Relevant bibliographies by topics / MRNA downregulation

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

Academic literature on the topic 'MRNA downregulation'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "MRNA downregulation"

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Yeilding, N. M., and W. M. Lee. "Coding elements in exons 2 and 3 target c-myc mRNA downregulation during myogenic differentiation." Molecular and Cellular Biology 17, no. 5 (May 1997): 2698–707. http://dx.doi.org/10.1128/mcb.17.5.2698.

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Downregulation in expression of the c-myc proto-oncogene is an early molecular event in differentiation of murine C2C12 myoblasts into multinucleated myotubes. During differentiation, levels of c-myc mRNA decrease 3- to 10-fold despite a lack of change in its transcription rate. To identify cis-acting elements that target c-myc mRNA for downregulation during myogenesis, we stably transfected C2C12 cells with mutant myc genes or chimeric genes in which various myc sequences were fused to the human beta-globin gene or to the bacterial chloramphenicol acetyltransferase (CAT) gene. Deletion of coding sequences from myc exon 2 or exon 3 abolished downregulation of myc mRNA during myogenic differentiation, while deletion of introns or sequences in the 5' or 3' untranslated regions (UTRs) did not, demonstrating that coding elements in both exons 2 and 3 are necessary for myc mRNA downregulation. Fusion of coding sequences from either myc exon 2 or 3 to beta-globin mRNA conferred downregulation onto the chimeric mRNA, while fusion of myc 3' UTR sequences or coding sequences from CAT or ribosomal protein L32 did not, demonstrating that coding elements in myc exons 2 and 3 specifically confer downregulation. These results present the apparent paradox that coding elements in either myc exon 2 or myc exon 3 are sufficient to confer downregulation onto beta-globin mRNA, but neither element alone was sufficient for myc mRNA downregulation, suggesting that some feature of beta-globin mRNA may potentiate the regulatory properties of myc exons 2 and 3. A similar regulatory function is not shared by all mRNAs because fusion of either myc exon 2 or myc exon 3 to CAT mRNA did not confer downregulation onto the chimeric mRNA, but fusion of the two elements together did. We conclude from these results that two myc regulatory elements, one exon 2 and one in exon 3, are required for myc mRNA downregulation. Finally, using a highly sensitive and specific PCR-based assay for comparing mRNA levels, we demonstrated that the downregulation mediated by myc exons 2 and 3 results in a decrease in cytoplasmic mRNA levels, but not nuclear mRNA levels, indicating that regulation is a postnuclear event.
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Asada, Sachie, Yoshitoshi Kasuya, Takeshi Sakurai, Tomoh Masaki, and Katsutoshi Goto. "Endothelin-1-Induced Downregulation of ETB Receptor mRNA." Journal of Cardiovascular Pharmacology 26 (1995): S272–275. http://dx.doi.org/10.1097/00005344-199526003-00082.

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Asada, Sachie, Yoshitoshi Kasuya, Takeshi Sakurai, Tomoh Masaki, and Katsutoshi Goto. "Endothelin-1-Induced Downregulation of ETB Receptor mRNA." Journal of Cardiovascular Pharmacology 26 (1995): S272–275. http://dx.doi.org/10.1097/00005344-199506263-00082.

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Liu, Jinyao, Ayako Hakucho, and Tatsuya Fujimiya. "Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/409350.

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The influences of angiotensinase C on ethanol-induced left ventricular (LV) systolic function were assessed in spontaneously hypertensive rats (SHRs). SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without ethanol and used as control. We evaluated LV systolic function, angiotensinase C mRNA and protein expressions, activation of the renin-angiotensin system (RAS), and the gene expressions of LV collagen (Col) III a1 and matrix metalloproteinases- (MMP-) 9. Compared to the WKY, LV systolic dysfunction (expressed by decreased fractional shortening and ejection fraction) was observed in the SHRs before ethanol treatment and further deteriorated by ethanol treatment. In the ethanol-treated SHRs, the following were observed: downregulations of angiotensinase C mRNA and protein, increased RAS activity with low collagen production as evidenced by angiotensin II and angiotensin type 1 receptor (AT1R) protein upregulation,AT1aR mRNA downregulation, and an MMP-9 mRNA expression upregulation trend with the downregulation of Col III a1 mRNA expression in LV. We conclude that chronic ethanol regimen is sufficient to promote the enhanced RAS activity-induced decrease in the production of cardiac collagen via downregulated angiotensinase C, leading to the further deterioration of LV systolic dysfunction in SHRs.
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Huang, Fu-Chen, Ying-Hsien Huang, Ho-Chang Kuo, and Sung-Chou Li. "Identifying Downregulation of Autophagy Markers in Kawasaki Disease." Children 7, no. 10 (October 4, 2020): 166. http://dx.doi.org/10.3390/children7100166.

