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1

Tang, Jinglong, and Masaya Baba. "MiT/TFE Family Renal Cell Carcinoma." Genes 14, no. 1 (2023): 151. http://dx.doi.org/10.3390/genes14010151.

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The microphthalmia-associated transcription factor/transcription factor E (MiT/TFE) family of transcription factors are evolutionarily conserved, basic helix–loop–helix leucine zipper (bHLH-Zip) transcription factors, consisting of MITF, TFEB, TFE3, and TFEC. MiT/TFE proteins, with the exception of TFEC, are involved in the development of renal cell carcinoma (RCC). Most of the MiT/TFE transcription factor alterations seen in sporadic RCC cases of MiT family translocation renal cell carcinoma (tRCC) are chimeric proteins generated by chromosomal rearrangements. These chimeric MiT/TFE proteins
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2

Lee, J. S., R. H. See, T. Deng, and Y. Shi. "Adenovirus E1A downregulates cJun- and JunB-mediated transcription by targeting their coactivator p300." Molecular and Cellular Biology 16, no. 8 (1996): 4312–26. http://dx.doi.org/10.1128/mcb.16.8.4312.

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Transcription factors and cofactors play critical roles in cell growth and differentiation. Alterations of their activities either through genetic mutations or by viral oncoproteins often result in aberrant cell growth and tumorigenesis. The transcriptional cofactor p300 has recently been shown to be complexed with transcription factors YY1 and CREB. Adenovirus E1A oncoproteins target these transcription complexes via physical interactions with p300, resulting in alterations of transcription mediated by these transcription factors. Here we show that p300 is also critical for repression by E1A
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3

Wilson, Hannah E., David A. Stanton, Stephanie Rellick, Werner Geldenhuys, and Emidio E. Pistilli. "Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG." American Journal of Physiology-Cell Physiology 320, no. 4 (2021): C577—C590. http://dx.doi.org/10.1152/ajpcell.00264.2020.

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The peroxisome proliferator-activated receptors (PPARs) have been previously implicated in the pathophysiology of skeletal muscle dysfunction in women with breast cancer (BC) and animal models of BC. This study investigated alterations induced in skeletal muscle by BC-derived factors in an in vitro conditioned media (CM) system and tested the hypothesis that BC cells secrete a factor that represses PPAR-γ (PPARG) expression and its transcriptional activity, leading to downregulation of PPARG target genes involved in mitochondrial function and other metabolic pathways. We found that BC-derived
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4

Orzechowska-Licari, Emilia J., Joseph F. LaComb, Aisharja Mojumdar, and Agnieszka B. Bialkowska. "SP and KLF Transcription Factors in Cancer Metabolism." International Journal of Molecular Sciences 23, no. 17 (2022): 9956. http://dx.doi.org/10.3390/ijms23179956.

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Tumor development and progression depend on reprogramming of signaling pathways that regulate cell metabolism. Alterations to various metabolic pathways such as glycolysis, oxidative phosphorylation, lipid metabolism, and hexosamine biosynthesis pathway are crucial to sustain increased redox, bioenergetic, and biosynthesis demands of a tumor cell. Transcription factors (oncogenes and tumor suppressors) play crucial roles in modulating these alterations, and their functions are tethered to major metabolic pathways under homeostatic conditions and disease initiation and advancement. Specificity
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5

Pazhani, Jayanthi, Vishnu Priya Veeraraghavan, and Selvaraj Jayaraman. "Transcription factors: a potential therapeutic target in head and neck squamous cell carcinoma." Epigenomics 15, no. 2 (2023): 57–60. http://dx.doi.org/10.2217/epi-2023-0046.

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Squamous cell carcinoma is the most common histopathological type of head and neck cancer; it often spreads to and involves the cervical lymph nodes. The tumorigenesis of head and neck squamous cell carcinoma (HNSCC) is a multistep process mediated by various transcription factors involved in progression and metastasis. Alterations in transcription factors such as FOSL1, YY1, FOXD1 and NF-κB have been associated with increased cell proliferation, cell migration and poor survival rates in patients with HNSCC. Stimulation of the NF-κB pathway results in transcriptional activation of other target
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6

Koch, Marilin, Stefan Czemmel, Felix Lennartz, et al. "CSIG-15. INHIBITION OF THE bHLH TRANSCRIPTIONAL NETWORKS BY A MUTATED E47 PROTEIN LEADS TO A STRONG ANTI-GLIOMA ACTIVITY IN VITRO AND IN VIVO." Neuro-Oncology 21, Supplement_6 (2019): vi47. http://dx.doi.org/10.1093/neuonc/noz175.185.

