Relevant bibliographies by topics / Alterations of transcription factors

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Academic literature on the topic 'Alterations of transcription factors'

Author: Grafiati
Published: 12 September 2023

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Journal articles on the topic "Alterations of transcription factors"

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Tang, Jinglong, and Masaya Baba. "MiT/TFE Family Renal Cell Carcinoma." Genes 14, no. 1 (January 5, 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 retain the bHLH-Zip structures and act as oncogenic transcription factors. The germline variant of MITF p.E318K has been reported as a risk factor for RCC. E 318 is present at the SUMOylation consensus site of MITF. The p.E318K variant abrogates SUMOylation on K 316, which results in alteration of MITF transcriptional activity. Only a few cases of MITF p.E318K RCC have been reported, and their clinical features have not yet been fully described. It would be important for clinicians to recognize MITF p.E318K RCC and consider MITF germline testing for undiagnosed familial RCC cases. This review outlines the involvement of the MiT/TFE transcription factors in RCC, both in sporadic and hereditary cases. Further elucidation of the molecular function of the MiT/TFE family is necessary for better diagnosis and treatment of these rare diseases.
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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 (September 1, 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 proteins (SPs) and Krüppel-like factors (KLFs) are closely related transcription factors characterized by three highly conserved zinc fingers domains that interact with DNA. Studies have demonstrated that SP and KLF transcription factors are expressed in various tissues and regulate diverse processes such as proliferation, differentiation, apoptosis, inflammation, and tumorigenesis. This review highlights the role of SP and KLF transcription factors in the metabolism of various cancers and their impact on tumorigenesis. A better understanding of the role and underlying mechanisms governing the metabolic changes during tumorigenesis could provide new therapeutic opportunities for cancer treatment.
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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 (August 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 of the activities of cJun and JunB, two members of the AP-1 transcriptional complexes. This repressive effect of E1A is dependent on the p300-binding domain of E1A and can be relieved by overexpression of p300. These results suggest that p300 serves as a mediator protein for downregulation of AP-1 activity by E1A. This hypothesis was further supported by the following observations: (i) in the absence of E1A, overexpression of p300 stimulated transcription both through an AP-1 site present in the collagenase promoter and through Jun proteins in GAL4 fusion protein-based assays; and (ii) overexpression of a mutant p300 lacking the E1A-interacting domain reduced the responsiveness of Jun-dependent transcription to E1A repression. As predicted from the functional results, p300 physically interacted with the Jun proteins. These findings thus established that p300 is a cofactor for cJun and JunB. We propose that p300 is a common mediator protein through which E1A gains control over multiple transcriptional regulatory pathways in the host cells.
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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 (April 1, 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 factors repress PPAR-mediated transcriptional activity without altering protein expression of PPARG. Furthermore, we show that BC-derived factors induce significant alterations in skeletal muscle mitochondrial function and lipid accumulation, which are rescued with exogenous expression of PPARG. The PPARG agonist drug rosiglitazone was able to rescue BC-induced lipid accumulation but did not rescue effects of BC-derived factors on PPAR-mediated transcription or mitochondrial function. These data suggest that BC-derived factors alter lipid accumulation and mitochondrial function via different mechanisms that are both related to PPARG signaling, with mitochondrial dysfunction likely being altered via repression of PPAR-mediated transcription, and lipid accumulation being altered via transcription-independent functions of PPARG.
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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 (January 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 genes associated with cell survival and proliferation. Understanding these molecular mechanisms will helps us develop new treatment strategies that target these transcription factors and may eventually decrease the morbidity and mortality associated with HNSCC.
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Koch, Marilin, Stefan Czemmel, Felix Lennartz, Sarah Beyeler, Justyna Przystal, Parameswari Govindarajan, Denis Canjuga, 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 (November 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 lines were transduced with a Doxycycline-inducible dnE47 lentivirus. Functional characterizations included immunocytochemistry, immunoblots, cytotoxicity and clonogenicity assays in vitro and latency until the onset of symptoms in vivo. CAGE and RNASeq were conducted for analyzing the dnE47-induced molecular profile. RESULTS The induction of dnE47 led to cytoplasmatic sequestration of HLH/bHLH transcription, reduced proliferation, increased cytotoxicity and reduced clonogenic survival in vitro and a prolonged latency until the onset of neurological symptoms in vivo. CAGE and RNASeq data revealed alterations in several cancer-relevant pathways. CONCLUSIONS A dnE47-mediated inhibition of the bHLH transcription network induced actionable molecular alterations in glioma cells that could be exploited for the design of novel therapies.
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Goodson, Michael, Brian A. Jonas, and Martin A. Privalsky. "Corepressors: Custom Tailoring and Alterations While you Wait." Nuclear Receptor Signaling 3, no. 1 (January 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 clear that the functions of both SMRT and N-CoR are further diversified through alternative mRNA splicing, yielding a series of corepressor protein variants that participate in distinctive transcription factor partnerships and display distinguishable repression properties. This review will discuss what is known about the structure and actions of SMRT, N-CoR, and their splicing variants, and how alternative splicing may allow the functions of these corepressors to be adapted and tailored to different cells and to different developmental stages.
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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 (September 16, 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 analysis we observed that these subtypes are determined by a distinct repertoire of lineage-specific transcription factors. Furthermore, specific pattern and abundance of copy number and DNA methylation changes at these TFs and targets, compared to other genes and to normal cells were observed. Overall, distinct transcriptional profiles are linked to genetic and epigenetic alterations at lineage-specific transcriptional regulators in breast cancer subtypes. Availability and implementation The analysis code and data are deposited at https://bitbucket.org/qzhu/breast.cancer.tf/. Supplementary information Supplementary data are available at Bioinformatics online.
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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 (January 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, or incubation with the p300 inhibitor curcumin. Histone H2AX phosphorylation and lysine acetylation were examined for oxidative DNA damage and p300 activation. Screening for transcription factors was performed with the Luminex system. Alterations of selected transcription factors were validated. mRNA expression of p300, endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and fibronectin (FN) and its splice variant EDB+FN and FN protein production were analyzed. HUVECs in 25 mmol/l glucose showed increased p300 production accompanied by increased binding of p300 to ET-1 and FN promoters, augmented histone acetylation, H2AX phosphorylation, activation of multiple transcription factors, and increased mRNA expression of vasoactive factors and ECM proteins. p300 overexpression showed a glucose-like effect on the mRNA expression of ET-1, VEGF, and FN. Furthermore, siRNA-mediated p300 blockade or chemical inhibitor of p300 prevented such glucose-induced changes. Similar mRNA upregulation was also seen in the organ culture of vascular tissues, which was prevented by p300 siRNA transfection. Data from these studies suggest that glucose-induced p300 upregulation is an important upstream epigenetic mechanism regulating gene expression of vasoactive factors and ECM proteins in endothelial cells and is a potential therapeutic target for diabetic complications.
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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 (October 15, 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 review the evidence suggesting a model in which cell-specific actions of SDTFs are the consequence of priming functions of lineage determining transcription factors. We also discuss recent findings relating lineage-determining and SDTF activity to alterations in the epigenetic landscape as well as the production and function of enhancer RNAs. These findings have implications for the understanding of how natural genetic variation impacts cell-specific programs of gene expression and suggest new approaches for altering gene expressionin vivo.
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Dissertations / Theses on the topic "Alterations of transcription factors"

