the bone marrow (BM), play a crucial role in MDS progression. In AML, we demonstrated that leukemic cells produced interferon (IFN)γ, allowing us to stratify them in INFGhigh and IFNGlow samples. Higher IFNγ levels remodelled the BM microenvironment, favouring the indoleamine 2,3-dioxygenase (IDO)1-depende

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Norton, Kacie A., Ross Humphreys, Chelsey Weatherill, et al. "Subfertility in young male mice mutant for chromatin remodeller CECR2." Reproduction 163, no. 2 (2022): 69–83. http://dx.doi.org/10.1530/rep-19-0507.

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Defects in spermatogenesis are an important cause of male infertility. Multiple aspects of spermatogenesis are controlled by chromatin remodellers, including regulating transcription. We previously described mutations in chromatin remodelling gene Cecr2 that resulted in the lethal neural tube defect exencephaly in most mutant mice and subfertility in mice that were non-penetrant for exencephaly. Here, we show that the severity of male subfertility is dependent on age. Cecr2GT/Del males contain two mutant alleles, one of which is hypomorphic and therefore produces a small amount of protein. The

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González-Medina, Alberto, Esther Pazo, Elena Hidalgo, and José Ayté. "SWI/SNF and RSC remodeler complexes bind to MBF-dependent genes." Cell Cycle 20, no. 24 (2021): 2652–61. http://dx.doi.org/10.1080/15384101.2021.2008203.

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Loesch, Robin, Linda Chenane, and Sabine Colnot. "ARID2 Chromatin Remodeler in Hepatocellular Carcinoma." Cells 9, no. 10 (2020): 2152. http://dx.doi.org/10.3390/cells9102152.

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Chromatin remodelers are found highly mutated in cancer including hepatocellular carcinoma. These mutations frequently occur in ARID (AT-rich Interactive Domain) genes, encoding subunits of the ATP-dependent SWI/SNF remodelers. The increasingly prevalent complexity that surrounds the functions and specificities of the highly modular BAF (BG1/BRM-associated factors) and PBAF (polybromo-associated BAF) complexes, including ARID1A/B or ARID2, is baffling. The involvement of the SWI/SNF complexes in diverse tissues and processes, and especially in the regulation of gene expression, multiplies the

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Poli, Jérôme, Susan M. Gasser, and Manolis Papamichos-Chronakis. "The INO80 remodeller in transcription, replication and repair." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1731 (2017): 20160290. http://dx.doi.org/10.1098/rstb.2016.0290.

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The accessibility of eukaryotic genomes to the action of enzymes involved in transcription, replication and repair is maintained despite the organization of DNA into nucleosomes. This access is often regulated by the action of ATP-dependent nucleosome remodellers. The INO80 class of nucleosome remodellers has unique structural features and it is implicated in a diverse array of functions, including transcriptional regulation, DNA replication and DNA repair. Underlying these diverse functions is the catalytic activity of the main ATPase subunit, which in the context of a multisubunit complex ca

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Soutourina, Julie, Véronique Bordas-Le Floch, Gabrielle Gendrel, et al. "Rsc4 Connects the Chromatin Remodeler RSC to RNA Polymerases." Molecular and Cellular Biology 26, no. 13 (2006): 4920–33. http://dx.doi.org/10.1128/mcb.00415-06.

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ABSTRACT RSC is an essential, multisubunit chromatin remodeling complex. We show here that the Rsc4 subunit of RSC interacted via its C terminus with Rpb5, a conserved subunit shared by all three nuclear RNA polymerases (Pol). Furthermore, the RSC complex coimmunoprecipitated with all three RNA polymerases. Mutations in the C terminus of Rsc4 conferred a thermosensitive phenotype and the loss of interaction with Rpb5. Certain thermosensitive rpb5 mutations were lethal in combination with an rsc4 mutation, supporting the physiological significance of the interaction. Pol II transcription of ca.

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Subtil-Rodríguez, Alicia, Elena Vázquez-Chávez, María Ceballos-Chávez, et al. "The chromatin remodeller CHD8 is required for E2F-dependent transcription activation of S-phase genes." Nucleic Acids Research 42, no. 4 (2013): 2185–96. http://dx.doi.org/10.1093/nar/gkt1161.