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Abstract OBJECTIVE The transcription factor E47 heterodimerizes with helix-loop-helix (HLH) and basic helix-loop-helix transcription (bHLH) factors like ID-1 and Olig2 that are overexpressed in glioblastoma. A dominant-negative variant of the E47 (dnE47) lacking the nuclear translocation signal, leads to cytoplasmatic sequestration of HLH and bHLH transcription factors. Here, we investigated combinations of dnE47-mediated inhibition of the bHLH transcriptional network with temozolomide and irradiation and explored the underlying molecular mechanisms. METHODS Long-term and stem cell glioma line
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7

Zhu, Qian, Xavier Tekpli, Olga G. Troyanskaya, and Vessela N. Kristensen. "Subtype-specific transcriptional regulators in breast tumors subjected to genetic and epigenetic alterations." Bioinformatics 36, no. 4 (2019): 994–99. http://dx.doi.org/10.1093/bioinformatics/btz709.

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Abstract Motivation Breast cancer consists of multiple distinct tumor subtypes, and results from epigenetic and genetic aberrations that give rise to distinct transcriptional profiles. Despite previous efforts to understand transcriptional deregulation through transcription factor networks, the transcriptional mechanisms leading to subtypes of the disease remain poorly understood. Results We used a sophisticated computational search of thousands of expression datasets to define extended signatures of distinct breast cancer subtypes. Using ENCODE ChIP-seq data of surrogate cell lines and motif
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8

Goodson, Michael, Brian A. Jonas, and Martin A. Privalsky. "Corepressors: Custom Tailoring and Alterations While you Wait." Nuclear Receptor Signaling 3, no. 1 (2005): nrs.03003. http://dx.doi.org/10.1621/nrs.03003.

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A diverse cadre of metazoan transcription factors mediate repression by recruiting protein complexes containing the SMRT (silencing mediator of retinoid and thyroid hormone receptor) or N-CoR (nuclear receptor corepressor) corepressors. SMRT and N-CoR nucleate the assembly of still larger corepressor complexes that perform the specific molecular incantations necessary to confer transcriptional repression. Although SMRT and N-CoR are paralogs and possess similar molecular architectures and mechanistic strategies, they nonetheless exhibit distinct molecular and biological properties. It is now c
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9

Chen, Shali, Biao Feng, Biju George, Rana Chakrabarti, Megan Chen, and Subrata Chakrabarti. "Transcriptional coactivator p300 regulates glucose-induced gene expression in endothelial cells." American Journal of Physiology-Endocrinology and Metabolism 298, no. 1 (2010): E127—E137. http://dx.doi.org/10.1152/ajpendo.00432.2009.

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Sustained hyperglycemia in diabetes causes alteration of a large number of transcription factors and mRNA transcripts, leading to tissue damage. We investigated whether p300, a transcriptional coactivator with histone acetyl transferase activity, regulates glucose-induced activation of transcription factors and subsequent upregulation of vasoactive factors and extracellular matrix (ECM) proteins in human umbilical vein endothelial cells (HUVECs). HUVECs were incubated in varied glucose concentrations and were studied after p300 small interfering RNA (siRNA) transfection, p300 overexpression, o
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10

Zhang, Dawn X., and Christopher K. Glass. "Towards an understanding of cell-specific functions of signal-dependent transcription factors." Journal of Molecular Endocrinology 51, no. 3 (2013): T37—T50. http://dx.doi.org/10.1530/jme-13-0216.

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The ability to regulate gene expression in a cell-specific manner is a feature of many broadly expressed signal-dependent transcription factors (SDTFs), including nuclear hormone receptors and transcription factors that are activated by cell surface receptors for extracellular signals. As the most plastic cells of the hematopoietic system, macrophages are responsive to a wide spectrum of regulatory molecules and provide a robust model system for investigation of the basis for cell-specific transcriptional responses at a genome-wide level. Here, focusing on recent studies in macrophages, we rev
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11

Cook, Tiffany, та Raul Urrutia. "TIEG proteins join the Smads as TGF-β-regulated transcription factors that control pancreatic cell growth". American Journal of Physiology-Gastrointestinal and Liver Physiology 278, № 4 (2000): G513—G521. http://dx.doi.org/10.1152/ajpgi.2000.278.4.g513.

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The control of epithelial cell proliferation, differentiation, and apoptosis requires a balance between signaling and transcriptional regulation. Recent developments in pancreatic cell research have revealed that transforming growth factor-β (TGF-β) signaling is important for the regulation of each of these phenomena. More importantly, perturbations in this pathway are associated with pancreatic cancer. A chief example of these alterations is the mutation in the TGF-β-regulated transcription factor Smad4/DPC4 that is found in a large percentage of pancreatic tumors. Surprisingly, studies on tr
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12

Liu, Shihua, Ya Qiu, Rong Xiang, and Peng Huang. "Characterization of H2O2-Induced Alterations in Global Transcription of mRNA and lncRNA." Antioxidants 11, no. 3 (2022): 495. http://dx.doi.org/10.3390/antiox11030495.

