Relevant bibliographies by topics / Transgenic muscle

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Transgenic muscle'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Transgenic muscle"

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Donoviel, D. B., M. A. Shield, J. N. Buskin, H. S. Haugen, C. H. Clegg, and S. D. Hauschka. "Analysis of muscle creatine kinase gene regulatory elements in skeletal and cardiac muscles of transgenic mice." Molecular and Cellular Biology 16, no. 4 (1996): 1649–58. http://dx.doi.org/10.1128/mcb.16.4.1649.

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Regulatory regions of the mouse muscle creatine kinase (MCK) gene, previously discovered by analysis in cultured muscle cells, were analyzed in transgenic mice. The 206-bp MCK enhancer at nt-1256 was required for high-level expression of MCK-chloramphenicol acetyltransferase fusion genes in skeletal and cardiac muscle; however, unlike its behavior in cell culture, inclusion of the 1-kb region of DNA between the enhancer and the basal promoter produced a 100-fold increase in skeletal muscle activity. Analysis of enhancer control elements also indicated major differences between their properties
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Tsika, G. L., J. L. Wiedenman, L. Gao, et al. "Induction of beta-MHC transgene in overloaded skeletal muscle is not eliminated by mutation of conserved elements." American Journal of Physiology-Cell Physiology 271, no. 2 (1996): C690—C699. http://dx.doi.org/10.1152/ajpcell.1996.271.2.c690.

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Mechanical overload leads to hypertrophy, increased type I fiber composition, and beta-myosin heavy chain (beta-MHC) induction in the fast-twitch plantaris muscle. To better understand the mechanism(s) involved in beta-MHC induction, we have examined inducible expression of transgenes carrying the simultaneous mutation of three DNA regulatory subregions [muscle CAT (MCAT), C-rich, and beta e3] in the context of either 5,600-base pair (bp; beta 5.6mut3) or 600-bp (beta 0.6mut3) beta-MHC promoter in overloaded plantaris muscles of transgenic mice. Protein extract from mechanically overloaded pla
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Wiedenman, J. L., I. Rivera-Rivera, D. Vyas, et al. "Beta-MHC and SMLC1 transgene induction in overloaded skeletal muscle of transgenic mice." American Journal of Physiology-Cell Physiology 270, no. 4 (1996): C1111—C1121. http://dx.doi.org/10.1152/ajpcell.1996.270.4.c1111.

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The hypertrophic responses of white fast-twitch muscle to mechanical overload has been investigated using transgenic mice. After 7 wk of overload, endogenous beta-myosin heavy chain (MHC) and slow myosin light chain 1 and 2 (SMLC1, SMLC2) protein were increased in the overloaded plantaris (OP) muscle compared with sham-operated control plantaris (CP)muscle. Concurrently, the levels of endogenous beta-MHC, SMLC1, SMLC2, and cardiac/slow troponin C (CTnC) mRNA transcripts were significantly increased in OP muscles, whereas skeletal troponin C (sTnC) mRNA transcript levels decreased. As an initia
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Sigmund, C. D., C. A. Jones, H. J. Jacob, et al. "Pathophysiology of vascular smooth muscle in renin promoter-T-antigen transgenic mice." American Journal of Physiology-Renal Physiology 260, no. 2 (1991): F249—F257. http://dx.doi.org/10.1152/ajprenal.1991.260.2.f249.

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The pathophysiological consequence of targeted production of SV-40 T-antigen to renin-expressing cells in the kidney of transgenic mice is reported. A histopathologic analysis of the kidney from adult transgenic mice (12–16 wk old) revealed the presence of severe vascular lesions manifested by marked atypical hyperplasia of vascular smooth muscle. The levels of plasma renin, kidney renin, and kidney renin mRNA were examined in 6- and 9-wk-old transgenic mice and were found to be significantly lower than their age-matched non-transgenic littermates and were nonresponsive to captopril treatment.
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Cho, Jun, Wilson Kuswanto, Christophe Benoist, and Diane Mathis. "T cell receptor specificity drives accumulation of a reparative population of regulatory T cells within acutely injured skeletal muscle." Proceedings of the National Academy of Sciences 116, no. 52 (2019): 26727–33. http://dx.doi.org/10.1073/pnas.1914848116.

