Relevant bibliographies by topics / Gene expression in C

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Gene expression in C'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Gene expression in C"

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Sathishkumar, Dr Balamurugan, Dr Akpojaro Jackson, and Ramalingam Dr. M. "Gene Expression Using Artificial Bee Colony besides Fuzzy C Means and NFDA." International Journal of Psychosocial Rehabilitation 24, no. 03 (February 19, 2020): 2028–36. http://dx.doi.org/10.37200/ijpr/v24i3/pr200949.

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Ding, Hao, Xiaoli Wu, and Andras Nagy. "Mice with Cre recombinase activatable PDGF-C expression." genesis 32, no. 2 (February 2002): 181–83. http://dx.doi.org/10.1002/gene.10065.

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SKRZYPCZAK, MACIEJ, JULITA ZIELEWICZ, STANISŁAW WINIARCZYK, JACEK WOJCIEROWSKI, ANNA KWAŚNIEWSKA, and JERZY JAKOWICKI. "Expression of c-MYC gene in neoplastic endometrium." PRZEGLĄD GINEKOLOGICZNO-POŁOŻNICZY 5, no. 1-1 (February 23, 2005): 15–20. http://dx.doi.org/10.1066/s10014040059.

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Ventura, Carlo, and Margherita Maioli. "Protein Kinase C Control of Gene Expression." Critical Reviews™ in Eukaryotic Gene Expression 11, no. 1-3 (2001): 26. http://dx.doi.org/10.1615/critreveukargeneexpr.v11.i1-3.120.

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Asselah, T., I. Bieche, A. Sabbagh, P. Bedossa, R. Moreau, D. Valla, M. Vidaud, and P. Marcellin. "Gene expression and hepatitis C virus infection." Gut 58, no. 6 (December 11, 2008): 846–58. http://dx.doi.org/10.1136/gut.2008.166348.

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Feng, Dingxia, Jenifer Saldanha, Qi Ye, and Jo Anne Powell-Coffman. "Oxygen-sensitive gene expression in C. elegans." Developmental Biology 356, no. 1 (August 2011): 257–58. http://dx.doi.org/10.1016/j.ydbio.2011.05.488.

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Xie, Yue, Changmin Chen, and David A. Hume. "Transcriptional Regulation of c-fms Gene Expression." Cell Biochemistry and Biophysics 34, no. 1 (2001): 001–16. http://dx.doi.org/10.1385/cbb:34:1:001.

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Zahn, Laura M. "Gene expression can point to disease risk." Science 364, no. 6445 (June 13, 2019): 1044.3–1045. http://dx.doi.org/10.1126/science.364.6445.1044-c.

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Evans, J. L., T. L. Moore, W. M. Kuehl, T. Bender, and J. P. Ting. "Functional analysis of c-Myb protein in T-lymphocytic cell lines shows that it trans-activates the c-myc promoter." Molecular and Cellular Biology 10, no. 11 (November 1990): 5747–52. http://dx.doi.org/10.1128/mcb.10.11.5747.

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The function of c-Myb protein was revealed by transfecting an expression vector containing the entire c-Myb protein-coding sequence into the murine CTLL-2 T-cell line. Expressions of high levels of c-Myb protein did not alter the expression of several T-cell markers, c-fos mRNA expression, responses to interleukin-2, and growth characteristics of these cells. Interestingly, expression of the c-myc gene was drastically increased in this clone. Further, the c-myb expression plasmid, but not a frameshift mutant of c-myb, enhanced the expression of a hybrid construct of c-myc promoter linked to a reporter gene by 8- to 14-fold. These results demonstrate a role of c-Myb protein in c-myc gene expression.
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Evans, J. L., T. L. Moore, W. M. Kuehl, T. Bender, and J. P. Ting. "Functional analysis of c-Myb protein in T-lymphocytic cell lines shows that it trans-activates the c-myc promoter." Molecular and Cellular Biology 10, no. 11 (November 1990): 5747–52. http://dx.doi.org/10.1128/mcb.10.11.5747-5752.1990.