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Morey, Ramonell Lluís. "Chromatin alterations imposed by the oncogenic transcription factor PML-RAR." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7138.

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En mamíferos, así como en plantas, mutaciones en AND helicasas/ATPasas del la família SNF2, no solo afectan a la estructura de la cromatina, sino que también afectan al patrón global de la metilación del ADN. Sugiriendo una relación funcional entre la estructura de la cromatina y la epigenética. El complejo NuRD, el cual posee una ATPasa de la familía SNF2, está relacionado con la represión de la transcripción y en el remodelamiento de la cromatina. Nuestro laboratorio demostró que la proteína leucémica PML-RARα reprime la transcripción de sus genes diana por el reclutamiento de DNMTs y el complejo PRC2. En esta tesis, demostramos una relación directa del complejo NuRD en la represión génica y en los cambios epigenéticos en la leucemia promielocítica aguda (APL). Mostramos que PML-RARα se une y recluta NuRD a sus genes diana, incluyendo el gen supresor de tumores RAR2, facilitando que el complejo de Polycomb se reclute y metile la lisina 27 de la histona H3. Tratamiento con Acido Retinóico (RA), el qual se utiliza en pacientes, reduce la ocupación de NuRD en células leucémicas. Eliminando NuRD no solo provoca que las histonas no se deacetilen y que la cromatina no se compacte, sino que también provoca que tanto la metilación del ADN y de las histonas no se produzca, así como la represión génica del gen RAR2, favoreciendo la diferenciación celular. Nuestros resultados caracterizan un nuevo papel del complejo NuRD en el establecimiento de los patrones epigenéticos en APL, demostrando una relación esencial entre la estructura de la cromatina y epigenética durante el desarrollo de la leucemia, pudiéndose aplicar a la terapia de esta enfermedad.
In mammals, as in plants, mutations in SNF2-like DNA helicases/ATPases were shown to affect not only chromatin structure but also global methylation patterns, suggesting a potential functional link between chromatin structure and epigentic marks. The SNF2-like containing NuRD complex is involved in gene transcriptional repression and chromatin remodeling. We have previously shown that the leukemogenic protein PMLRARα represses target genes through recruitment of DNMTs and Polycomb complex. In this thesis, we demonstrate a direct role of the NuRD complex in aberrant gene repression and transmission of epigenetic repressive marks in acute promyelocytic leucemia (APL). We show that PML-RARα binds and recruits NuRD to target genes, including to the tumor-suppressor gene RAR2. In turn, the NuRD complex facilitates Polycomb binding and histone methylation at lysine 27. Retinoic acid treatment reduced the promoter occupancy of the NuRD complex. Knock-down of the NuRD complex in leukemic cells not only prevented histone deacetylation and chromatin compaction, but also impaired DNA and histone methylation as well as stable silencing, thus favoring cellular differentiation. These results unveil an important role for NuRD in the establishment of altered epigenetic marks in APL, demonstrating an essential link between chromatin structure and epigenetics in leukemogenesis that could be exploited for therapeutic intervention.
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Ruiz, Emmanuelle. "Coopération entre les inducteurs de l’EMT (EMT-TF/miRNA) et les altérations oncogéniques dans la tumorigenèse mammaire." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10069.