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Kawasaki disease (KD) is the most common cause of heart disease acquired in childhood. Even if treated with high-dose intravenous immunoglobulin G (IVIG) at the early stage; children are still at risk of developing coronary artery lesions. Accumulating evidence suggests that autophagy is enhanced in various heart diseases. Evaluating the pathogenic role of autophagy in KD and coronary artery lesions (CAL) may aid in identifying a potential therapeutic target for the treatment or prevention of the disease. Blood samples were obtained from 20 children with KD at the onset of disease and 21 days after IVIG therapy. Twenty children with other causes of febrile disease and 20 healthy children were included as controls. Total RNA was extracted from white blood cells; and autophagy-related gene mRNA expression levels were measured using real-time polymerase chain reaction. The patients with KD had downregulated levels of LC3B mRNA (0.50 ± 0.06 vs. 1.67 ± 0.15; p < 0.001), BECN1 mRNA (0.70 ± 0.08 vs. 1.43 ± 0.23; p < 0.05), and ATG16L1 mRNA (0.28 ± 0.04 vs. 0.96 ± 0.16; p < 0.01) compared to the febrile control group. The values of these parameters all increased significantly 21 days after the IVIG therapy as follows: LC3B mRNA (1.77 ± 0.29 vs. 0.50 ± 0.06; p < 0.001), BECN1 mRNA (1.67 ± 0.36 vs. 0.70 ± 0.08; p < 0.05), and ATG16L1 mRNA (2.96 ± 0.43 vs. 0.28 ± 0.04; p < 0.001), while the level of ATG16L1 mRNA persists low in KD patients with CAL. Our results showed the autophagy-related genes expressions in KD and their change after IVIG administration. This suggests that autophagy may have a protective effect on KD.
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Ichiki, Toshihiro, Kotaro Takeda, and Akira Takeshita. "Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II." Hypertension 36, suppl_1 (October 2000): 688. http://dx.doi.org/10.1161/hyp.36.suppl_1.688-b.

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58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.
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Tao, Xianzun, and Guangxia Gao. "Tristetraprolin Recruits Eukaryotic Initiation Factor 4E2 To Repress Translation of AU-Rich Element-Containing mRNAs." Molecular and Cellular Biology 35, no. 22 (September 14, 2015): 3921–32. http://dx.doi.org/10.1128/mcb.00845-15.

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Tristetraprolin (TTP) regulates the expression of AU-rich element-containing mRNAs through promoting the degradation and repressing the translation of target mRNA. While the mechanism for promoting target mRNA degradation has been extensively studied, the mechanism underlying translational repression is not well established. Here, we show that TTP recruits eukaryotic initiation factor 4E2 (eIF4E2) to repress target mRNA translation. TTP interacted with eIF4E2 but not with eIF4E. Overexpression of eIF4E2 enhanced TTP-mediated translational repression, and downregulation of endogenous eIF4E2 or overexpression of a truncation mutant of eIF4E2 impaired TTP-mediated translational repression. Overexpression of an eIF4E2 mutant that lost the cap-binding activity also impaired TTP's activity, suggesting that the cap-binding activity of eIF4E2 is important in TTP-mediated translational repression. We further show that TTP promoted eIF4E2 binding to target mRNA. These results imply that TTP recruits eIF4E2 to compete with eIF4E to repress the translation of target mRNA. This notion is supported by the finding that downregulation of endogenous eIF4E2 increased the production of tumor necrosis factor alpha (TNF-α) protein without affecting the mRNA levels in THP-1 cells. Collectively, these results uncover a novel mechanism by which TTP represses target mRNA translation.
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Latham, K. E., and I. R. Konigsberg. "Mitogen stimulation affects contractile protein mRNA abundance and translation in embryonic quail myocytes." Molecular and Cellular Biology 9, no. 8 (August 1989): 3203–11. http://dx.doi.org/10.1128/mcb.9.8.3203.