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The function of c-Myb protein was revealed by transfecting an expression vector containing the entire c-Myb protein-coding sequence into the murine CTLL-2 T-cell line. Expressions of high levels of c-Myb protein did not alter the expression of several T-cell markers, c-fos mRNA expression, responses to interleukin-2, and growth characteristics of these cells. Interestingly, expression of the c-myc gene was drastically increased in this clone. Further, the c-myb expression plasmid, but not a frameshift mutant of c-myb, enhanced the expression of a hybrid construct of c-myc promoter linked to a reporter gene by 8- to 14-fold. These results demonstrate a role of c-Myb protein in c-myc gene expression.
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Dissertations / Theses on the topic "Gene expression in C"

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Sasmono, R. Tedjo. "Transcriptional regulation of c-fms gene expression /." [St. Lucia, Qld.], 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17479.pdf.

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John, Christopher Robert. "Gene expression associated with the evolution of C₄ photosynthesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709401.

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David, John M. "The control of apolipoprotein C-I gene expression during adipocyte differentiation." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 4.92 Mb., p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:1435920.

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Thirumalai, Avinash N. "Regulation of C-reactive Protein Gene Expression and Function." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etd/2467.

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Human C-reactive protein (CRP) is the prototypic acute phase protein whose serum concentration increases rapidly during inflammation. CRP is also associated with atherosclerosis; it is deposited at lesion sites where it may interact with modified lipoproteins. There are 2 major questions regarding CRP: 1. How is the serum concentration of CRP regulated? 2. What are the functions of CRP in atherosclerosis? Our first aim was to determine the role of the constitutively expressed transcription factor Oct-1 in regulating CRP gene expression. We found that Oct-1 overexpression inhibited (IL-6+IL-1β)- induced CRP gene expression; maximal inhibition required the binding of Oct-1 to an octamer motif at (-59 to -66) on the CRP promoter. Oct-1 overexpression inhibited both (IL-6+IL-1β)- induced and C/EBPβ-induced CRP gene expression even when the Oct-1 site was deleted. These findings suggest that Oct-1 is a repressor of CRP gene expression that acts via binding to its cognate site on the CRP promoter as well as through indirect interactions with other promoterbound transcription factors. Our second aim was to investigate the interaction of CRP with oxidized low density lipoprotein (ox-LDL). Acidic pH, a hallmark of atherosclerotic lesions, reversibly alters CRP structure and exposes a hidden binding site that enables CRP to bind ox-LDL. Using site-directed mutagenesis we constructed a CRP mutant (E42Q) that showed significant binding to ox-LDL at physiological pH. E42Q CRP required a less acidic pH for maximal binding and bound ox-LDL more efficiently than wild type CRP at any pH. We then examined if reactive oxygen species also induced CRP – ox-LDL interaction. H2O2-treated CRP bound ox-LDL at physiological pH. Like acidic pH, H2O2-treatment induced only a local structural change exposing the ox-LDL binding site. E42Q and H2O2-modified CRP are tools to study the function of CRP in animal models of atherosclerosis, which may not have an inflammatory environment sufficient to modify CRP and induce binding to atherogenic ox-LDL. We conclude that Oct-1 is one of the critical regulators of CRP gene expression, and that CRP can be modified in vitro to convert it into an atherogenic LDL-binding molecule.
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Paradis, François William François William. "The expression of cellulomomas fimi cellulase genes in Brevibacterium lactofermentum and characterization of recombinant C. fimi B-glucosidase A from E coli." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30586.