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Les cellules cancéreuses sont capables de réactiver la transition Epithélio-Mésenchymateuse (EMT), mécanisme embryonnaire, pour acquérir une mobilité et une capacité de dédifférenciation. L'EMT conduit à une reprogrammation génétique avec la réactivation d'inducteurs de l'EMT, qui sont en majorité des facteurs de transcription (EMT-TF), et conduit à l'inhibition de miARN. Par ailleurs des stress oncogéniques sont essentiels à la progression tumorale. Le but de mon projet de thèse était de comprendre comment les événements de reprogrammation génétique survenant au cours de l'EMT coopèrent avec des stress oncogéniques dans la transformation tumorale mammaire.Premièrement, un criblage basé sur la coopération oncogénique en soft agar assay, entre les EMT-TFs et les stress oncogénique a été réalisé. Suite à une analyse bioinformatique, différentes signatures d'EMT-TF associés à un stress oncogénique ont été identifiées. Ainsi, par exemple, l'expression de l'EMT-TF Zeb1 et l'EMT-TF GSC sont associés à la délétion du gène suppresseur de tumeur PTEN pour transformer des cellules mammaires immortalisées. Une analyse en immuno-histochimie sur un set de 558 tumeurs du sein triple négatives a validé in vivo la présence d'une corrélation entre l'expression de GSC et l'expression de PTEN. Cependant cette association semble être plus complexe. En effet, l'expression de GSC est négativement associée à l'expression nucléaire de PTEN tandis qu'elle est positivement associée à l'expression de PTEN cytoplasmique. Enfin une analyse sur des métadonnées publiques de cancers telles que le TCGA ou le METABRIC est en cours pour valider ces signatures in vitro et plus largement pour déterminer comment l'EMT ou les signatures associées aux EMT-TF se corrèlent avec les voies oncogéniques classiques. Deuxièmement, une analyse in silico à partir d'algorithmes prédictifs de cibles de miARN, a été réalisée pour sélectionner les miARN capables d'inhiber l'expression de plusieurs EMT-TF. Deux miARN (miR-495 et 590-3p) ont été identifiés ciblant plusieurs membres des 4 principales familles d'EMT-TF (FoxC, Snail, bHLH et ZEB). Des tests in vitro ont été réalisés pour valider ces régulations identifiant Slug comme une cible de miR-590-3p. De plus, l'expression de ces miARN dans des lignées cellulaires mammaires est négativement associée à l'expression des EMT-TF et des marqueurs de l'EMT. Un traitement au TGF, inducteur de l'EMT, diminue leur expression, signifiant potentiellement que ces miARN peuvent négativement réguler l'EMT. En parallèle, plusieurs EMT-TF sont capables de réprimer l'expression de miR-590-3p, agissant directement sur son promoteur, créant ainsi des boucles de régulation. Des études fonctionnelles utilisant des vecteurs d'expression stable de miR-590-3p sembleraient montrer un rôle secondaire de ce miARN dans la régulation de l'EMT car mir-590-3p dérégule des marqueurs secondaires de l'EMT comme la N-cadhérine. Des études de restauration de fonctions sont envisagées pour déterminer quelle est l'importance de ces boucles de régulation dans la progression tumorale mammaire. Plus largement, l'expression des miARN identifiés va être corrélée avec les signatures associées aux EMT-TF et aux voies oncogéniques classiques pour déterminer le lien entre ces trois composants dans la tumorigenèse mammaire. Mes travaux de thèse ont montré qu'il existait un intéractome entre des inducteurs de l'EMT, des stress oncogéniques et des miARNs au cours de la transformation mammaire humaine
Cancer cells are able to reactivate the Epithelio-Mesenchymal Transition (EMT), an embryonic mechanism, to acquire mobility and dedifferentiation capacities. EMT leads to a genetic reprogramming with the reactivation of EMT inductors, mainly transcription factors (EMT-TF) and the inhibition of miRNA. Otherwise, oncogenic stresses are essentials to tumor progression. The aim of my thesis project was to have a better understanding about the cooperation between events of genetic reprogramming occurring during EMT and oncogenic stresses during mammary tumor transformation. First, a screening based on oncogenic cooperation in soft agar assay, between EMT-TFs and oncogenic stresses was performed. Following a bioinformatics analysis, different EMT-TFs signatures associated with an oncogenic stress were identified. Thus, for example, the expression of EMT-TF ZEB1 and GSC were associated with the deletion of tumor suppressor gene PTEN to transform immortalized mammary epithelial cells. An immunohistochemistry analysis on a set of 558 triple negative breast cancers validated in vivo the presence of a correlation between the expressions of GSC and PTEN. However, this association seems to be more complex. Indeed, the expression of GSC is negatively associated with the nuclear expression of PTEN while it’s positively associated with the cytoplasmic expression of PTEN. Finally, an analysis of public metadata on cancer samples as TCGA or METABRIC is ongoing to validate these in vitro signatures and wider to determine how EMT or EMT-TFs associated signatures correlate with classical oncogenic pathways.Secondly, an in silico analysis, from predictive algorithms of miRNA targets, was performed to select miRNA able to inhibit the expression of several EMT-TFs. Two miRNA (miR-495 and miR-590-3p) were identified targeting several members of four principal’s families of EMT-TFs (FOXC, Snail, bHLH and ZEB). In vitro tests were realized to validate these regulations identifying Slug as a target of miR-590-3p. Moreover, these miRNAs expression in mammary cell lines is negatively correlated with EMT-TFs expression and EMT markers. A treatment with TGF-, a major EMT inductor, decreases their expression, potentially meaning that these miRNA can negatively regulate EMT. In parallel, several EMT-TFs are able to repress the expression of miR-590-3p, acting directly on its promotor, thus creating feedback loops. Functional studies using stable expression vector of miR-590-3p suggest a secondary role of this miRNA in the regulation of EMT because miR-590-3p deregulates EMT secondary markers as N-Cadherin. Functions restauration studies are planned to determine how important these feedback loops in mammary tumor progression are. To open the project, expression of these identified miRNA will be correlated with EMT-TF associated signatures and with classical oncogenic pathways to determine the link between these three components in mammary tumorigenesis. My thesis works are shown that there is an interactome between EMT inductors, oncogenic stresses and miRNA during human mammary transformation
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McElwee, Joshua J. "A comparative analysis of transcriptional alterations in long-lived insulin/IGF-1-like signaling mutants in Caenorhabditis elegans and Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4982.

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Jamrog, Laura. "Impact des altérations génétiques de PAX5 sur le développement de la lignée lymphoïde B et dans la leucémogenèse des LAL-B." Electronic Thesis or Diss., Toulouse 3, 2021. http://www.theses.fr/2021TOU30306.