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Foxp3+CD4+regulatory T cells (Tregs) play important roles in controlling both homeostatic processes and immune responses at the tissue and organismal levels. For example, Tregs promote muscle regeneration in acute or chronic injury models by direct effects on local muscle progenitor cells, as well as on infiltrating inflammatory cells. Muscle Tregs have a transcriptome, a T cell receptor (TCR) repertoire, and effector capabilities distinct from those of classical, lymphoid-organ Tregs, but it has proven difficult to study the provenance and functions of these unique features due to the rarity
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NOSEK, THOMAS M., MARCO A. P. BROTTO, DAVID A. ESSIG, et al. "Functional properties of skeletal muscle from transgenic animals with upregulated heat shock protein 70." Physiological Genomics 4, no. 1 (2000): 25–33. http://dx.doi.org/10.1152/physiolgenomics.2000.4.1.25.

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The influence of inducible heat stress proteins on protecting contracting skeletal muscle against fatigue-induced injury was investigated. A line of transgenic mice overexpressing the inducible form of the 72-kDa heat shock protein (HSP72) in skeletal muscles was used. We examined the relationship between muscle contractility and levels of the constitutive (HSC73) and inducible (HSP72) forms of the 72-kDa heat shock protein in intact, mouse extensor digitorum longus (EDL), soleus (SOL), and the diaphragm (DPH). In all transgenic muscles, HSP72 was expressed at higher levels compared with trans
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Nalbantoglu, J., N. Larochelle, E. Wolf, G. Karpati, H. Lochmuller, and P. C. Holland. "Muscle-Specific Overexpression of the Adenovirus Primary Receptor CAR Overcomes Low Efficiency of Gene Transfer to Mature Skeletal Muscle." Journal of Virology 75, no. 9 (2001): 4276–82. http://dx.doi.org/10.1128/jvi.75.9.4276-4282.2001.

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ABSTRACT Significant levels of adenovirus (Ad)-mediated gene transfer occur only in immature muscle or in regenerating muscle, indicating that a developmentally regulated event plays a major role in limiting transgene expression in mature skeletal muscle. We have previously shown that in developing mouse muscle, expression of the primary Ad receptor CAR is severely downregulated during muscle maturation. To evaluate how global expression of CAR throughout muscle affects Ad vector (AdV)-mediated gene transfer into mature skeletal muscle, we produced transgenic mice that express the CAR cDNA und
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Kelly, R., S. Alonso, S. Tajbakhsh, G. Cossu, and M. Buckingham. "Myosin light chain 3F regulatory sequences confer regionalized cardiac and skeletal muscle expression in transgenic mice." Journal of Cell Biology 129, no. 2 (1995): 383–96. http://dx.doi.org/10.1083/jcb.129.2.383.

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The myosin light chain IF/3F locus contains two independent promoters, MLC1F and MLC3F, which are differentially activated during skeletal muscle development. Transcription at this locus is regulated by a 3' skeletal muscle enhancer element, which directs correct temporal and tissue-specific expression from the MLC1F promoter in transgenic mice. To investigate the role of this enhancer in regulation of the MLC3F promoter in vivo, we have analyzed reporter gene expression in transgenic mice containing lacZ under transcriptional control of the mouse MLC3F promoter and 3' enhancer element. Our re
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Azpiazu, Iñaki, Jill Manchester, Alexander V. Skurat, Peter J. Roach, and John C. Lawrence. "Control of glycogen synthesis is shared between glucose transport and glycogen synthase in skeletal muscle fibers." American Journal of Physiology-Endocrinology and Metabolism 278, no. 2 (2000): E234—E243. http://dx.doi.org/10.1152/ajpendo.2000.278.2.e234.