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Hydrogen peroxide (H2O2) is an important reactive oxygen species that plays a major role in redox signaling. Although H2O2 is known to regulate gene expression and affect multiple cellular processes, the characteristics and mechanisms of such transcriptional regulation remain to be defined. In this study, we utilized transcriptome sequencing to determine the global changes of mRNA and lncRNA transcripts induced by H2O2 in human pancreatic normal epithelial (HPNE) and pancreatic cancer (PANC-1) cells. Promoter analysis using PROMO and TRRUST revealed that mRNAs and lncRNAs largely shared the sa
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13

Rossi, Chiara, Anna Fernàndez, Pascual Torres, et al. "Cell Stress Induces Mislocalization of Transcription Factors with Mitochondrial Enrichment." International Journal of Molecular Sciences 22, no. 16 (2021): 8853. http://dx.doi.org/10.3390/ijms22168853.

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Previous evidence links the formation of extranuclear inclusions of transcription factors, such as ERK, Jun, TDP-43, and REST, with oxidative, endoplasmic-reticulum, proteasomal, and osmotic stress. To further characterize its extranuclear location, we performed a high-content screening based on confocal microscopy and automatized image analyses of an epithelial cell culture treated with hydrogen peroxide, thapsigargin, epoxomicin, or sorbitol at different concentrations and times to recreate the stresses mentioned above. We also performed a subcellular fractionation of the brain from transgen
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14

Desvergne, Béatrice, Liliane Michalik, and Walter Wahli. "Transcriptional Regulation of Metabolism." Physiological Reviews 86, no. 2 (2006): 465–514. http://dx.doi.org/10.1152/physrev.00025.2005.

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Our understanding of metabolism is undergoing a dramatic shift. Indeed, the efforts made towards elucidating the mechanisms controlling the major regulatory pathways are now being rewarded. At the molecular level, the crucial role of transcription factors is particularly well-illustrated by the link between alterations of their functions and the occurrence of major metabolic diseases. In addition, the possibility of manipulating the ligand-dependent activity of some of these transcription factors makes them attractive as therapeutic targets. The aim of this review is to summarize recent knowle
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15

Lefevre, Pascal, Svitlana Melnik, Nicola Wilson, Arthur D. Riggs, and Constanze Bonifer. "Developmentally Regulated Recruitment of Transcription Factors and Chromatin Modification Activities to Chicken Lysozyme cis-Regulatory Elements In Vivo." Molecular and Cellular Biology 23, no. 12 (2003): 4386–400. http://dx.doi.org/10.1128/mcb.23.12.4386-4400.2003.

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ABSTRACT Expression of the chicken lysozyme gene is upregulated during macrophage differentiation and reaches its highest level in bacterial lipopolysaccharide (LPS)-stimulated macrophages. This is accompanied by complex alterations in chromatin structure. We have previously shown that chromatin fine-structure alterations precede the onset of gene expression in macrophage precursor cells and mark the lysozyme chromatin domain for expression later in development. To further examine this phenomenon and to investigate the basis for the differentiation-dependent alterations of lysozyme chromatin,
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16

Zhang, Bo, Zhi-Wen Xu, Kun-Hao Wang, Tian-Cheng Lu, and Ye Du. "Complex Regulatory Network of MicroRNAs, Transcription Factors, Gene Alterations in Adrenocortical Cancer." Asian Pacific Journal of Cancer Prevention 14, no. 4 (2013): 2265–68. http://dx.doi.org/10.7314/apjcp.2013.14.4.2265.

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17

Xu, Z., D. Cawthon, K. A. McCastlain, et al. "Selective Alterations of Transcription Factors in MPP+-Induced Neurotoxicity in PC12 Cells." NeuroToxicology 26, no. 4 (2005): 729–37. http://dx.doi.org/10.1016/j.neuro.2004.12.008.

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18

Kgatle, Mankgopo M., Asgar A. Kalla, Muhammed M. Islam, Mike Sathekge, and Razia Moorad. "Prostate Cancer: Epigenetic Alterations, Risk Factors, and Therapy." Prostate Cancer 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/5653862.

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Prostate cancer (PCa) is the most prevalent urological cancer that affects aging men in South Africa, and mechanisms underlying prostate tumorigenesis remain elusive. Research advancements in the field of PCa and epigenetics have allowed for the identification of specific alterations that occur beyond genetics but are still critically important in the pathogenesis of tumorigenesis. Anomalous epigenetic changes associated with PCa include histone modifications, DNA methylation, and noncoding miRNA. These mechanisms regulate and silence hundreds of target genes including some which are key compo
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19

Yang, Haopeng, and Michael R. Green. "Harnessing lymphoma epigenetics to improve therapies (article not eligible for CME credit)." Hematology 2020, no. 1 (2020): 95–100. http://dx.doi.org/10.1182/hematology.2020006908.