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Le gène PAX5 (Paired boX 5) code un facteur de transcription essentiel pour la différenciation lymphoïde B. Nous avons montré que les deux isoformes PAX5A et PAX5B étaient différentiellement régulées mais pouvaient exercer une fonction équivalente durant l'induction de la différenciation lymphoïde B et pourraient présenter des différences fonctionnelles à la suite de l'activation des lymphocytes B. Le contrôle précis de leur expression peut ainsi refléter un moyen d'ajuster finement le dosage de PAX5 pendant le processus de différenciation des cellules de la lignée lymphoïde B. PAX5 est la cible principale d'une large diversité d'altérations somatiques dans les LAL-B de l'enfant et de l'adulte. Cependant, le rôle des protéines de fusion impliquant PAX5 dans l'initiation et la transformation des LAL-B est encore méconnu. Nous avons précédemment décrit une nouvelle translocation chromosomique récurrente t(7;9)(q11;p13) dans les LAL-B qui juxtapose PAX5 à la séquence codante du gène de l'élastine (ELN). Pour étudier la fonction de la protéine de fusion résultante, PAX5-ELN, au cours du développement leucémique, nous avons créé un modèle murin dans lequel le transgène PAX5-ELN est exprimé spécifiquement dans le compartiment B. Les souris exprimant PAX5-ELN développent un phénotype de LAL-B avec une pénétrance de 80%. Leur transformation leucémique est associée à l'acquisition de mutations secondaires récurrentes des gènes Ptpn11, Kras, Pax5, et Jak3 affectant d'importantes voies de signalisation requises pour la prolifération cellulaire. Nos études fonctionnelles ont démontré que PAX5-ELN altérait in vitro et in vivo le développement lymphoïde B et pouvait induire une expansion aberrante du compartiment progéniteur B (pro-B) au stade préleucémique. Nos approches moléculaires et computationnelles ont identifié des gènes-candidats régulés par PAX5-ELN et pouvant être impliqués dans l'initiation leucémique. Nos données fournissent ainsi un nouveau modèle d'étude in vivo récapitulant la leucémogenèse multi-étapes des LAL-B décrites chez les patients et impliquent fortement les protéines de fusion engageant PAX5 en tant que puissantes oncoprotéines dans le développement leucémique. Par ailleurs, il existe de plus en plus de preuves d'une base génétique héréditaire de prédisposition aux LAL-B pédiatriques. Dans ce contexte, quatre cas de familles non-apparentées affectées par des LAL-B et exprimant des mutations ponctuelles germinales et hétérozygotes de PAX5 ont récemment été rapportés : la mutation PAX5 G183S altérant le domaine octapeptide de PAX5 a été décrite chez trois familles alors que la mutation PAX5 R38H altérant le domaine de liaison à l'ADN de PAX5 a été identifiée chez une autre. Nous avons renforcé l'hypothèse du caractère héréditaire des LAL-B familiales avec la description de trois nouveaux cas de LAL-B au sein d'une même famille exprimant la mutation germinale PAX5 R38H. Pour étudier l'effet intrinsèque de la protéine mutée PAX5 R38H dans le développement lymphoïde B, nous avons effectué des tests fonctionnels in vitro et in vivo combinés à une analyse d'expression génique, basés sur une approche de complémentation rétrovirale. Nos résultats ont indiqué que PAX5 R38H agissait comme un fort variant hypomorphique qui échouait à induire la différenciation lymphoïde B et n'exerçait pas d'effet dominant-négatif sur la forme sauvage de PAX5. Des transplantations syngéniques de cellules exprimant PAX5 R38H ont démontré qu'elles maintenaient une capacité de prise de greffe et menaient au développement leucémique chez la souris. Notre analyse transcriptomique a confirmé la perte de fonction de PAX5 sur ses gènes cibles et a révélé une signature moléculaire spécifique au mutant. Nos données mettent ainsi en évidence l'importance de la dérégulation transcriptionnelle dans la leucémogenèse des LAL-B familiales, en particulier des gènes impliqués dans la différenciation lymphoïde B
The PAX5 (Paired boX 5) gene encodes a key transcription factor crucial for B-cell differentiation. We showed that the two PAX5 isoforms are differentially regulated but have equivalent function during early B-cell differentiation. Indeed, PAX5A and PAX5B isoforms can both induce B-cell program but may have functional differences after B-cell activation. The tight control of their expression may thus reflect a way to finely tune PAX5 dosage during B-cell differentiation process. PAX5 is a well-known haploinsufficient tumor suppressor gene in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and is the main target of a wide diversity of somatic alterations in childhood and adult BCP-ALL, occurring in one third of sporadic cases. However, the role of PAX5 fusion proteins in BCP-ALL initiation and transformation is ill-known. We previously reported a new recurrent t(7;9)(q11;p13) chromosomal translocation in human BCP-ALL that juxtaposed PAX5 to the coding sequence of elastin (ELN). To study the function of the resulting PAX5-ELN fusion protein in BCP-ALL development, we generated a mouse model in which the PAX5-ELN transgene is expressed specifically in B cells. PAX5-ELN-expressing mice efficiently developed BCP-ALL phenotype with a penetrance of 80%. Leukemic transformation was associated with clonal Immunoglobulin gene rearrangement and recurrent secondary mutations in Ptpn11, Kras, Pax5, and Jak3 genes affecting key signaling pathways required for cell proliferation. Our functional studies demonstrated that PAX5-ELN impairs B-cell development in vitro and in vivo and induces an aberrant expansion of the pro-B cell compartment at the preleukemic stage. Our molecular and computational approaches identified PAX5-ELN-regulated candidate genes that establish the molecular bases of the preleukemic state to drive BCP-ALL initiation. In conclusion, our study provides a new in vivo model recapitulating the multistep leukemogenesis process of human BCP-ALL and strongly implicates PAX5 fusion proteins as potent oncoproteins in leukemia development. Furthermore, there is increasing evidence for an inherited genetic basis of susceptibility to childhood BCP-ALL. In this context, four unrelated families with childhood BCP-ALL expressing heterozygous PAX5 germline point mutations were recently reported: the recurrent mutation PAX5 G183S affecting the octapeptide domain of PAX5 has been described in three families while PAX5 R38H affecting its DNA-binding paired domain has been identified in another one. We strengthen the hypothesis of inherited character of familial BCP-ALL with the description of three novel familial BCP-ALL cases in related patients that express the germline PAX5 R38H mutation. To uncover the intrinsic effect of PAX5 R38H mutant in B-cell development, we performed in vitro, and in vivo functional assays combined with a gene expression analysis, based on a retroviral complementation approach. Our results indicated that PAX5 R38H mutant acts as a strong hypomorphic variant that fails to drive B-cell differentiation and does not exert a dominant-negative effect on wild-type PAX5. Syngeneic transplantation of PAX5 R38H-expressing cells demonstrated maintenance of engraftment capacity and led to development of BCP-ALL phenotype in mice. Our transcriptomic analysis of these PAX5 R38H-expressing cells showed that PAX5 R38H drastically alters the pattern of expression of PAX5 target genes but also revealed a distinct molecular signature specific to PAX5 R38H. Together with previous unrelated family study, our observations allow to establish the recurrence of the germline PAX5 R38H mutation associated with BCP-ALL. Our data also highlight the importance of transcriptional dysregulation in leukemogenesis of familial BCP-ALL, particularly of genes involved in B-cell differentiation
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Redondo, Monte Enric [Verfasser], and Philipp [Akademischer Betreuer] Greif. "Investigation of transcription factor alterations in core binding factor leukemia : implications in clonal expansion, cell metabolism and lineage fate decisions / Enric Redondo Monte ; Betreuer: Philipp Greif." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/122568269X/34.