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The effects of transgenic overexpression of glycogen synthase in different types of fast-twitch muscle fibers were investigated in individual fibers from the anterior tibialis muscle. Glycogen synthase was severalfold higher in all transgenic fibers, although the extent of overexpression was twofold greater in type IIB fibers. Effects of the transgene on increasing glycogen and phosphorylase and on decreasing UDP-glucose were also more pronounced in type IIB fibers. However, in any grouping of fibers having equivalent malate dehydrogenase activity (an index of oxidative potential), glycogen wa
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Rao, M. V., M. J. Donoghue, J. P. Merlie, and J. R. Sanes. "Distinct regulatory elements control muscle-specific, fiber-type-selective, and axially graded expression of a myosin light-chain gene in transgenic mice." Molecular and Cellular Biology 16, no. 7 (1996): 3909–22. http://dx.doi.org/10.1128/mcb.16.7.3909.

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The fast alkali myosin light chain 1f/3f (MLC1f/3f) gene is developmentally regulated, muscle specific, and preferentially expressed in fast-twitch fibers. A transgene containing an MLC1f promoter plus a downstream enhancer replicates this pattern of expression in transgenic mice. Unexpectedly, this transgene is also expressed in a striking (approximately 100-fold) rostrocaudal gradient in axial muscles (reviewed by J. R. Sanes, M. J. Donoghue, M. C. Wallace, and J. P. Merlie, Cold Spring Harbor Symp. Quant. Biol. 57:451-460, 1992). Here, we analyzed the expression of mutated transgenes to map
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Dissertations / Theses on the topic "Transgenic muscle"

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Ning, Jie. "Estrogen receptor [alpha] and [beta] knock-out effects on skeletal muscle in mature female and male mice, and aromatase knock-out effects on skeletal muscle in mature male mice." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/6273.

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Thesis (M.S.)--University of Missouri-Columbia, 2007.<br>"August 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.
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Chen, Paula Renee. "Muscle Fiber Hyperplasia in Leg Muscle of Transgenic Quail Overexpressing anAlternative Splicing Variant of Myostatin." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1462207424.

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Sjuve, Rolf. "Function of contractile and cytoskeletal proteins in smooth muscle effects of hypertrophy and age and of desmin removal in a transgenic animal /." Lund : Dept. of Physiology and Neuroscience, Lund University, 1998. http://books.google.com/books?id=ccFqAAAAMAAJ.

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Chalothorn, Dan. "Cellular trafficking properties and physiological functions of the [alpha]1-adrenoceptor subtypes." Lexington, Ky. : [University of Kentucky Libraries], 2003. http://lib.uky.edu/ETD/ukypham2003d00083/Chalothorn.pdf.

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Thesis (Ph. D.)--University of Kentucky, 2003.<br>Title from document title page. Document formatted into pages; contains x, 192p. : ill. Includes abstract. Includes bibliographical references (p. 165-189).
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Sonner, Martha Jean. "Investigating Anatomical and Molecular Aspects of Proprioceptive Sensory Neuron Diversity Using a Transgenic Mouse Model." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1420817202.

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Bogomolovas, Julius, Jennifer R. Fleming, Brian R. Anderson, et al. "Exploration of pathomechanisms triggered by a single-nucleotide polymorphism in titin's I-band: the cardiomyopathy-linked mutation T2580I." ROYAL SOC, 2016. http://hdl.handle.net/10150/621990.

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Missense single-nucleotide polymorphisms (mSNPs) in titin are emerging as a main causative factor of heart failure. However, distinguishing between benign and disease-causing mSNPs is a substantial challenge. Here, we research the question of whether a single mSNP in a generic domain of titin can affect heart function as a whole and, if so, how. For this, we studied the mSNP T2850I, seemingly linked to arrhythmogenic right ventricular cardiomyopathy (ARVC). We used structural biology, computational simulations and transgenic muscle in vivo methods to track the effect of the mutation from the m
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Brittsan, Angela Gail. "TRANSGENIC APPROACHES TO ELUCIDATE THE ROLE OF PHOSPHOLAMBAN IN BASAL CONTRACTILITY AND DURING BETA-ADRENERGIC STIMULATION OF THE HEART." University of Cincinnati / OhioLINK, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=ucin960908353.