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Abstract Affinity maturation and terminal differentiation of B cells via the germinal center reaction is a complex multistep process controlled by transcription factors that induce or suppress large dynamic transcriptional programs. This occurs via the recruitment of coactivator or corepressor complexes that epigenetically regulate gene expression by post-translationally modifying histones and/or remodeling chromatin structure. B-cell–intrinsic developmental programs both regulate and respond to interactions with other cells in the germinal center that provide survival and differentiation sign
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20

Yang, Haopeng, and Michael R. Green. "Harnessing lymphoma epigenetics to improve therapies." Blood 136, no. 21 (2020): 2386–91. http://dx.doi.org/10.1182/blood.2020006908.

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Abstract Affinity maturation and terminal differentiation of B cells via the germinal center reaction is a complex multistep process controlled by transcription factors that induce or suppress large dynamic transcriptional programs. This occurs via the recruitment of coactivator or corepressor complexes that epigenetically regulate gene expression by post-translationally modifying histones and/or remodeling chromatin structure. B-cell–intrinsic developmental programs both regulate and respond to interactions with other cells in the germinal center that provide survival and differentiation sign
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21

Chauhan, Gaurav, and Hannelore V. Heemers. "Somatic Alterations Impact AR Transcriptional Activity and Efficacy of AR-Targeting Therapies in Prostate Cancer." Cancers 13, no. 16 (2021): 3947. http://dx.doi.org/10.3390/cancers13163947.

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Inhibiting the activity of the ligand-activated transcription factor androgen receptor (AR) is the default first-line treatment for metastatic prostate cancer (CaP). Androgen deprivation therapy (ADT) induces remissions, however, their duration varies widely among patients. The reason for this heterogeneity is not known. A better understanding of its molecular basis may improve treatment plans and patient survival. AR’s transcriptional activity is regulated in a context-dependent manner and relies on an interplay between its associated transcriptional regulators, DNA recognition motifs, and li
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22

Ries, Rhonda E., Hamid Bolouri, Jason E. Farrar, et al. "Alteration of Chromatin Modifiers and Misregulation of Transcription Factors Define the Genomic Profile of Infant AML." Blood 128, no. 22 (2016): 774. http://dx.doi.org/10.1182/blood.v128.22.774.774.

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Abstract AML is a malignancy of hematopoietic progenitor cells characterized by differentiation arrest leading to hematopoietic insufficiency secondary to the accumulation of hematopoietic progenitors. While much is known about the karyotypic and immunophenotypic makeup of AML, comprehensive genomic data is still emerging. The Therapeutically Applicable Research to Generate Effective Treatments (TARGET) AML project, a cooperative effort between the National Cancer Institute (NCI) and the Children's Oncology Group (COG), has sought to deepen the knowledge-base of genomic alterations that are pr
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Puustinen, Mikael Christer, and Lea Sistonen. "Molecular Mechanisms of Heat Shock Factors in Cancer." Cells 9, no. 5 (2020): 1202. http://dx.doi.org/10.3390/cells9051202.

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Malignant transformation is accompanied by alterations in the key cellular pathways that regulate development, metabolism, proliferation and motility as well as stress resilience. The members of the transcription factor family, called heat shock factors (HSFs), have been shown to play important roles in all of these biological processes, and in the past decade it has become evident that their activities are rewired during tumorigenesis. This review focuses on the expression patterns and functions of HSF1, HSF2, and HSF4 in specific cancer types, highlighting the mechanisms by which the regulat
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Chen, Li, Moli Huang, Jasmine Plummer, et al. "Master transcription factors form interconnected circuitry and orchestrate transcriptional networks in oesophageal adenocarcinoma." Gut 69, no. 4 (2019): 630–40. http://dx.doi.org/10.1136/gutjnl-2019-318325.

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ObjectiveWhile oesophageal squamous cell carcinoma remains infrequent in Western populations, the incidence of oesophageal adenocarcinoma (EAC) has increased sixfold to eightfold over the past four decades. We aimed to characterise oesophageal cancer-specific and subtypes-specific gene regulation patterns and their upstream transcription factors (TFs). DesignTo identify regulatory elements, we profiled fresh-frozen oesophageal normal samples, tumours and cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematical modelling was performed to establish (super)-enhancers land
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Yotova, Iveta, Emily Hsu, Catherine Do, et al. "Epigenetic Alterations Affecting Transcription Factors and Signaling Pathways in Stromal Cells of Endometriosis." PLOS ONE 12, no. 1 (2017): e0170859. http://dx.doi.org/10.1371/journal.pone.0170859.

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26

Doerfler, Walter. "Adenovirus oncogenesis: alterations in cellular methylation and transcription patterns− factors in viral oncogenesis?" Gene Function & Disease 2, no. 4 (2001): 139–50. http://dx.doi.org/10.1002/1438-826x(200112)2:4<139::aid-gnfd139>3.0.co;2-8.