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Borralleras, Fumaña Cristina 1988. "Correlation between cognitive phenotype, neural morphology and molecular alterations in mouse models of Williams-Beuren syndrome : new therapeutic approaches." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/388032.

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Williams-Beuren syndrome (WBS) is a rare neurodevelopmental disorder caused by a heterozygous deletion of 26-28 contiguous genes in the 7q11.23 region. So far, a great deal of attention has been focused on its unique and distinctive neurocognitive profile. Although important progress has been made with regards to clinical characterization or genotype-phenotype correlations, a much deeper insight into the neuropathological features of WBS would be of great interest. In this thesis project, we have used a WBS mouse model carrying a heterozygous deletion that mimics the most common deletion found in patients. We have characterized the cognitive and behavioral phenotype of these mice and we have indentified molecular and neuroanatomical alterations relevant for the disease. Moreover, we have attempted two novel therapeutic strategies: a gene therapy and a pharmacological approach. The results obtained highlight the utility of this animal model to study the mechanisms underlying the disease as well as to evaluate novel therapeutic strategies.
La síndrome de Williams-Beuren (SWB) és una malaltia rara del neurodesenvolupament causada per una deleció heterozigota d’entre 26 i 28 gens contigus a la regió 7q11.23. Fins ara, una gran part de l’atenció s’ha centrat en el seu característic perfil neurocognitiu. Tot i que s’han fet progressos molt importants pel que fa a la caracterització clínica o a les correlacions genotip-fenotip, seria de gran interès aprofundir en les característiques neuropatològiques de la SWB. En aquesta tesi, hem utilitzat un model de ratolí del SWB amb una deleció heterozigota que mimetitza la deleció més comuna d’aquests pacients. Hem caracteritzat el fenotip cognitiu i comportamental d’aquests ratolins i hem identificat alteracions moleculars i neuroanatòmiques rellevants per a la malaltia. Per altra banda, hem dut a terme dues estratègies terapèutiques: una teràpia gènica i un tractament farmacològic. Els resultats obtinguts remarquen la utilitat d’aquest model animal per a l’estudi dels mecanismes subjacents a la malaltia així com també per a avaluar noves aproximacions terapèutiques.
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Chanapai, Seni. "Photocontrol of artificial transcription factors." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58014/.

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The design of a photoswitchable homeodomain artificial transcription factor (PATF), modelled on an engrailed homeodomain, for the purpose of controlling DNA binding affinity and controlling the transcription process in cells using light has been investigated. This study was conducted using a 3,3’-bis(sulfo)- 4,4’bis(chloroacetamino)azobenzene crosslinker, alkylated between two cysteine residues with different spacings (i, i+4, i, i+7 and i, i+11) and either a rigid or flexible linker domain. In previous studies, basic leucine zipper transcription activators have been photocontrolled in living cells by incorporating a photoswitchable azobenzene crosslinker. Circular dichroism spectroscopy showed the conformation of crosslinked PATF (XLPATF) peptides (i, i+11 spacing) containing rigid and flexible linkers could be controlled reversibly by light. Fluorescence anisotropy experiments using labelled DNA confirmed the in vitro DNA binding affinity of PATF was considerably higher with the crosslinker in the trans (ground state) configuration than in the cis (photoexcited state) configuration. Further studies of peptides with i, i+4 and i, i+7 spacings with a semirigid and rigid linker domains showed increased binding affinity with the crosslinker in the cis configuration. Initiation of transcription was investigated by an in vitro transcription assay to measure the ability of PATF molecules to moderate the production of RNA by irradiation with UV light. PATF molecules with i, i+11 spacings showed increased transcriptional activation with the crosslinker in the ground state configuration and i, i+4 and i, i+7 spacings resulted in increased transcription activation with the crosslinker in the excited state conformation. Control of 50% of transcriptional activity was achieved for i, i+11 v spacings, and PATFs with a rigid linker domain were more effective switches than those with flexible linkers. Using i, i+4 and i, i+7 spacings in PATFs resulted in a lower degree of control but, as anticipated, transcriptional activation was increased after irradiation.
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Pinacho, Garcia Raquel. "SP Transcription factors in psychotic disorders." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/327025.