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In cultures of differentiated, fusion-blocked muscle cells obtained from embryonic Japanese quail (Coturnix coturnix japonica), mitogen stimulation leads to an immediate reduction in the rates of synthesis of skeletal muscle myosin heavy chain (MHC) and alpha-actin. The molecular mechanisms responsible for this downregulation were examined. The cellular abundances of the alpha-actin and MHC mRNAs were affected differently by mitogen stimulation; alpha-actin mRNA abundance declined by an amount which quantitatively accounted for the observed decrease in alpha-actin synthesis, whereas MHC mRNA abundance remained virtually unchanged during the first 6 h following mitogen stimulation, a period during which MHC synthesis declined by more than 70%. MHC mRNA abundance did decline between 6 and 12 h after mitogen stimulation. Downregulation of MHC synthesis therefore involves an initial block in mRNA translation combined with a later loss of MHC mRNA from the cytoplasma, while alpha-actin synthesis is regulated at the level of mRNA abundance. These observations are consistent with the hypothesis that, in addition to transcriptional activation of muscle-specific genes, skeletal muscle differentiation normally involves cell cycle-dependent modulations in cellular factors which control message stability and message translation.
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Latham, K. E., and I. R. Konigsberg. "Mitogen stimulation affects contractile protein mRNA abundance and translation in embryonic quail myocytes." Molecular and Cellular Biology 9, no. 8 (August 1989): 3203–11. http://dx.doi.org/10.1128/mcb.9.8.3203-3211.1989.

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In cultures of differentiated, fusion-blocked muscle cells obtained from embryonic Japanese quail (Coturnix coturnix japonica), mitogen stimulation leads to an immediate reduction in the rates of synthesis of skeletal muscle myosin heavy chain (MHC) and alpha-actin. The molecular mechanisms responsible for this downregulation were examined. The cellular abundances of the alpha-actin and MHC mRNAs were affected differently by mitogen stimulation; alpha-actin mRNA abundance declined by an amount which quantitatively accounted for the observed decrease in alpha-actin synthesis, whereas MHC mRNA abundance remained virtually unchanged during the first 6 h following mitogen stimulation, a period during which MHC synthesis declined by more than 70%. MHC mRNA abundance did decline between 6 and 12 h after mitogen stimulation. Downregulation of MHC synthesis therefore involves an initial block in mRNA translation combined with a later loss of MHC mRNA from the cytoplasma, while alpha-actin synthesis is regulated at the level of mRNA abundance. These observations are consistent with the hypothesis that, in addition to transcriptional activation of muscle-specific genes, skeletal muscle differentiation normally involves cell cycle-dependent modulations in cellular factors which control message stability and message translation.
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10

Nanbu, R., P. A. Menoud, and Y. Nagamine. "Multiple instability-regulating sites in the 3' untranslated region of the urokinase-type plasminogen activator mRNA." Molecular and Cellular Biology 14, no. 7 (July 1994): 4920–28. http://dx.doi.org/10.1128/mcb.14.7.4920.