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27

Jeong, Mira, Min Luo, Deqiang Sun, et al. "HSC Aging Epigenome: Widespread Alterations in DNA Methylation and Transcription." Blood 120, no. 21 (2012): 2329. http://dx.doi.org/10.1182/blood.v120.21.2329.2329.

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Abstract Abstract 2329 Age is the most important risk factor for myelodysplastic syndrome (MDS), a premalignant state that transforms into acute myelogenous leukemia in one third of cases. Indeed with normal aging, hematopoietic stem cell (HSC) regenerative potential diminishes and differentiation skews from lymphopoiesis toward myelopoiesis. The expansion in the HSC pool with aging provides sufficient but abnormal blood production, and animals experience a decline in immune function. Previous studies from our lab established that the DNA methyltransferase 3a (Dnmt3a) enables efficient differe
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Bach, Duc-Hiep, Nguyen Long, Thi-Thu-Trang Luu, Nguyen Anh, Sung Kwon, and Sang Lee. "The Dominant Role of Forkhead Box Proteins in Cancer." International Journal of Molecular Sciences 19, no. 10 (2018): 3279. http://dx.doi.org/10.3390/ijms19103279.

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Forkhead box (FOX) proteins are multifaceted transcription factors that are significantly implicated in cancer, with various critical roles in biological processes. Herein, we provide an overview of several key members of the FOXA, FOXC, FOXM1, FOXO and FOXP subfamilies. Important pathophysiological processes of FOX transcription factors at multiple levels in a context-dependent manner are discussed. We also specifically summarize some major aspects of FOX transcription factors in association with cancer research such as drug resistance, tumor growth, genomic alterations or drivers of initiati
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29

Belluti, Silvia, Giovanna Rigillo, and Carol Imbriano. "Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates." Cells 9, no. 3 (2020): 760. http://dx.doi.org/10.3390/cells9030760.

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Alternative splicing (AS) is a finely regulated mechanism for transcriptome and proteome diversification in eukaryotic cells. Correct balance between AS isoforms takes part in molecular mechanisms that properly define spatiotemporal and tissue specific transcriptional programs in physiological conditions. However, several diseases are associated to or even caused by AS alterations. In particular, multiple AS changes occur in cancer cells and sustain the oncogenic transcriptional program. Transcription factors (TFs) represent a key class of proteins that control gene expression by direct bindin
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Felger, J. C., S. W. Cole, T. W. W. Pace та ін. "Molecular signatures of peripheral blood mononuclear cells during chronic interferon-α treatment: relationship with depression and fatigue". Psychological Medicine 42, № 8 (2011): 1591–603. http://dx.doi.org/10.1017/s0033291711002868.

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BackgroundInterferon-alpha (IFN-α) treatment for infectious disease and cancer causes high rates of depression and fatigue, and has been used to investigate the impact of inflammatory cytokines on brain and behavior. However, little is known about the transcriptional impact of chronic IFN-α on immune cellsin vivoand its relationship to IFN-α-induced behavioral changes.MethodGenome-wide transcriptional profiling was performed on peripheral blood mononuclear cells (PBMCs) from 21 patients with chronic hepatitis C virus (HCV) either awaiting IFN-α therapy (n=10) or at 12 weeks of IFN-α treatment
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Aliya, Nishat, Saifur Rahman, Zafar K. Khan, and Pooja Jain. "Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective." Leukemia Research and Treatment 2012 (February 9, 2012): 1–15. http://dx.doi.org/10.1155/2012/984754.

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Cell type specificity of human T cell leukemia virus 1 has been proposed as a possible reason for differential viral outcome in primary target cells versus secondary. Through chromatin remodeling, the HTLV-1 transactivator protein Tax interacts with cellular factors at the chromosomally integrated viral promoter to activate downstream genes and control viral transcription. RNA interference is the host innate defense mechanism mediated by short RNA species (siRNA or miRNA) that regulate gene expression. There exists a close collaborative functioning of cellular transcription factors with miRNA
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Khan, Zia A., and Subrata Chakrabarti. "Cellular Signaling and Potential New Treatment Targets in Diabetic Retinopathy." Experimental Diabetes Research 2007 (2007): 1–12. http://dx.doi.org/10.1155/2007/31867.

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Dysfunction and death of microvascular cells and imbalance between the production and the degradation of extracellular matrix (ECM) proteins are a characteristic feature of diabetic retinopathy (DR). Glucose-induced biochemical alterations in the vascular endothelial cells may activate a cascade of signaling pathways leading to increased production of ECM proteins and cellular dysfunction/death. Chronic diabetes leads to the activation of a number of signaling proteins including protein kinase C, protein kinase B, and mitogen-activated protein kinases. These signaling cascades are activated in
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Agris, Paul F. "Targeting Gene Transcription Prevents Antibiotic Resistance." Antibiotics 14, no. 4 (2025): 345. https://doi.org/10.3390/antibiotics14040345.