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Psychotic disorders including bipolar disorder and schizophrenia are a leading cause of disability across the world but the underlying pathophysiological mechanisms remain poorly understood. Available treatments are inadequate for some sets of symptoms as is the case for negative symptoms in schizophrenia. Alterations in brain connectivity, synaptic plasticity, N-methyl D aspartate receptor (NMDAR) signalling and calcium homeostasis have been suggested to contribute to these disorders. However, the particular transcriptional programmes altered in these disorders are not fully characterised. Previous data suggested that the transcription factors specificity protein 4 (SP4) and SP1 may be involved in the pathophysiology of psychotic disorders. We hypothesized that the expression and/or function of SP4 and SP1 may be altered in psychotic disorders through the regulation of transcriptional programmes involved in neuronal patterning, synaptic plasticity and glutamate signalling. In this doctoral Thesis we aimed to characterise the contribution of SP4 and SP1 transcription factors to the pathophysiology of psychotic disorders. By using real time quantitative RT-PCR and/or immunoblot techniques, we analysed the expression of SP factors, of SP4 S770 phosphorylation and/or of selected SP-regulated gene targets in at least one of the following substrates: (i) rat cerebellar granule neurons (CGNs), (ii) the postmortem brains of bipolar disorder, schizophrenia and control subjects, (iii) peripheral mononuclear blood cells (PMBC) of first-episode psychosis, and (iv) the rodent hippocampus after NMDAR blockade and antipsychotic treatment. We found that membrane depolarisation regulates SP4 protein levels in CGNs by preventing SP4 degradation via the ubiquitin-proteasoma pathway and that lithium prevents SP4 degradation and increases SP1 gene expression in non-depolarising conditions. In postmortem human tissue, we found a reduction in protein but not mRNA expression of SP4 and SP1 in the cerebellum in subjects with bipolar disorder and in subjects with more severe negative symptoms in schizophrenia. We have also found reduced expression of protein and mRNA levels of SP4 in the prefrontal cortex in bipolar disorder and of SP1 in the same region in schizophrenia, suggesting a disorder-specific regulation in this area. In contrast, both SP4 and SP1 protein and mRNA levels were increased in the hippocampus in schizophrenia. Consistent with this, we also observed an increase of SP1 and SP4 protein levels in the hippocampus of a mouse model of psychosis, but not in the hippocampus of a rat model of chronic antipsychotic treatment, suggesting that this upregulation may be present from the early stages of psychosis. We further characterised the phosphorylation of SP4 at serine 770 (S770), which is regulated by membrane depolarisation and NMDAR activity. We found an increase of SP4 S770 phosphorylation in conditions where SP4 protein levels are reduced, namely in the cerebellum of bipolar disorder and of schizophrenia patients with more severe negative symptoms, as well as in PMBC in first-episode psychotic patients. These results suggest that an imbalance in SP4 abundance may be regulated by NMDAR-dependent SP4 phosphorylation in the brain. Moreover, we found that reduced expression of NR2A and DRD2 in the cerebellum of schizophrenia patients correlated with more severe negative symptoms and SP protein levels. Additionally, we show here evidence for an imbalance in the SP4-NWK2-NR1 pathway in the cerebellum of patients with bipolar disorder. This pathway is involved in NR1 subunit availability on the cell surface, suggesting that SP4 could contribute to altered NR1 receptor trafficking in psychotic disorders. Together, the results presented in this Thesis suggest an imbalance in SP4 and SP1 transcription factors in the brains of patients with bipolar disorder and schizophrenia that may contribute to alterations in NMDAR receptor signalling and thereby to the impaired synaptic plasticity and altered brain connectivity observed in psychotic disorders.
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Müller, Susanne. "Transcription factors regulating the Btk promoter /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2717-0.

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Paik, Elizabeth Jae-Eun. "Caudal Transcription Factors in Hematopoietic Development." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10254.

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During embryogenesis, hematopoietic cells arise from the lateral plate mesoderm (LPM) following gastrulation. The transcriptional program required for this LPM to blood switch is not fully understood. Previous work on a zebrafish mutant with a deletion in the cdx4 gene demonstrated the importance of this caudal transcription factor in the LPM to blood transition. To explain how cdx4 regulates embryonic hematopoiesis, two main approaches were taken in this thesis. The first part of the thesis describes a chemical genetics screen that identified cdx4 interacting pathways. To find small molecules that could rescue the loss of red blood cells caused by the cdx4 deletion, cdx4 mutant embryos were incubated with 2640 compounds from the beginning of the gastrula stage to the 10-somite stage. Two related psoralen compounds, Bergapten (Ber) and 8-methoxypsoralen (8-MOP), rescued the erythroid progenitors in the cdx4 mutants. This rescue is closely linked to the compounds' effects on anteriorposterior patterning, reminiscent of retinoic acid pathway compounds. The second part of my thesis identifies a Cdx4-Sall4 transcriptional module in the LPM. Chromatin-immunoprecipitation coupled to sequencing (ChIP-seq) and microarray analysis revealed that Cdx4 directly regulates cdx4 and a zinc finger transcription factor spalt-like 4 (sall4) transcription. Sall4 ChIP-seq showed that Sall4 also binds to its own locus and to the cdx4 locus, suggesting an auto- and cross-regulation between two transcription factors. In addition, Cdx4 and Sall4 bind to common genomic regions proximal to mesodermal progenitor (tbx16 and mespa) and hematopoietic genes (scl, gata2a, and ldb1a), indicating Cdx4 and Sall4 co-regulate key genes that are required for LPM and blood specification. sall4 knockdown in the cdx4 mutants demonstrated that Sall4 synergizes with Cdx4 in regulating embryonic hematopoiesis. These findings suggest that auto- and cross-regulation of Cdx4 and Sall4 establish a stable circuit in the LPM that facilitates the activation of blood-specific program as development proceeds. How undifferentiated germ layers transition into various tissues is a key question in developmental biology. My thesis establishes a model based on LPM to blood transition, which is also applicable to other studies on germ layer specification.
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Books on the topic "Alterations of transcription factors"

1

Ravid, Katya, and Jonathan D. Licht, eds. Transcription Factors. New York, USA: John Wiley & Sons, Inc., 2000. http://dx.doi.org/10.1002/0471223883.

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Gossen, Manfred, Jörg Kaufmann, and Steven J. Triezenberg, eds. Transcription Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6.

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Higgins, Paul J., ed. Transcription Factors. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-738-9.

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1947-, Locker Joseph, ed. Transcription factors. Oxford: BIOS, 2001.