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Abstract The precise regulation of S-phase–specific genes is critical for cell proliferation. How the repressive chromatin configuration mediated by the retinoblastoma protein and repressor E2F factors changes at the G1/S transition to allow transcription activation is unclear. Here we show ChIP-on-chip studies that reveal that the chromatin remodeller CHD8 binds ∼2000 transcriptionally active promoters. The spectrum of CHD8 target genes was enriched in E2F-dependent genes. We found that CHD8 binds E2F-dependent promoters at the G1/S transition but not in quiescent cells. Consistently, CHD8 wa

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Chutani, Namita, Sandhya Ragula, Khajamohiddin Syed, and Suresh B. Pakala. "Novel Insights into the Role of Chromatin Remodeler MORC2 in Cancer." Biomolecules 13, no. 10 (2023): 1527. http://dx.doi.org/10.3390/biom13101527.

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A newly discovered chromatin remodeler, MORC2, is a Microrchidia (MORC) family member. MORC2 acts as a chromatin remodeler by binding to the DNA and changing chromatin conformation using its ATPase domain. MORC2 is highly expressed in a variety of human cancers. It controls diverse signaling pathways essential for cancer development through its target genes and interacting partners. MORC2 promotes cancer cells’ growth, invasion, and migration by regulating the expression of genes involved in these processes. MORC2 is localized primarily in the nucleus and is also found in the cytoplasm. In the

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Yao, Wei, Devin A. King, Sean L. Beckwith, et al. "The INO80 Complex Requires the Arp5-Ies6 Subcomplex for Chromatin Remodeling and Metabolic Regulation." Molecular and Cellular Biology 36, no. 6 (2016): 979–91. http://dx.doi.org/10.1128/mcb.00801-15.

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ATP-dependent chromatin remodeling complexes are essential for transcription regulation, and yet it is unclear how these multisubunit complexes coordinate their activities to facilitate diverse transcriptional responses. In this study, we found that the conserved Arp5 and Ies6 subunits of theSaccharomyces cerevisiaeINO80 chromatin-remodeler form an abundant and distinct subcomplexin vivoand stimulate INO80-mediated activityin vitro. Moreover, our genomic studies reveal that the relative occupancy of Arp5-Ies6 correlates with nucleosome positioning at transcriptional start sites and expression

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Song, Yawei, Zhengyu Liang, Jie Zhang, et al. "CTCF functions as an insulator for somatic genes and a chromatin remodeler for pluripotency genes during reprogramming." Cell Reports 39, no. 1 (2022): 110626. http://dx.doi.org/10.1016/j.celrep.2022.110626.

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Chohra, Ilyas, Keshi Chung, Subhajit Giri, and Brigitte Malgrange. "ATP-Dependent Chromatin Remodellers in Inner Ear Development." Cells 12, no. 4 (2023): 532. http://dx.doi.org/10.3390/cells12040532.

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During transcription, DNA replication and repair, chromatin structure is constantly modified to reveal specific genetic regions and allow access to DNA-interacting enzymes. ATP-dependent chromatin remodelling complexes use the energy of ATP hydrolysis to modify chromatin architecture by repositioning and rearranging nucleosomes. These complexes are defined by a conserved SNF2-like, catalytic ATPase subunit and are divided into four families: CHD, SWI/SNF, ISWI and INO80. ATP-dependent chromatin remodellers are crucial in regulating development and stem cell biology in numerous organs, includin

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Bogliotti, Y. S., L. B. Ferré, D. J. Humpal, and P. J. Ross. "68 EPIGENETIC REMODELING OF HISTONE 3 MARKS DURING BOVINE PRE-IMPLANTATION DEVELOPMENT." Reproduction, Fertility and Development 26, no. 1 (2014): 148. http://dx.doi.org/10.1071/rdv26n1ab68.

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During pre-implantation development, substantial epigenetic changes occur that are thought to play key roles in achieving embryonic genome activation and totipotency. Embryonic genome activation occurs at the 8- to 16-cell stage in cattle and, although it is a crucial step of development, the specific mechanisms involved are still poorly understood. The aim of this study was to determine whether 4 histone 3 marks associated with active genes are remodelled during oocyte and early embryo development in cattle. The dynamics of acetylation of lysine 27 (H3K27ac), di-methylation of lysine 79 (H3K7

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Yu, Xiaoming, Xinchao Meng, Yutong Liu, et al. "The chromatin remodeler ZmCHB101 impacts expression of osmotic stress-responsive genes in maize." Plant Molecular Biology 97, no. 4-5 (2018): 451–65. http://dx.doi.org/10.1007/s11103-018-0751-8.