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Innovative strategies are needed to curb the global health challenge of antibiotic resistance. The World Health Organization predicts that antibiotic resistance could lead to millions of deaths annually. Pharmaceutical experience has shown that modest alterations of commonly-used broad-spectrum antibiotics readily elicit resistant strains. Thus, continued simple iterative improvements on current antibiotics are not sustainable. Traditional strategies target single sites with the goal of a broad-spectrum antibiotic. In comparison, a novel strategy targets multiple sites in single- or multidrug-
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Gebrie, Alemu. "Transcription factor EB as a key molecular factor in human health and its implication in diseases." SAGE Open Medicine 11 (January 2023): 205031212311572. http://dx.doi.org/10.1177/20503121231157209.

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Transcription factor EB, as a component of the microphthalmia family of transcription factors, has been demonstrated to be a key controller of autophagy–lysosomal biogenesis. Transcription factor EB is activated by stressors such as nutrition and deprivation of growth factors, hypoxia, lysosomal stress, and mitochondrial injury. To achieve the ultimate functional state, it is controlled in a variety of modes, such as in its rate of transcription, post-transcriptional control, and post-translational alterations. Due to its versatile role in numerous signaling pathways, including the Wnt, calciu
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Divvela, Satya Srirama Karthik, Darius Saberi, and Beate Brand-Saberi. "Atoh8 in Development and Disease." Biology 11, no. 1 (2022): 136. http://dx.doi.org/10.3390/biology11010136.

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Atoh8 belongs to a large superfamily of transcriptional regulators called basic helix-loop-helix (bHLH) proteins. bHLH proteins have been identified in a wide range of organisms from yeast to humans. The members of this special group of transcription factors were found to be involved not only in embryonic development but also in disease initiation and its progression. Given their importance in several fundamental processes, the translation, subcellular location and turnover of bHLH proteins is tightly regulated. Alterations in the expression of bHLH proteins have been associated with multiple
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Crispino, John D., and Mitchell J. Weiss. "Erythro-megakaryocytic transcription factors associated with hereditary anemia." Blood 123, no. 20 (2014): 3080–88. http://dx.doi.org/10.1182/blood-2014-01-453167.

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Abstract Most heritable anemias are caused by mutations in genes encoding globins, red blood cell (RBC) membrane proteins, or enzymes in the glycolytic and hexose monophosphate shunt pathways. A less common class of genetic anemia is caused by mutations that alter the functions of erythroid transcription factors (TFs). Many TF mutations associated with heritable anemia cause truncations or amino acid substitutions, resulting in the production of functionally altered proteins. Characterization of these mutant proteins has provided insights into mechanisms of gene expression, hematopoietic devel
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Mori, Luisa P., Michael J. Corley, Andrew T. McAuley, et al. "Transcriptional and methylation outcomes of didehydro-cortistatin A use in HIV-1–infected CD4+T cells." Life Science Alliance 7, no. 10 (2024): e202402653. http://dx.doi.org/10.26508/lsa.202402653.

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Ongoing viral transcription from the reservoir of HIV-1 infected long-lived memory CD4+T cells presents a barrier to cure and associates with poorer health outcomes for people living with HIV, including chronic immune activation and inflammation. We previously reported that didehydro-cortistatin A (dCA), an HIV-1 Tat inhibitor, blocks HIV-1 transcription. Here, we examine the impact of dCA on host immune CD4+T-cell transcriptional and epigenetic states. We performed a comprehensive analysis of genome-wide transcriptomic and DNA methylation profiles upon long-term dCA treatment of primary human
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Catizone, Allison N., Gizem Karsli Uzunbas, Petra Celadova, Sylvia Kuang, Daniel Bose, and Morgan A. Sammons. "Locally acting transcription factors regulate p53-dependent cis-regulatory element activity." Nucleic Acids Research 48, no. 8 (2020): 4195–213. http://dx.doi.org/10.1093/nar/gkaa147.

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Abstract The master tumor suppressor p53 controls transcription of a wide-ranging gene network involved in apoptosis, cell cycle arrest, DNA damage repair, and senescence. Recent studies revealed pervasive binding of p53 to cis-regulatory elements (CREs), which are non-coding segments of DNA that spatially and temporally control transcription through the combinatorial binding of local transcription factors. Although the role of p53 as a strong trans-activator of gene expression is well known, the co-regulatory factors and local sequences acting at p53-bound CREs are comparatively understudied.
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Jones, Cheyenne A., William P. Tansey, and April M. Weissmiller. "Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation." Epigenetics Insights 15 (January 2022): 251686572211156. http://dx.doi.org/10.1177/25168657221115656.