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Yamaguchi, Nobutoshi, ed. Plant Transcription Factors. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8657-6.

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Link, Wolfgang, ed. FOXO Transcription Factors. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8900-3.

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Yuan, Ling, and Sharyn E. Perry, eds. Plant Transcription Factors. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-154-3.

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Maiese, Kenneth, ed. Forkhead Transcription Factors. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1599-3.

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Latchman, David S. Eukaryotic transcription factors. 5th ed. Amsterdam: Elsevier/Academic Press, 2008.

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Eukaryotic transcription factors. 4th ed. Oxford: Academic, 2004.

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Book chapters on the topic "Alterations of transcription factors"

1

Carlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 57–73. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7741-4_4.

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Arampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso, et al. "Transcription Factors." In Encyclopedia of Exercise Medicine in Health and Disease, 867. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3139.

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Gooch, Jan W. "Transcription Factors." In Encyclopedic Dictionary of Polymers, 929. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14992.

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Carlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 55–70. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7905-1_4.

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Herrera, F. J., D. D. Shooltz, and S. J. Triezenberg. "Mechanisms of Transcriptional Activation in Eukaryotes." In Transcription Factors, 3–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_1.

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Sheen, J. H., and R. B. Dickson. "c-Myc in Cellular Transformation and Cancer." In Transcription Factors, 309–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_10.

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Lasar, A., R. Marienfeld, T. Wirth, and B. Baumann. "NF-κB: Critical Regulator of Inflammation and the Immune Response." In Transcription Factors, 325–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_11.

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Kumar, V., and D. P. Sarkar. "Hepatitis B Virus X Protein: Structure-Function Relationships and Role in Viral Pathogenesis." In Transcription Factors, 377–407. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_12.

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Pascussi, J. M., Z. Dvorák, S. Gerbal-Chaloin, E. Assenat, L. Drocourt, P. Maurel, and M. J. Vilarem. "Regulation of Xenobiotic Detoxification by PXR, CAR, GR, VDR and SHP Receptors: Consequences in Physiology." In Transcription Factors, 409–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_13.

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Morishita, R., N. Tomita, Y. Kaneda, and T. Ogihara. "Potential of Transcription Factor Decoy Oligonucleotides as Therapeutic Approach." In Transcription Factors, 439–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_14.

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Conference papers on the topic "Alterations of transcription factors"

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Zhang, Ji, and Morton H. Friedman. "The Adaptive Response of Endothelial Transcription to Increased Shear Stress In Vitro." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19318.

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Previous studies have shown a substantial effect of shear stress on endothelial phenotype and functions such as production of nitric oxide, secretion of growth factors, inflammatory responses, production of reactive oxygen species, permeability to macromolecules and cytoskeletal remodeling [1–3]. However, the dynamics of the endothelial adaptive response to changes in shear stress are largely unknown. The response of vascular endothelial cells to alterations in shear stress is an essential component of normal endothelial physiology, since local shear stress can be altered in vivo by the global hemodynamic changes that are caused by daily activities such as exercise, sleep, smoking and stress. The duration of these changes ranges from minutes to hours. When adapting to the altered shear stress, endothelial cells undergo a series of structural remodeling and morphological changes, and a transient alteration of endothelial phenotype will be induced. An understanding of the transient regulation of endothelial phenotype will not only improve our knowledge of normal endothelial physiology but also yield insights into mechanisms underlying atherogenesis.
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Collins, Corolyn J., Richard B. Levene, Christina P. Ravera, Marker J. Dombalagian, David M. Livingston, and Dennis C. Lynch. "MOLECULAR CLONING OF THE HUMAN GENE FOR VON WILLEBRAND FACTOR AND IDENTIFICATION OF THE TRANSCRIPTION INITIATION SITE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642830.

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Most patients with von Willebrand's disease appear to have a defect affecting the level of expression of the von Willebrand factor (vWf) gene. Thus, an understanding of the pathogenesis of von Willebrand's disease will require an analysis of the structure and function of the vWf gene in normals and in patients. To begin such analyses, we have screened a human genomic cosmid library with probes obtained from vWf cDNA and isolated a colinear segment spanning ≈175 kb in five overlapping clones. This segment extends ≈25 kb upstream and ≈5 kb downstream of the transcription start and stop sites for vWf mRNA, implying the vWf gene has a length of ≈150 kb. Within one of these clones, the vWf transcription initiation sites have been mapped. A portion of the promoter region has been sequenced, revealing a typical TATA box, a downstream CCAAT box, and a perfect downstream repeat of the 8 base pairs containing the major transcription start site. Primer extension analysis suggests that sequences contained within the downstream repeat of the transcription start site may be used as minor initiation sites in endothelial cells. Transfection studies are underway to evaluate the role of sequences within this promoter region in gene regulatory activity. Comparative restriction analyses of cloned and chromosomal DNA segments strongly suggests that no major alterations ocurred during cloning and that there is only one complete copy of the vWf gene in the human haploid genome. Similar analyses of DNA from vWf-expressing endothelial cells and non-expressing white blood cells suggests that no major rearrangements are associated with vWf gene expression. Finally, cross hybridization patterns among seven mammalian species suggests a strong conservation of genomic sequences encoding the plasma portion of vWf, but a lower degree of conservation of sequences encoding the N terminal region of provWf.
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Abdel-Sayed, Philippe, Arne Vogel, and Dominique P. Pioletti. "Dissipation Can Act as a Mechanobiological Signal in Cartilage Differentiation." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-62268.