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In the first part of this thesis, I describe the expression of C. fimi cellulase genes in the closely related Brevibacterium lactofermentum by generating a shuttle vector able to replicate selectively in the latter and carrying full length cellulase-encoding genes. The expression of those genes apparently originated from some unpredicted regulatory sequences, possibly located within the vector itself. The enzymatic activity was mostly found in the culture medium in B. lactofermentum indicating that the organism secreted the enzymes. The putative C. fimi promoter sequences did not function in B. lactofermentum, making difficult the analysis of their roles in expression of C. fimi cellulase genes. In the second part of this thesis, I describe the characterization of a recombinant C. fimi exo-ϐ-1,4-glucosidase (CbgA) expressed in E. coli. The purified enzyme had a Mr of 183 kDa and hydrolysed various ϐ-glucosides with a preference for cello-oligosaccharides in the order C5>C4>C3>C2. The intact CbgA polypeptide was not required for enzymatic activity since removal of about 700 residues from the amino terminus did not reduce activity. The purified enzyme was used to raise polyclonal antibodies which in turn were used to identify the corresponding enzyme in C. fimi. During the fractionation of C. fimi ϐ-glucosidases, several enzymes hydrolyzing various ϐ-glucosides were isolated together with the native CbgA, which was present in the culture medium as part of a protein aggregate. Part of the nucleotide sequence of the 7.2 kb insert was determined. Alignments of the N-terminal amino acid sequences of the purified CbgA and truncated polypeptides with the partial nucleotide sequence of the cloned C. fimi DNA showed that precise excision was responsible for the appearance of a truncated form of CbgA. Alignment of the amino-terminal sequence of a CbgA:CexCBD fusion peptide indicated that the pre-mature CbgA starts with a putative leader sequence of 49 amino acids which is followed by a region rich in Pro and Ala residues. Two GTG translational initiation codons followed by sequences resemblingprokaryotic ribosome binding sites and separated by a large open reading frame were identified from data obtained after in vitro site-directed mutagenesis of the most upstream initiation codon suggesting that internal re-initiation may occur and that upstream regulatory sequences had not been isolated.
Medicine, Faculty of
Medical Genetics, Department of
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Ball, Sarah Elizabeth. "A study of c-fms in myeloid leukaemias." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252976.

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Xue, Lin. "A VISUALIZATION TOOL FOR CROSS-EXPERIMENT GENE EXPRESSION ANALYSIS OF C. ELEGANS." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_theses/472.

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Forty-six genomic gene expression studies of free living soil nematode C. eleganshave been published. To facilitate exploratory analysis of those studies, we constructed adatabase containing all the published C. elegans expression datasets. A Perl CGIprogram, called Microarray Analysis Display (MAdisplay), allows gene expressionclustergrams of any combination of entered genes and datasets to be viewed(http://elegans.uky.edu/gl/madisplay). Perl programs were used to preprocess the rawdata from different sources into a common format and to transform the data to displaythe expression changes relative to each experiment's controls. Three hundred lists ofgenes from figures and tables were extracted from the publications and made available inthe GeneLists database, which also contains Gene Ontology and KEGG gene lists. Weused these tools to examine in a systematic fashion the mean expression of gene lists inthe set of microarray and SAGE experiments. Seventy-nine percent of publicationderived gene lists show a strong expression change (p-value andlt;0.001) in more than oneexperiment with the median being fourteen out of the 127 experiments that are derivedfrom the forty-six publications. This indicates that groups of genes identified in onepublication typically show an expression effect in many other experiments.
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Voleti, Bhavya. "Mechanism of Transcriptional Regulation of C-Reactive Protein Gene Expression." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2058.