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In LLC-PK1 cells urokinase-type plasminogen activator (uPA) mRNA has a short half-life. It is stabilized by inhibition of protein synthesis and by downregulation of protein kinase C (PKC). In the present study on uPA mRNA metabolism, we focused our attention on the 3' untranslated region (3'UTR) of the uPA mRNA, as this region is long and highly conserved among several mammalian species, including mice and humans. To investigate the possible role of the 3'UTR of uPA mRNA in mRNA metabolism, we inserted this region into the 3'UTR of the rabbit beta-globin gene that is linked to the cytomegalovirus promoter and stably transfected it into LLC-PK1 cells. While the parental globin mRNA was stable, the chimeric mRNA was degraded as rapidly as endogenous uPA mRNA, suggesting that the 3'UTR of uPA mRNA contains most of the information required for its rapid turnover. Further analysis showed that there are at least three independent determinants of instability in the 3'UTR; one is an AU-rich sequence located immediately 3' of the poly(A) addition signal, and one is a sequence containing a stem structure. One determinant seems to require ongoing RNA synthesis for its activity. All chimeric unstable globin mRNAs became stable in the presence of cycloheximide, a protein synthesis inhibitor, suggesting that the stabilization of mRNA by protein synthesis inhibition is not through a specific sequence in the mRNA. In PKC-downregulated cells, globin mRNAs with the complete 3'UTR or the AU-rich sequence were stabilized, suggesting that PKC downregulation stabilizes uPA mRNA through the AU-rich sequence. Here we discuss the significance of multiple, independently acting instability determinants in the regulation of uPA mRNA metabolism.
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Dissertations / Theses on the topic "MRNA downregulation"

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Victor, Xylophone Vijai Aasee. "Angiotensin II-mediated Regulation of the Human Angiotensin II Type 1 Receptor Gene." Diss., CLICK HERE for online access, 2005. http://contentdm.lib.byu.edu/ETD/image/etd952.pdf.

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Wu, Yan-Yun, and 吳雁韻. "Downregulation of Zfp36l2 mRNA by TTP and functional characterization of Zfp36l2 in LPS-stimulated mouse macrophage RAW264.7 cells." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/22428487734492194222.

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碩士
國立臺灣大學
生化科學研究所
101
Post-transcriptional control comprises regulation of the stability or translational efficiency of mRNA. Microarray analyses have revealed that 40-50% of changes in gene expression in response to cellular signals occur at the level of mRNA stability. Adenine and uridine -rich element mediated decay is one of several mechanisms the degrade mRNAs in the post-transcriptional regulations. AU-rich elements are always found in 3’UTR of a variety of transcripts that encode immediate response genes such as cytokines and inflammatory mediators, like proto-oncogenes and transcription factors. TTP family proteins bind to ARE of target mRNA by zinc finger domain and promote degradation. There are four members belong to TTP family: TTP (ZFP36), ZFP36L1, ZFP36L2 and ZFP36L3 which is specifically expressed in the placenta and extraembryonic tissues. Currently, the gene regulation and functional characterization of Zfp36l2 are unclear. We observed that Zfp36l2 mRNA expression was decreased in LPS-stimulated RAW264.7 cells. RNA pull down assay have improved that the downregulation of Zfp36l2 mRNA was caused by TTP binding to its ARE, which was induced by NFкB signaling pathway in LPS-stimulated RAW264.7 cells. On the other hand, we have identified two mRNA targets of Zfp36l2, Cox2 and Mkp-1 mRNA, in resting RAW264.7 cells. To investigate the molecular mechanism of Zfp36l2-specific Cox2 mRNA downregulation, we characterized the functional domains of Zfp36l2 by using some deletion constructs. In Immunofluorescence staining, WT- Zfp36l2 dispersed in the cytoplasm evenly, whereas Zfp36l2-N-TZF formed distinct foci and located at processing body, and Zfp36l2 –TZF-C tended to gather at the nuclear membranes. The luciferase reporter analysis showed that N-terminus of Zfp36l2 is required for its mRNA downregulation activity. In addition, we observed that the LPS treatment would lead to a lasting decrease of Zfp36l2 expression for more than 16 h, which might cause a higher induction of anti-inflammatory Mkp-1and IL-10 mRNA and a lower induction of pro-inflammatory cytokine TNFα in response to the second LPS treatment. Our results indicate that the expression levels of Zfp36l2 are tightly controlled to regulate intracellular inflammatory response in LPS-stimulated macrophages.
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Book chapters on the topic "MRNA downregulation"

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Gorter, J. A., E. M. Aronica, T. Opitz, M. V. L. Bennett, J. A. Connor, and R. S. Zukin. "Global Ischemia Induces Downregulation of GIuR2 mRNA and Increases AMPA Receptor-Mediated Ca2+ Influx in Hippocampal CA1 Neurons." In Maturation Phenomenon in Cerebral Ischemia III, 321–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58602-6_41.