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Sanford, Jamie Lynn. "Analysis of the cell junction proteins CASK and claudin-5 in skeletal and cardiac muscle." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1117553681.

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Thesis (Ph. D.)--Ohio State University, 2005.<br>Title from first page of PDF file. Document formatted into pages; contains xv, 188 p.; also includes graphics (some col.) Includes bibliographical references (p. 166-188). Available online via OhioLINK's ETD Center
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Pritchard, Tracy J. "Expression and function of the Na+-K +ATPase a-isoforms in smooth muscle: evidence from transgenic mice /." Cincinnati, Ohio : University of Cincinnati, 2007. http://www.ohiolink.edu/etd/view.cgi?ucin1186672962.

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Thesis (Ph. D. )--University of Cincinnati, 2007.<br>Advisor: Dr. Richard J. Paul Title from electronic thesis title page (viewed Nov. 23, 2007). Includes abstract. Keywords: transgenic mice; hypertension; vascular smooth muscle; Na+-Ca2+ exchanger Includes bibliographical references.
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Tanaka, Tomohiro. "Skeletal muscle AMP-activated protein kinase phosphorylation parallels metabolic phenotype in leptin transgenic mice under dietary modification." Kyoto University, 2006. http://hdl.handle.net/2433/143868.

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Book chapters on the topic "Transgenic muscle"

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Rudnicki, Michael A., Thomas Braun, Hans-Henning Arnold, and Rudolf Jaenisch. "Targeted Inactivation of the Muscle Regulatory Genes Myf-5 and MyoD: Effect on Muscle and Skeletal Development." In Transgenic Animals as Model Systems for Human Diseases. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_9.

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Schilz, Robert, and Jack A. Elias. "Transgenic Animals and the Modelling of Asthma." In Airways Smooth Muscle: Modelling the Asthmatic Response In Vivo. Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9000-7_11.

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Nguyen, Phong D., and Peter D. Currie. "Using Transgenic Zebrafish to Study Muscle Stem/Progenitor Cells." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6771-1_6.

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Paul, R. J., G. E. Shull, and E. G. Kranias. "The Sarcoplasmic Reticulum and Smooth Muscle Function: Evidence from Transgenic Mice." In Role Of The Sarcoplasmic Reticulum In Smooth Muscle. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470853050.ch17.

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Yaffe, David, Uri Nudel, Moshe Shani, et al. "Expression of Cloned Muscle-Specific Genes in Transfected Cells and Transgenic Mice." In Coordinated Regulation of Gene Expression. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2245-0_15.

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Buonanno, Andres, Lucia Casabo, Jon Kornhauser, C. Michael Crowder, and John P. Merlie. "Transcriptional Regulation of Acetylcholine Receptor Genes in Transfected Muscle Cells and Transgenic Mice." In Molecular Biology of Neuroreceptors and Ion Channels. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74155-5_43.

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Tai, Phillip W. L., Catherine L. Smith, John C. Angello, and Stephen D. Hauschka. "Analysis of Fiber-Type Differences in Reporter Gene Expression of β-Gal Transgenic Muscle." In Methods in Molecular Biology. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-343-1_26.

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Terauchi, Yasuo, and Takashi Kadowaki. "Transgenic Approach to Insulin Signaling." In Muscle Metabolism. CRC Press, 2002. http://dx.doi.org/10.1201/9780203166420.ch12.

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Leturque, Armelle, and Anna-Maria Lombardi. "Transgenic Models to Study Glucose Transport and Metabolism in Skeletal Muscle." In Muscle Metabolism. CRC Press, 2002. http://dx.doi.org/10.1201/9780203166420.ch13.

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Mora, Silvia, and Jeffrey Pessin. "The Use of Mouse Transgenic and Homologous Recombination Technologies to Analyze the Physiologic Basis of Glucose Homeostasis." In Muscle Metabolism. CRC Press, 2002. http://dx.doi.org/10.1201/9780203166420.pt4.