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Morillon, Antonin. "Is histone loss a common feature of DNA metabolism regulation?This paper is one of a selection of papers published in this Special Issue, entitled 27th International West Coast Chromatin and Chromosome Conference, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 4 (2006): 450–52. http://dx.doi.org/10.1139/o06-070.

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Chromatin modifications play a crucial role in regulating DNA metabolism. Chromatin structures can be remodeled by covalently modifying histones, by shifting nucleosomes along the DNA, and by changing the histone composition of nucleosomes. Lately, nucleosome displacement has been extensively described within transcribed genes and DNA breaks. This review focuses on recently published work that describes the relationships between histone modification/exchange and nucleosome displacement.

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Feng, Ying, Yan Zhang, Zhiqing Lin, et al. "Chromatin remodeler Dmp18 regulates apoptosis by controlling H2Av incorporation in Drosophila imaginal disc development." PLOS Genetics 18, no. 9 (2022): e1010395. http://dx.doi.org/10.1371/journal.pgen.1010395.

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Programmed Cell Death (PCD) or apoptosis is a highly conserved biological process and plays essential roles both in the development and stress context. In Drosophila, expression of pro-apoptotic genes, including reaper (rpr), head involution defective (hid), grim, and sickle (skl), is sufficient to induce cell death. Here, we demonstrate that the chromatin remodeler Dmp18, the homolog of mammalian Znhit1, plays a crucial role in regulating apoptosis in eye and wing development. We showed that loss of Dmp18 disrupted eye and wing development, up-regulated transcription of pro-apoptotic genes, a

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Padilla-Benavides, Teresita, Monserrat Olea-Flores, Tapan Sharma, et al. "Differential Contributions of mSWI/SNF Chromatin Remodeler Sub-Families to Myoblast Differentiation." International Journal of Molecular Sciences 24, no. 14 (2023): 11256. http://dx.doi.org/10.3390/ijms241411256.

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Mammalian SWI/SNF (mSWI/SNF) complexes are ATP-dependent chromatin remodeling enzymes that are critical for normal cellular functions. mSWI/SNF enzymes are classified into three sub-families based on the presence of specific subunit proteins. The sub-families are Brm- or Brg1-associated factor (BAF), ncBAF (non-canonical BAF), and polybromo-associated BAF (PBAF). The biological roles for the different enzyme sub-families are poorly described. We knocked down the expression of genes encoding unique subunit proteins for each sub-family, Baf250A, Brd9, and Baf180, which mark the BAF, ncBAF, and P

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Gidh-Jain, Madhavi, Boyu Huang, Praveer Jain, and Nabil El-Sherif. "Differential Expression of Voltage-Gated K+Channel Genes in Left Ventricular Remodeled Myocardium After Experimental Myocardial Infarction." Circulation Research 79, no. 4 (1996): 669–75. http://dx.doi.org/10.1161/01.res.79.4.669.

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Causton, Helen C., Bing Ren, Sang Seok Koh, et al. "Remodeling of Yeast Genome Expression in Response to Environmental Changes." Molecular Biology of the Cell 12, no. 2 (2001): 323–37. http://dx.doi.org/10.1091/mbc.12.2.323.

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We used genome-wide expression analysis to explore how gene expression in Saccharomyces cerevisiae is remodeled in response to various changes in extracellular environment, including changes in temperature, oxidation, nutrients, pH, and osmolarity. The results demonstrate that more than half of the genome is involved in various responses to environmental change and identify the global set of genes induced and repressed by each condition. These data implicate a substantial number of previously uncharacterized genes in these responses and reveal a signature common to environmental responses that

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Reddy, B. Ashok, Prashanth Kumar Bajpe, Andrew Bassett, et al. "Drosophila Transcription Factor Tramtrack69 Binds MEP1 To Recruit the Chromatin Remodeler NuRD." Molecular and Cellular Biology 30, no. 21 (2010): 5234–44. http://dx.doi.org/10.1128/mcb.00266-10.