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C-reactive protein (CRP) is an acute phase protein produced by hepatocytes whose serum concentration increases in inflammatory conditions including cardiovascular complications. Statins that are used in the treatment of cardiovascular diseases to reduce cholesterol also lower serum CRP levels. In human hepatoma Hep3B cells, CRP is induced in response to cytokines IL-6 and IL-1β. The objective of the study was to determine the mechanism of regulation of CRP gene expression in Hep3B cells in response to cytokines and to determine the effect of statins on CRP expression. Key findings of our research were: 1. IL-1β-activated NF-κB p50/p65 acted synergistically with IL-6-activated C/EBPβ in inducing CRP transactivation through the proximal CRP promoter. 2. A NF-κB site was localized in the proximal CRP promoter centered at position -69 overlapping the known OCT-1/HNF-1/HNF-3 sites. 3. The synergy between IL-6 and IL-1β in inducing CRP gene expression was partially mediated through the NF-κB site. 4. In the absence of C/EBPβ, a complex containing C/EBPζ and RBP-Jκ was formed at the C/EBP-p50-site. 5. Overexpressed C/EBPζ repressed both (IL-6+IL-1β)-induced and C/EBPβ-induced CRP expression. 6. OCT-1 repressed (IL-6+IL-1β)-induced CRP transactivation through the proximal CRP promoter. 7. Statins reduce cytokine-induced CRP gene expression at the transcriptional level. These findings led us to conclude that: 1. CRP transcription is determined by the relative levels of various transcription factors such as C/EBPβ, C/EBPζ, NF-κB and OCT-1 and their interaction with the proximal CRP promoter. 2. Inhibition of CRP transcription by statins is not due to an anti-inflammatory effect but due to the direct effect on CRP gene expression.
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Hachicha, Mohamed. "Regulation of C-C and C-X-C chemokine gene expression in synovial fibroblasts and peripheral blood neutrophils." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ25241.pdf.

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Dörr, Katrin Zaragoza. "Molecular mechanisms of gene activation and gene expression mediated by CCAAT/enhancer binding proteins." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15873.

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Der Transkriptionsfaktor CCAAT/Enhancer-Binding Protein alpha (C/EBPa) koordiniert Proliferationshemmung und Differenzierung von myeloiden VorlŠuferzellen und Adipozyten. C/EBPa ist ein transkriptioneller Aktivator von abstammungspezifischen Genen und blockiert den Zellzyklus durch Repression von proliferationsfšrdernden E2F Zielgenen. Die hier gezeigten Daten zeigen, dass auch umgekehrt E2F die transkriptionelle und differenzierungsfšrdernde AktivitŠt von C/EBPa entgegenwirkt. Somit besitzen E2F-C/EBPa eine zentrale Schalterfunktion zwischen Proliferation und Differenzierung. Der Repressionsmechanismus durch E2F ist in mehreren Aspekten neuartig: Zum erstenmal wurde gezeigt, dass E2F einen anderen Transkriptionsfaktor reprimieren kann. E2F reprimiert die transkriptionelle AktivitŠt von C/EBPa ohne Bindung an cis-regulatorischen Elemente, sondern durch direkte Protein-Protein Interaktionen, die die Bindung von C/EBPa an DNA verhindern. Diese Form der transkriptionellen Repression geschieht unabhŠngig von "Pocket-Proteinen''". Patienten mit Akuter Myeloiden LeukŠmie (AML) weisen hŠufig eine gestšrte DNA Bindung von C/EBPa auf, welche ursachlich fŸr granulozitŠren Funktionsstšrungen sein kšnnte. Daher wŠre es wichtig zu analysieren ob E2F die DNA Bindung von C/EBPa in AML Patienten beeintrŠchtigt und ob auf E2F gerichtete Therapien granulozitŠre Reifung wiederherstellen. C/EBPa blockiert Zellproliferation durch vielseitigen Mechanismen. Hier wurde gezeigt, dass C/EBPa mit UBF1, dem Co-Aktivator der RNA Polymerase I, an chromosomalen Foci positioniert wird. Eine €hnlichkeit zu anderen fokalen Strukturen suggeriert, dass C/EBPa die Transkription von Polymerase I regulierten rRNA Gene reprimieren und somit ribosomale Biogenese beeintrŠchtigen kšnnte. Die Assoziation zwischen C/EBPa und UBF1 wird durch die Histon-Methyltransferase SUV39H1 stimuliert. Demnach kšnnte die antiproliferative Funktion von C/EBPa nicht nur auf der Regulierung von RNA Pol II-abhŠngiger Transkription, sondern auch auf der Repression von RNA Pol I regulierter rRNA Synthese basieren.
The transcription factor CCAAT/Enhancer-Binding Protein alpha (C/EBPa) coordinates proliferation arrest and differentiation of myeloid progenitors and adipocytes. C/EBPa acts as a transcriptional activator of lineage specific genes and blocks the cell cycle by repressing transcription of E2F-regulated genes. Data presented here suggest that also inversely E2F interferes with the transcriptional activity of C/EBPa, counteracting C/EBPa-mediated differentiation processes. Thus, E2F-C/EBPa are part of a switch mechanism between proliferation and differentiation. The mechanism by which E2F suppresses C/EBPa-mediated transactivation is novel in several aspects. E2F acts as a co-repressor of another transcription factor, C/EBPa, without binding to cis-regulatory elements, but by direct protein-protein interactions that abolish the binding of C/EBPa to DNA. This mechanism of transcriptional repression occurs independent of pocket proteins. Disturbed DNA binding of C/EBPa is often observed in AML patients suggesting a causative role in granulocytic disorders. Thus, it would be of main interest to analyze whether E2F mediates disruption of C/EBPa''s DNA-binding in AML patients and whether therapies directed against E2F could restore granulocytic maturation. Despite the extensive knowledge of mechanisms involved in the inhibitory function of C/EBPa, it has not been addressed whether C/EBPa may impinge on cell proliferation by affecting the ribosomal biogenesis of a cell. This work demonstrates an association of C/EBPa to the RNA Pol I transcription factor UBF1, both proteins retained in large chromosomal foci. Similarities to other focal structures associated to UBF1, suggest that C/EBPa may repress transcription of Pol I-transcribed rRNA genes, and thus affect ribosomal biogenesis. The enrichment of C/EBPa at sites of UBF1 is induced by the histone methyltransferase SUV39H1. Thus, C/EBPa may not only control lineage commitment and cell proliferation by regulating genes transcribed by RNA Pol II, but also may act as a repressor of RNA Pol I mediated rRNA synthesis.
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Books on the topic "Gene expression in C"