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Conference papers on the topic "Transgenic muscle"

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Rizzuto, E., A. Musarò, A. Catizone, and Z. Del Prete. "Morpho-Functional Interaction Between Muscle and Tendon in Hypertrophic MLC/mIGF-1 Mice." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19332.

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Tendons and ligaments are uniaxial viscoelastic connective tissues and, during normal activity, tendons transmit forces from muscles to bones, while ligaments stabilize the joints. Many experiments have been carried out to study ligaments and tendons mechanical properties [1], and the effects of training protocols [2] or specific pathologies. Recently, different transgenic mice models have been proposed as a new way to study in depth tendons’ function and development [3]. Within this context, we made use of pathological and transgenic animal models to investigate the morpho-functional interact
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Hong, So Gun, Hyun Ju Oh, Jung Eun Park, et al. "Dog recloning from muscle fibroblasts in transgenic cloned beagle: Regeneration of an identical transgenic dog." In 2010 International Conference on Chemistry and Chemical Engineering (ICCCE). IEEE, 2010. http://dx.doi.org/10.1109/iccceng.2010.5560421.

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Suzumura, K., K. Funakoshi, T. Hoshino, et al. "A light-regulated bio-micro-actuator powered by transgenic Drosophila melanogaster muscle tissue." In 2011 IEEE 24th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2011. http://dx.doi.org/10.1109/memsys.2011.5734383.

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Hirooka, Masaya, Sze Ping Beh, Toshifumi Asano, et al. "Evaluation and optical control of somatic muscle micro bioactuator of channelrhodopsin transgenic Drosophila melanogaster." In 2014 IEEE 27th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2014. http://dx.doi.org/10.1109/memsys.2014.6765608.

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Rodinova, Marie, Jana Krizova, Hana Stufkova, et al. "B12 Longitudinal view of mitochondrial bioenergetics in skeletal muscle of premanifest transgenic minipig model for huntington’s disease." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.64.

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Matovu, Jacob, and Ahmet Alçiçek. "Investigations and Concerns about the Fate of Transgenic DNA and Protein in Livestock." In International Students Science Congress. Izmir International Guest Student Association, 2021. http://dx.doi.org/10.52460/issc.2021.011.

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The fate of transgenic DNA (tDNA) and protein from feed derived from Genetically Modified organisms (GMOs) in animals has been a major issue since their commercialization in 1996. Several studies have investigated the risks of horizontal gene transfer (HGT) of tDNA and protein to bacteria or animal cells/tissues, but some of the reported data are controversial. Previous reports showed that tDNA fragments or proteins derived from GM plants could not be detected in tissues, fluids, or edible products from livestock. Other researchers have shown that there is a possibility of small fragments ente
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Elliot, John, Alan James, Kimberley Wang, et al. "Transforming growth factor alpha increases extracellular matrix within the airway smooth muscle layer in a transgenic mouse model of airway disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa894.

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Ünlü, Elif Işılay, and Ahmet Çınar. "Lesion Detection on Skin Images Using Improved U-Net." In International Students Science Congress. Izmir International Guest Student Association, 2021. http://dx.doi.org/10.52460/issc.2021.022.

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The fate of transgenic DNA (tDNA) and protein of feeds from Genetically Modified organisms (GMOs) in animals has been an important topic since their commercialization in 1996. Several studies have investigated about risks of horizontal gene transfer (HGT) of tDNA and proteins to bacteria or animal cells/tissues, however, the reported data is at times controversial. Earlier reports showed that tDNA fragments or protein derived from GM plants have not been detected in tissues, fluids, or edible products of farm animals. Other researchers have come out to demonstrate that there is the possibility
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Körner, S., N. Thau-Habermann, and S. Petri. "Die Expression des Axon-guidance Protein Rezeptor Neuropilin 1 ist im Rückenmark von transgenen SOD1G93A ALS Mäusen erhöht und im Muskel erniedrigt." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685003.

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