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ABSTRACT ATP-dependent chromatin-remodeling complexes (remodelers) are essential regulators of chromatin structure and gene transcription. How remodelers can act in a gene-selective manner has remained enigmatic. A yeast two-hybrid screen for proteins binding the Drosophila transcription factor Tramtrack69 (TTK69) identified MEP1. Proteomic characterization revealed that MEP1 is a tightly associated subunit of the NuRD remodeler, harboring the Mi2 enzymatic core ATPase. In addition, we identified the fly homolog of human Deleted in oral cancer 1 (DOC1), also known as CDK2-associated protein 1

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Muñoz, Sofía, Francesca Passarelli, and Frank Uhlmann. "Conserved roles of chromatin remodellers in cohesin loading onto chromatin." Current Genetics 66, no. 5 (2020): 951–56. http://dx.doi.org/10.1007/s00294-020-01075-x.

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Abstract Cohesin is a conserved, ring-shaped protein complex that topologically entraps DNA. This ability makes this member of the structural maintenance of chromosomes (SMC) complex family a central hub of chromosome dynamics regulation. Besides its essential role in sister chromatid cohesion, cohesin shapes the interphase chromatin domain architecture and plays important roles in transcriptional regulation and DNA repair. Cohesin is loaded onto chromosomes at centromeres, at the promoters of highly expressed genes, as well as at DNA replication forks and sites of DNA damage. However, the fea

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Zhang, Heng, Brett Bishop, Whitney Ringenberg, William M. Muir, and Joe Ogas. "The CHD3 Remodeler PICKLE Associates with Genes Enriched for Trimethylation of Histone H3 Lysine 27." Plant Physiology 159, no. 1 (2012): 418–32. http://dx.doi.org/10.1104/pp.112.194878.

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Poupeau, Audrey, Christian Garde, Karolina Sulek, et al. "Genes controlling the activation of natural killer lymphocytes are epigenetically remodeled in intestinal cells from germ‐free mice." FASEB Journal 33, no. 2 (2018): 2719–31. http://dx.doi.org/10.1096/fj.201800787r.

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Melvin, Andrew, Sharon Mudie, and Sonia Rocha. "The chromatin remodeler ISWI regulates the cellular response to hypoxia: role of FIH." Molecular Biology of the Cell 22, no. 21 (2011): 4171–81. http://dx.doi.org/10.1091/mbc.e11-02-0163.

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The hypoxia-inducible factor (HIF) is a master regulator of the cellular response to hypoxia. Its levels and activity are controlled by dioxygenases called prolyl-hydroxylases and factor inhibiting HIF (FIH). To activate genes, HIF has to access sequences in DNA that are integrated in chromatin. It is known that the chromatin-remodeling complex switch/sucrose nonfermentable (SWI/SNF) is essential for HIF activity. However, no additional information exists about the role of other chromatin-remodeling enzymes in hypoxia. Here we describe the role of imitation switch (ISWI) in the cellular respon

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Crosswhite, Patrick L. "ATP-dependent chromatin remodeling complexes in embryonic vascular development and hypertension." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 3 (2019): H575—H580. http://dx.doi.org/10.1152/ajpheart.00147.2019.

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Hypertension, a chronic elevation in blood pressure, is the largest single contributing factor to mortality worldwide and the most common preventable risk factor for cardiovascular disease. High blood pressure increases the risk for someone to experience a number of adverse cardiovascular events including heart failure, stroke, or aneurysm. Despite advancements in understanding factors that contribute to hypertension, the etiology remains elusive and there remains a critical need to develop innovative study approaches to develop more effective therapeutics. ATP-dependent chromatin remodelers a

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Singh, Parul, Jacques Serizay, Justine Couble, et al. "High-resolution map of the Plasmodium falciparum genome reveals MORC/ApiAP2-mediated links between distant, functionally related genes." Nature Microbiology 10, no. 7 (2025): 1665–83. https://doi.org/10.1038/s41564-025-02038-z.

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Abstract Genome organization plays an important role in silencing compacted, heterochromatinized genes in the most virulent human malaria parasite, Plasmodium falciparum. However, it remains unclear how these genes spatially cluster or whether active genes are also organized in a specific manner. We used Micro-C to achieve near-nucleosome resolution DNA–DNA contact maps, which revealed previously undescribed inter- and intrachromosomal heterochromatic and euchromatic structures in the blood-stage parasite. We observed subtelomeric fold structures that facilitate interactions among heterochroma

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Li, Shitao, Lingyan Wang, Michael Berman, and Martin Dorf. "Mapping a dynamic innate immunity protein interaction network regulating type I interferon production (108.2)." Journal of Immunology 188, no. 1_Supplement (2012): 108.2. http://dx.doi.org/10.4049/jimmunol.188.supp.108.2.