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The SWI/SNF chromatin remodeling complex uses the energy of ATP hydrolysis to alter contacts between DNA and nucleosomes, allowing regions of the genome to become accessible for biological processes such as transcription. The SWI/SNF chromatin remodeler is also one of the most frequently altered protein complexes in cancer, with upwards of 20% of all cancers carrying mutations in a SWI/SNF subunit. Intense studies over the last decade have probed the molecular events associated with SWI/SNF dysfunction in cancer and common themes are beginning to emerge in how tumor-associated SWI/SNF mutation
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Khamit, Ali, Payal Chakraborty, Szabolcs Zahorán, Zoltán Villányi, Hajnalka Orvos, and Edit Hermesz. "Stress-Induced Changes in Nucleocytoplasmic Localization of Crucial Factors in Gene Expression Regulation." International Journal of Molecular Sciences 25, no. 7 (2024): 3895. http://dx.doi.org/10.3390/ijms25073895.

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This study investigates the toxic effect of harmful materials, unfiltered by the placenta, on neonatal umbilical cord (UC) vessels, focusing on stress-induced adaptations in transcriptional and translational processes. It aims to analyze changes in pathways related to mRNA condensate formation, transcriptional regulation, and DNA damage response under maternal smoking-induced stress. UC vessels from neonates born to smoking (Sm) and nonsmoking mothers (Ctr) were examined. Immunofluorescence staining and confocal microscopy assessed the localization of key markers, including Transcription Compl
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Cheng, Jinping, Guiqian Zhang, Linhao Xu, Chang Liu, and Hua Jiang. "Altered H3K27 trimethylation contributes to flowering time variations in polyploid Arabidopsis thaliana ecotypes." Journal of Experimental Botany 73, no. 5 (2021): 1402–14. http://dx.doi.org/10.1093/jxb/erab470.

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Abstract Polyploidy is a widespread phenomenon in flowering plant species. Polyploid plants frequently exhibit considerable transcriptomic alterations after whole-genome duplication (WGD). It is known that the transcriptomic response to tetraploidization is ecotype-dependent in Arabidopsis; however, the biological significance and the underlying mechanisms are unknown. In this study, we found that 4x Col-0 presents a delayed flowering time whereas 4x Ler does not. The expression of FLOWERING LOCUS C (FLC), the major repressor of flowering, was significantly increased in 4x Col-0 but only a sub
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Plaza-Diaz, Julio, David Izquierdo, Álvaro Torres-Martos, Aiman Tariq Baig, Concepción M. Aguilera, and Francisco Javier Ruiz-Ojeda. "Impact of Physical Activity and Exercise on the Epigenome in Skeletal Muscle and Effects on Systemic Metabolism." Biomedicines 10, no. 1 (2022): 126. http://dx.doi.org/10.3390/biomedicines10010126.

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Exercise and physical activity induces physiological responses in organisms, and adaptations in skeletal muscle, which is beneficial for maintaining health and preventing and/or treating most chronic diseases. These adaptations are mainly instigated by transcriptional responses that ensue in reaction to each individual exercise, either resistance or endurance. Consequently, changes in key metabolic, regulatory, and myogenic genes in skeletal muscle occur as both an early and late response to exercise, and these epigenetic modifications, which are influenced by environmental and genetic factors
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Hayashi, Kaori. "Altered DNA methylation in kidney disease: useful markers and therapeutic targets." Clinical and Experimental Nephrology 26, no. 4 (2022): 309–15. http://dx.doi.org/10.1007/s10157-022-02181-5.

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AbstractRecent studies have demonstrated the association of altered epigenomes with lifestyle-related diseases. Epigenetic regulation promotes biological plasticity in response to environmental changes, and such plasticity may cause a ‘memory effect’, a sustained effect of transient treatment or an insult in the course of lifestyle-related diseases. We investigated the significance of epigenetic changes in several genes required for renal integrity, including the nephrin gene in podocytes, and the sustained anti-proteinuric effect, focusing on the transcription factor Krüppel-like factor 4 (KL
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Owen, R. D., and M. C. Ostrowski. "Rapid and selective alterations in the expression of cellular genes accompany conditional transcription of Ha-v-ras in NIH 3T3 cells." Molecular and Cellular Biology 7, no. 7 (1987): 2512–20. http://dx.doi.org/10.1128/mcb.7.7.2512-2520.1987.

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Hormone treatment of NIH 3T3 cells that contain recombinant fusions between the mouse mammary virus long terminal repeat and the v-ras gene of Harvey murine sarcoma virus results in conditional expression of the ras p21 gene product. Levels of ras mRNA and p21 are maximal after 2 to 4 h of hormone treatment. Analysis of cellular RNA by Northern blotting and nuclease S1 protection assays indicates that the expression of two cellular RNA species increases with kinetics similar to v-ras: v-sis-related RNA and retrovirus-related VL30 RNA. Run-on transcription in isolated nuclei shows that the incr
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45

Owen, R. D., and M. C. Ostrowski. "Rapid and selective alterations in the expression of cellular genes accompany conditional transcription of Ha-v-ras in NIH 3T3 cells." Molecular and Cellular Biology 7, no. 7 (1987): 2512–20. http://dx.doi.org/10.1128/mcb.7.7.2512.