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Conference papers on the topic "MRNA downregulation"

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Iwaya, Takeshi, Takeo Fukagawa, Yutaka Suzuki, Tomoya Sudo, Kaoru Ishida, Kohei Kume, Satoshi Nishizuka, et al. "Abstract 5201: MicroRNA 760 regulates gastric cancer progression by downregulation of histone mRNA expression." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5201.

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Rynko, Abby E., Allison D. Fryer, and David B. Jacoby. "Etanercept Blocks Parainfluenza Downregulation Of M2 Muscarinic Receptor MRNA In Parasympathetic Nerves In Vivo." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2150.

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Zheng, Ying, and Wilson S. Meng. "Polycation Coated Polymeric Particles as Vehicles of RNA Delivery Into Immune Cells." In ASME 2010 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2010. http://dx.doi.org/10.1115/smasis2010-3714.

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The purpose of this work is to develop a carrier system for delivering RNA molecules aimed to downregulate specific functions in T cells. In many forms of cancer, T cells that express the protein Forkhead Box P3 (Foxp3) are associated with cancer progression. These cells can be identified by CD4 and CD25, molecules express on the cell surface. Studies have shown that downregulation of Foxp3 can increase the ability of other immune cells to destroy tumors. A class of RNA molecules, commonly referred to as “siRNA”, bind to and degrade specific messenger RNA (mRNA) in a sequence-dependent manner such that expression of the encoded protein is terminated. Because mRNA molecules are located inside cells, a carrier system is required to facilitate the uptake of siRNA, which does not passively diffuse through the plasma membrane. To this end, nanosized polymeric particles coated with the polycation, ornithinex10-histidinex6 (or O10H6) were used to adsorb siRNA that bind to the mRNA encoding Foxp3. The RNA-loaded particles are spherical and uniform in size (normally distributed, polydispersity index = 0.072). Loading of RNA to the particles was confirmed using gel electrophoresis. RNA complexed with the particles are protected from serum destabilization: 83.1% of RNA were recovered compared to 36.1% in RNA that were not associated with the particles. Association with the particles increased the uptake of the RNA in mouse T cells from 3.2±0.2% (free RNA) to 20.1±3.9%. Specifically, uptake of the RNA in T cells that express CD4 increased from 2.7±0.2% to 27.1±1.3% when particles were employed. These differences are statistically significant in three experiments conducted (p &lt; 0.01). Internalization of the RNA into T cells was confirmed using confocal imaging. Flow cytometric analysis showed that the particle-complexed RNA reduced the percentage of T cells that express both CD4 and CD25 in mice carrying tumors from 24.0% when free RNA molecules were used to 13.5%. In these cells, the level of Foxp3 mRNA was reduced by 30%. In conclusion, the particles facilitate the uptake of siRNA molecules into a population of T cells that is known to promote cancer growth.
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Kooshki, Mitra, Christine Naczki, Michael E. Robbins, and Linda J. Metheny-Barlow. "Abstract 1792: Radiation-induced downregulation of GLT-1 glutamate transporter mRNA expression is reversed by renin-angiotensin system inhibitors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1792.

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Tian, Zhongxian, Honglei Jin, Jingxia Li, Chao Huang, and Chuanshu Huang. "Abstract 1062: Downregulation of miR-200c stabilizes XIAP mRNA and contributes to invasion and lung metastasis of bladder cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1062.

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Ngan, Hoi Lam, and Vivian W. Y. Lui. "Abstract 5712: Potential clinical significance of downregulation of MAPK pathway components mRNA expression in head and neck squamous cell carcinoma (HNSCC)." 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.am2017-5712.

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Zhang, Jingjie, Weiming Ouyang, Jingxia Li, Yonghui Yu, Xuejun Li, and Chuanshu Huang. "Abstract 4703: SAHA downregulation of HuR expression is responsible for reduction of cyclin D1 mRNA stability and cell transformation by EGF in Cl41 cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4703.

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.
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Londino, J. D., J. Adair, D. Farkas, and R. K. Mallampalli. "Influenza Infection Stabilizes Interferon Lambda Receptor mRNA by Downregulating microRNA." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4172.

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