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Knee cartilage is a soft tissue having viscoelastic properties. Under cyclic loadings, viscoelastic materials dissipate mechanical loadings through heat generation. In knee cartilage, this heat might not be convected because of the tissue avascularity, resulting thus to a local temperature increase. As cells are sensitive to temperature, these thermo-mechanical phenomena of energy dissipation could influence their metabolism. The goal of this study is to evaluate the effect of thermogenesis on chondrogenic differentiation. First, we focused our work in quantifying the heat generated in cartilage as a result to deformation. On a cellular level, the effect of thermal alterations on cell metabolism was assessed looking at the gene expression of transcription factors involved in chondrogenesis. Hence, human chondro-progenitor cells were cultured at 33°C and 37°C for 48 h and 96 h. An up-regulation in mRNA expression levels of Sox9 and its co-activator PGC-1α has been observed. These results point to a thermal contribution to chondrogenic gene expression.
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Gaykalova, Daria A., Chad A. Glazer, Rajita Vatapalli, Sheetal Bhan, Chunbo Shao, Patrick K. Ha, and Joseph A. Califano. "Abstract 2042: Cancer-specific transcription factor BORIS has different effects on expression of its target genes via chromatin structure alterations." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2042.

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Hussain, Showket, Neha Singh, Irfana Salam, Mohammad A. Bhat, Nandita Kakkar, Mohammad M. Mir, Mushtaq A. Siddiqi, et al. "Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2722.

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Ponomarenko, J., T. Merkulova, G. Orlova, E. Gorshkova, O. Fokin, and M. Ponomarenko. "Mining genome variation to associate disease with transcription factor binding site alteration." In Proceedings 2nd Annual IEEE International Symposium on Bioinformatics and Bioengineering (BIBE 2001). IEEE, 2001. http://dx.doi.org/10.1109/bibe.2001.974424.

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"Neuronal transcription factors in lifespan control." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-405.

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Ismail, Ayman M., and Hussam B. Khalail. "Urban design factors associated with coastal alterations." In 2010 International Conference on Environmental Engineering and Applications (ICEEA). IEEE, 2010. http://dx.doi.org/10.1109/iceea.2010.5596087.

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Tsai, Zing Tsung-Yeh, Grace Tzu-Wei Huang, and Huai-Kuang Tsai. "Simultaneous Identification for Synergistic Transcription Factors and their Transcription Factor Binding Sites." In 2011 International Conference on Complex, Intelligent and Software Intensive Systems (CISIS). IEEE, 2011. http://dx.doi.org/10.1109/cisis.2011.90.

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Verdine, Gregory L. "Abstract IA1-2: Drugging oncogenic transcription factors." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-ia1-2.

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Reports on the topic "Alterations of transcription factors"

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Arazi, Tzahi, Vivian Irish, and Asaph Aharoni. Micro RNA Targeted Transcription Factors for Fruit Quality Improvement. United States Department of Agriculture, July 2008. http://dx.doi.org/10.32747/2008.7592651.bard.

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Fruits are unique to flowering plants and represent an important component of human and animal diets. Development and maturation of tomato fruit is a well-programmed process, and yet, only a limited number of factors involved in its regulation have been characterized. Micro-RNAs (miRNAs) are small, endogenous RNAs that regulate gene expression in animals and plants. Plant miRNAs have a vital role in the generation of plant forms through post-transcriptional regulation of the accumulation of developmental regulators, especially transcription factors. Recently, we and others have demonstrated that miRNAs and other type of small RNAs are expressed in tomato fruit, and target putative transcription factors during its development and maturation. The original objectives of the approved proposal were: 1. To identify fruit miRNA transcription factor target genes through a bioinformatic approach. 2. To identify fruit miRNA transcription factor target genes up-regulated in tomato Dicer-like 1 silenced fruit. 3. To establish the biological functions of selected transcription factors and examine their utility for improving fleshy fruit quality trait. This project was approved by BARD as a feasibility study to allow initial experiments to peruse objective 2 as described above in order to provide initial evidence that miRNAs do play a role in fruit development. The approach planned to achieve objective 2, namely to identify miRNA transcription factor targets was to clone and silence the expression of a tomato DCL1 homolog in different stages of fruit development and examine alterations to gene expression in such a fruit in order to identify pathways and target genes that are regulated by miRNA via DCL1. In parallel, we characterized two transcription factors that are regulated by miRNAs in the fruit. We report here on the cloning of tomato DCL1 homolog, characterization of its expression in fruit flesh and peel of wild type and ripening mutants and generation of transgenic plants that silence SlDCL1 specifically in the fruit. Our results suggest that the tomato homolog of DCL1, which is the major plant enzyme involved in miRNA biogenesis, is present in fruit flesh and peel and differentially expressed during various stages of fruit development. In addition, its expression is altered in ripening mutants. We also report on the cloning and expression analysis of Sl_SBP and Sl_ARF transcription factors, which serve as targets of miR157 and miR160, respectively. Our data suggest that Sl_SBP levels are highest during fruit ripening supporting a role for this gene in that process. On the other hand Sl_ARF is strongly expressed in green fruit up to breaker indicating a role for that gene at preripening stage which is consistent with preliminary in_situ analyses that suggest expression in ovules of immature green fruit. The results of this feasibility study together with our previous results that miRNAs are expressed in the fruit indeed provide initial evidence that these regulators and their targets play roles in fruit development and ripening. These genes are expected to provide novel means for genetic improvement of tomato fleshy fruit.
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Michelotti, Julia M. Identification of Mammary Specific Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada303179.

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Sederoff, Ronald, Ross Whetten, David O'Malley, and Malcolm Campbell. Transcription Factors in Xylem Development. Final report. Office of Scientific and Technical Information (OSTI), July 1999. http://dx.doi.org/10.2172/760586.

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Iyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436905.

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Iyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada485280.

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Lyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada455791.

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Lyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470576.

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Grotewold, Erich. Engineering phenolics metabolism in the grasses using transcription factors. Office of Scientific and Technical Information (OSTI), July 2013. http://dx.doi.org/10.2172/1088660.

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Schaber, John D. Expression and Activation of STAT Transcription Factors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 1998. http://dx.doi.org/10.21236/ad1012061.

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Charles J. Daniels. The Role of Multiple Transcription Factors In Archaeal Gene Expression. Office of Scientific and Technical Information (OSTI), September 2008. http://dx.doi.org/10.2172/937513.

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