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Abstract We use co-immunoprecipitation and mass spectrometry to identify antiviral signaling networks which regulate innate immune responses. Fifty-eight baits were associated with 260 interacting proteins forming a Human Innate Immunity Interactome of 401 unique interactions; 21% of interactions were remodeled following RNA, DNA, or LPS stimulation. Overexpression and depletion analyses identified 22 novel genes which regulate NF-kB and ISRE reporter activity, viral replication, or virus-induced interferon production. The innate immune interactome provides a dynamic physical and regulatory ne

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Zhao, Haixin, Zhijun Han, Xinyuan Liu, et al. "The chromatin remodeler Chd4 maintains embryonic stem cell identity by controlling pluripotency- and differentiation-associated genes." Journal of Biological Chemistry 292, no. 20 (2017): 8507–19. http://dx.doi.org/10.1074/jbc.m116.770248.

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Hussain, Shahid, Debasis Nayak, Sajad A. Wani, et al. "Abstract 6346: The chromatin remodeler SMARCA5 selectively shapes nuclear receptor signaling in African American prostate cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 6346. https://doi.org/10.1158/1538-7445.am2025-6346.

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Abstract SMARCA5 is found in distinct chromatin remodeling complexes where it regulates ATP hydrolysis to control nucleosome positioning required for gene expression and DNA repair. Previously, we established the chromatin remodeling enzyme SMARCA5 is significantly down-regulated in African American (AA) compared to European Americans (EA) prostate cancer (PCa). We have now explored how SMARCA5 distorts the epigenome and impacts transcription, as well as cell phenotypes. Firstly, we revealed that the H3K27ac cistrome had significantly different distributions between AA (RC43N) and EA (HPr1AR)

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Walter, Korden, Constanze Bonifer, and Hiromi Tagoh. "Stem cell–specific epigenetic priming and B cell–specific transcriptional activation at the mouse Cd19 locus." Blood 112, no. 5 (2008): 1673–82. http://dx.doi.org/10.1182/blood-2008-02-142786.

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Abstract Low-level expression of multiple lineage-specific genes is a hallmark of hematopoietic stem cells (HSCs). HSCs predominantly express genes specific for the myeloid or megakaryocytic-erythroid lineages, whereas the transcription of lymphoid specific genes appears to begin after lymphoid specification. It has been demonstrated for a number of genes that epigenetic priming occurs before gene expression and lineage specification; however, little is known about how epigenetic priming of lymphoid genes is regulated. To address the question of how B cell–restricted expression is established,

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Sperlazza, Justin, Mohamed Rahmani, Jason Beckta, et al. "Depletion of the chromatin remodeler CHD4 sensitizes AML blasts to genotoxic agents and reduces tumor formation." Blood 126, no. 12 (2015): 1462–72. http://dx.doi.org/10.1182/blood-2015-03-631606.

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Key Points CHD4 depletion sensitizes AML cells but not normal CD34+ progenitors to genotoxic agents by relaxing chromatin and impairing DSB repair. CHD4 depletion modulates expression of AML cell genes that regulate tumor formation in vivo and colony formation in vitro.

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Qiu, Hongfang, Emily Biernat, Chhabi K. Govind, et al. "Chromatin remodeler Ino80C acts independently of H2A.Z to evict promoter nucleosomes and stimulate transcription of highly expressed genes in yeast." Nucleic Acids Research 48, no. 15 (2020): 8408–30. http://dx.doi.org/10.1093/nar/gkaa571.

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Abstract The chromatin remodelers SWI/SNF and RSC function in evicting promoter nucleosomes at highly expressed yeast genes, particularly those activated by transcription factor Gcn4. Ino80 remodeling complex (Ino80C) can establish nucleosome-depleted regions (NDRs) in reconstituted chromatin, and was implicated in removing histone variant H2A.Z from the −1 and +1 nucleosomes flanking NDRs; however, Ino80C’s function in transcriptional activation in vivo is not well understood. Analyzing the cohort of Gcn4-induced genes in ino80Δ mutants has uncovered a role for Ino80C on par with SWI/SNF in e

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