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Radzio, Renate. Heterologe Genexpression in dem Cephalosporin C produzierenden Hyphenpilz Acremonium chrysogenum. Berlin: J. Cramer, 1997.

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Krasnoshtein, Flora. Analysis of the pattern of expression of the fanconi anemia group C (Fac) gene during murine development. Ottawa: National Library of Canada, 1995.

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The nonlinear workbook: Chaos, fractals, cellular automata, genetic algorithms, gene expression programming, support vector machine, wavelets, hidden Markov models, fuzzy logic with C++, Java and symbolic C++ programs. 6th ed. Hackensack, New Jersey: World Scientific, 2015.

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Karin, Michael, ed. Gene Expression. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6811-3.

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The nonlinear workbook: Chaos, fractals, cellular automata, neural networks, genetic algorithms, gene expression programming, support vector machine, wavelets, hidden Markov models, Fuzzy logic with C++, Java and SymbolicC++ programs. 5th ed. New Jersey: World Scientific, 2011.

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The nonlinear workbook: Chaos, fractals, cellular automata, neural networks, genetic algorithms, gene expression programming, support vector machine, wavelets, hidden Markov models, Fuzzy logic with C++, Java and SymbolicC++ programs. 3rd ed. Hackensack, NJ: World Scientific, 2005.

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The nonlinear workbook: Chaos, fractals, cellular automata, neural networks, genetic algorithms, gene expression programming, support vector machine, wavelets, hidden Markov models, Fuzzy logic with C++, Java and SymbolicC++ programs. 5th ed. New Jersey: World Scientific, 2011.