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Hormone treatment of NIH 3T3 cells that contain recombinant fusions between the mouse mammary virus long terminal repeat and the v-ras gene of Harvey murine sarcoma virus results in conditional expression of the ras p21 gene product. Levels of ras mRNA and p21 are maximal after 2 to 4 h of hormone treatment. Analysis of cellular RNA by Northern blotting and nuclease S1 protection assays indicates that the expression of two cellular RNA species increases with kinetics similar to v-ras: v-sis-related RNA and retrovirus-related VL30 RNA. Run-on transcription in isolated nuclei shows that the incr
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46

Khakhar, Arjun, Cecily Wang, Ryan Swanson, et al. "VipariNama: RNA viral vectors to rapidly elucidate the relationship between gene expression and phenotype." Plant Physiology 186, no. 4 (2021): 2222–38. http://dx.doi.org/10.1093/plphys/kiab197.

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Abstract Synthetic transcription factors have great promise as tools to help elucidate relationships between gene expression and phenotype by allowing tunable alterations of gene expression without genomic alterations of the loci being studied. However, the years-long timescales, high cost, and technical skill associated with plant transformation have limited their use. In this work, we developed a technology called VipariNama (ViN) in which vectors based on the tobacco rattle virus are used to rapidly deploy Cas9-based synthetic transcription factors and reprogram gene expression in planta. W
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Tebbi, Cameron K., Jiyu Yan, Eva Sahakian, et al. "Mycovirus-Containing Aspergillus flavus Alters Transcription Factors in Normal and Acute Lymphoblastic Leukemia Cells." International Journal of Molecular Sciences 25, no. 19 (2024): 10361. http://dx.doi.org/10.3390/ijms251910361.

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Transcription factors control genes to maintain normal hemopoiesis, and dysregulation of some factors can lead to acute lymphoblastic leukemia (ALL). Mycoviruses are known to alter the genetics of their fungal host. The present study evaluates the effects of the products of a mycovirus-containing Aspergillus flavus (MCAF), isolated from the home of a patient with ALL, on certain transcription factors of normal and ALL cell lines. Our published studies have shown that ALL patients have antibodies to MCAF, and that exposure of the mononuclear leukocytes of patients in complete remission to its p
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Ruiz-Roig, Clàudia, Núria Noriega, Alba Duch, Francesc Posas, and Eulàlia de Nadal. "The Hog1 SAPK controls the Rtg1/Rtg3 transcriptional complex activity by multiple regulatory mechanisms." Molecular Biology of the Cell 23, no. 21 (2012): 4286–96. http://dx.doi.org/10.1091/mbc.e12-04-0289.

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Cells modulate expression of nuclear genes in response to alterations in mitochondrial function, a response termed retrograde (RTG) regulation. In budding yeast, the RTG pathway relies on Rtg1 and Rtg3 basic helix-loop-helix leucine Zipper transcription factors. Exposure of yeast to external hyperosmolarity activates the Hog1 stress-activated protein kinase (SAPK), which is a key player in the regulation of gene expression upon stress. Several transcription factors, including Sko1, Hot1, the redundant Msn2 and Msn4, and Smp1, have been shown to be directly controlled by the Hog1 SAPK. The mech
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Yang, Bing, Dingyu Zhang, Zitong Meng, et al. "NAC047/052/104 Synergistically Regulate the Dark-Induced Leaf Senescence in Non-Heading Chinese Cabbage." International Journal of Molecular Sciences 26, no. 5 (2025): 2340. https://doi.org/10.3390/ijms26052340.

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Non-heading Chinese cabbage (NHCC) is an important vegetable, and its leaves are harvested for consumption. Thus, the initiation and progression of leaf senescence in NHCC directly impact its yield and quality. In multiple plant species, NAC transcription factors are known to act as critical regulators of leaf senescence. However, in NHCC, the NAC transcription factors contributing to leaf senescence regulation remain to be identified, and the mechanisms underlying dark-induced leaf senescence remain unclear. To explore the molecular mechanisms of leaf senescence in NHCC, we stored NHCC away f
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Eguchi, Asuka, Garrett O. Lee, Fang Wan, Graham S. Erwin, and Aseem Z. Ansari. "Controlling gene networks and cell fate with precision-targeted DNA-binding proteins and small-molecule-based genome readers." Biochemical Journal 462, no. 3 (2014): 397–413. http://dx.doi.org/10.1042/bj20140400.

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Transcription factors control the fate of a cell by regulating the expression of genes and regulatory networks. Recent successes in inducing pluripotency in terminally differentiated cells as well as directing differentiation with natural transcription factors has lent credence to the efforts that aim to direct cell fate with rationally designed transcription factors. Because DNA-binding factors are modular in design, they can be engineered to target specific genomic sequences and perform pre-programmed regulatory functions upon binding. Such precision-tailored factors can serve as molecular t
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