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The nonlinear workbook: Chaos, fractals, cellular automata, neural networks, genetic algorithms, gene expression programming, support vector machine, wavelets, hidden Markov models, Fuzzy logic with C++, Java and SymbolicC++ programs. 4th ed. New Jersey: World Scientific, 2008.

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Measuring gene expression. New York: Taylor & Francis, 2007.

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Zhang, Jun, and Gregg Rokosh, eds. Cardiac Gene Expression. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-030-0.

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Book chapters on the topic "Gene expression in C"

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Lanctôt, Christian, and Peter Meister. "Microscopic Analysis of Chromatin Localization and Dynamics in C. elegans." In Imaging Gene Expression, 153–72. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-526-2_11.

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Cahill, Michael A., Ralf Janknecht, and Alfred Nordheim. "Signal uptake by the c-fos serum response element." In Inducible Gene Expression, Volume 2, 39–72. Boston, MA: Birkhäuser Boston, 1995. http://dx.doi.org/10.1007/978-1-4684-6837-3_2.

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Sotiroudis, Theodore G., Symeon M. Kyriakidis, Leonidas G. Baltas, Vasilis G. Zevgolis, and Athanasios E. Evangelopoulos. "Ca2+-Calmodulin-Dependent Protein Kinases and Protein Kinase C: Functional Similarities." In Evolutionary Tinkering in Gene Expression, 59–69. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5664-6_6.

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Cantrell, D. A., A. A. Davies, G. Krissansen, and M. J. Crumpton. "Interactions between protein kinase C and the T3/T cell antigen receptor complex." In Regulation of Immune Gene Expression, 119–33. Totowa, NJ: Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5014-2_11.

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Tripp, Vanessa, and Lennart Randau. "Evolution of C/D Box sRNAs." In RNA Metabolism and Gene Expression in Archaea, 201–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65795-0_9.

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Belasco, Joel G., Ann-Bin Shyu, and Michael E. Greenberg. "Rapid Degradation of the c-FOS Proto-Oncogene Transcript." In Post-Transcriptional Control of Gene Expression, 65–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75139-4_7.

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Duarte, T. L., and I. F. Almeida. "Vitamin C, gene expression and skin health." In Handbook of diet, nutrition and the skin, 114–27. Wageningen: Wageningen Academic Publishers, 2012. http://dx.doi.org/10.3920/978-90-8686-729-5_7.

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Sherman, Fred, Richard P. Moerschell, Susumu Tsunasawa, Rolf Sternglanz, and Mark E. Dumont. "Co- and Posttranslational Processes and Mitochondrial Import of Yeast Cytochrome c." In Translational Regulation of Gene Expression 2, 117–41. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2894-4_6.

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Sherman, Fred. "Protein Modifications and Mitochondrial Import of Yeast Cytochrome c: An Overview." In Post-Transcriptional Control of Gene Expression, 637–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75139-4_59.

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Rossi, P., C. Sette, A. Bevilacqua, F. Mangia, and R. Geremia. "Role of c-kit in Egg Activation." In Testicular Function: From Gene Expression to Genetic Manipulation, 253–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03671-6_13.

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Conference papers on the topic "Gene expression in C"

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Wang, Yu, and Maia Angelova. "Weighted Kernel Fuzzy C-Means Method for Gene Expression Analysis." In 2012 Spring Congress on Engineering and Technology (S-CET). IEEE, 2012. http://dx.doi.org/10.1109/scet.2012.6342018.

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Zhang, Mingrui, Beya Adamu, Chi-Cheng Lin, and Ping Yang. "Gene expression analysis with integrated fuzzy C-means and pathway analysis." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090211.

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Finigan, JH, A. Boueiz, R. Damico, HH Pae, DN Grigoryev, C. Cheadle, and PM Hassoun. "Gene Expression Changes Mediated by Activated Protein C in Ventilator Associated Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5551.

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Suzuki, Motoshi, Yasuhiro Kamei, Shunsuke Yuba, and Shin Takagi. "A technique enabling the controlled gene expression in targeted single cells of C. elegans." In 2006 IEEE International Symposium on MicroNanoMechanical and Human Science. IEEE, 2006. http://dx.doi.org/10.1109/mhs.2006.320244.

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Novianti, Titta, Febriana Wahyuni, It Jamilah, and Syafruddin Ilyas. "The Peak of Cytochrome-c (Cyt-c) Gene Expression in Inflammatory Stage after Amputation of Digit Tip Mice (Mus musculus)." In 1st International Conference on Health. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0009566300780082.

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Taber, Larry A., Dmitry A. Voronov, Mathieu C. Re´mond, Kimberly S. Latacha, and Patrick W. Alford. "Mechanical Forces Involved in Cardiac C-Looping." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59270.

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Cardiac looping is a vital morphogenetic process that transforms the initially straight heart tube into a curved tube normally directed toward the right side of the embryo. We examined the role of biomechanical forces during the initial stages of looping, when the heart bends and rotates into a c-shaped tube (c-looping). C-looping consists of two primary deformation components: ventral bending and dextral (rightward) rotation (torsion). Embryonic chick hearts were subjected to mechanical and chemical perturbations, and the experiments were simulated using a computational model. The results suggest that bending is driven primarily by actin polymerization within the heart tube, while rotation is driven by external loads due to the splanchnopleure and omphalomesenteric veins. The results of this study may help investigators searching for the link between gene expression and the mechanical processes that drive looping.
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"Mining Association Rules that Incorporate Transcription Factor Binding Sites and Gene Expression Patterns in C. elegans." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2013. http://dx.doi.org/10.5220/0004252300810089.

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Stur, Elaine, Shelia Thomas, Francine Rezzoug, and Donald Miller. "Abstract 1520: Down-regulation of c-MYC and hTERT gene expression in triple negative breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1520.

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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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Tao, Yongguang, Shuang Liu, and Yiqun Jiang. "Abstract 4317: EGLN1/c-Myc induced lymphoid-specific helicase inhibits ferroptosis through lipid metabolic gene expression changes." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4317.

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Reports on the topic "Gene expression in C"

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Melkoumian, Zaroui. Regulation of C-myc Gene Expression by Potassium Channel Blocker Quindine in MCF-7 Human Breast Cancer Cell Line. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384096.

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Horio, M., F. R. Collart, and E. Huberman. Heterogeneity in c-jun gene expression in normal and malignant cells exposed to either ionizing radiation or hydrogen peroxide. Office of Scientific and Technical Information (OSTI), January 1993. http://dx.doi.org/10.2172/10173201.

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Ye, Shanli. DNA Sequences Involved in the Regulation of Human c-myc Gene Expression by Herpes Simplex Virus Type 1 (HSV-1). Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7097.

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Hrushesy, William, Phillip Bulkhaults, and Shaojin You. Sage Gene Expression Profiles Characterizing Cure. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada462344.

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Geballe, Adam. Translational Regulation of HER2 Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/ada339298.

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Gerald, William L. Gene Expression Analysis of Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada437751.

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Wang, Xuefel, Huining Kang, Chris Fields, Jim R. Cowie, George S. Davidson, David Michael Haaland, Valeriy Sibirtsev, et al. Application of multidisciplinary analysis to gene expression. Office of Scientific and Technical Information (OSTI), January 2004. http://dx.doi.org/10.2172/918393.

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Peterson, Blake R. Anticar Inhibitors of AR-Mediated Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada446982.

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Synold, Timothy W. In Vivo Imaging of MDR1A Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada433034.

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Woloschak, G. E., T. Paunesku, C. M. Chang-Liu, L. Loberg, J. Gauger, and D. McCormick. Changes in gene expression following EMF exposure. Office of Scientific and Technical Information (OSTI), October 1997. http://dx.doi.org/10.2172/563249.

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