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Journal articles on the topic 'Gene upregulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Christman, Karen L., Richard Sievers, Fang Qizhi, Kenneth Colley, and Randall J. Lee. "Myocardial ischemia induced upregulation of pleitrophin gene." Journal of the American College of Cardiology 41, no. 6 (March 2003): 393. http://dx.doi.org/10.1016/s0735-1097(03)81133-6.

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2

Lee, H. "MUC8 mucin gene upregulation in chronic rhinosinusitis." Otolaryngology - Head and Neck Surgery 129, no. 2 (August 2003): P175—P176. http://dx.doi.org/10.1016/s0194-5998(03)01081-7.

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3

Ozcan, Onder, Ahmet Korkut Belli, Esin Sakalli Cetin, Murat Kara, Ozgur Ilhan Celik, Mehmet Kaplan, Selami Ilgaz Kayilioglu, Cem Donmez, and Murat Polat. "Upregulation of SIRT1 gene in gastric adenocarcinoma." Turkish Journal of Gastroenterology 30, no. 4 (April 15, 2019): 326–30. http://dx.doi.org/10.5152/tjg.2019.18550.

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4

Kok, C. H., A. L. Brown, P. G. Ekert, and R. J. D'Andrea. "Gene expression analysis reveals HOX gene upregulation in trisomy 8 AML." Leukemia 24, no. 6 (April 29, 2010): 1239–43. http://dx.doi.org/10.1038/leu.2010.85.

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5

Suradhat, Sanipa, and Roongroje Thanawongnuwech. "Upregulation of interleukin-10 gene expression in the leukocytes of pigs infected with porcine reproductive and respiratory syndrome virus." Journal of General Virology 84, no. 10 (October 1, 2003): 2755–60. http://dx.doi.org/10.1099/vir.0.19230-0.

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Recent studies suggest that porcine reproductive and respiratory syndrome virus (PRRSV) may have immunomodulatory effects on the host immune system by upregulating interleukin (IL)-10 gene expression. To determine the effect of PRRSV on porcine cytokine gene expression in vivo, we infected pigs with either the European or North American strain of PRRSV and monitored cytokine gene expression in peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage cells (BALC) using a multiplex PCR assay. Our results showed that both European and North American strains of PRRSV significantly upregulated IL-10 gene expression in PBMC of infected pigs from 5 days post-infection (p.i.). In addition, upregulation of IL-10 and interferon (IFN)-γ gene expression was observed in BALC starting from 9 days p.i. The upregulation of cytokine gene expression in BALC was observed concurrent with an increased percentage of lymphocytes in the BALC population, suggesting a role for peripheral leukocytes in cytokine production in lungs. Our results showed that PRRSV infection resulted in an upregulation of IL-10 gene expression in vivo and that both European and North American strains induced comparable levels of IL-10 gene expression in the infected pigs, despite differences in the clinical signs. Our data support the notion that induction of IL-10 production may be one of the strategies used by PRRSV to modulate the host's immune responses, and this may contribute to the unique clinical picture observed following PRRSV infection.

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Schrimpf, C., K. Tim, U. Böer, M. Klingenberg, O. Teebken, and M. Wilhelmi. "Shear Stress Induces Vasoprotective Gene Upregulation in Pericytes." European Journal of Vascular and Endovascular Surgery 47, no. 6 (June 2014): 696–97. http://dx.doi.org/10.1016/j.ejvs.2014.03.035.

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7

Simakou, Theodoros, Robin Freeburn, and Fiona L. Henriquez. "Gene expression during THP-1 differentiation is influenced by vitamin D3 and not vibrational mechanostimulation." PeerJ 9 (July 14, 2021): e11773. http://dx.doi.org/10.7717/peerj.11773.

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Background In injury or infection, monocytes migrate into the affected tissues from circulation and differentiate into macrophages which are subsequently involved in the inflammatory responses. Macrophage differentiation and activation have been studied in response to multiple chemokines and cytokines. However, mechanical, and physical stimuli can also influence macrophage differentiation, activation, cytokine production, and phagocytic activity. Methods In this study the macrophage differentiation from THP-1 monocytes was assessed upon the stimulation with 1,25-dihydroxyvitamin D3 and 1,000 Hz vibrations, using qPCR for quantification of transcript expression. Vitamin D binds the vitamin D receptor (VDR) and subsequently modulates the expression of a variety of genes in monocytes. The effects of the 1,000 Hz vibrational stimulation, and the combined treatment of vitamin D3 and 1000 Hz vibrations were unknown. The differentiation of macrophages was assessed by looking at transcription of macrophage markers (e.g., CD14, CD36), antigen presenting molecules (e.g., HLA-DRA), transcription factors (e.g., LEF-1, TCF7L2), and mechanosensors (e.g., PIEZO1 and PKD2). Results The results showed that vitamin D3 induced THP-1 macrophage differentiation, which was characterized by upregulation of CD14 and CD36, downregulation of HLA-DRA, upregulation of the PKD2 (TRPP2), and an inverse relationship between TCF7L2 and LEF-1, which were upregulated and downregulated respectively. The 1,000 Hz vibrations were sensed from the cells which upregulated PIEZO1 and TCF3, but they did not induce expression of genes that would indicate macrophage differentiation. The mRNA transcription profile in the cells stimulated with the combined treatment was comparable to that of the cells stimulated by the vitamin only. The 1,000 Hz vibrations slightly weakened the effect of the vitamin for the regulation of CD36 and HLA-DMB in the suspension cells, but without causing changes in the regulation patterns. The only exception was the upregulation of TCF3 in the suspension cells, which was influenced by the vibrations. In the adherent cells, the vitamin D3 cancelled the upregulating effect of the 1,000 Hz vibrations and downregulated TCF3. The vitamin also cancelled the upregulation of PIEZO1 gene by the 1,000 Hz vibrations in the combined treatment. Conclusion The mechanical stimulation with 1,000 Hz vibrations resulted in upregulation of PIEZO1 in THP-1 cells, but it did not affect the differentiation process which was investigated in this study. Vitamin D3 induced THP-1 macrophage differentiation and could potentially influence M2 polarization as observed by upregulation of CD36 and downregulation of HLA-DRA. In addition, in THP-1 cells undergoing the combined stimulation, the gene expression patterns were influenced by vitamin D3, which also ablated the effect of the mechanical stimulus on PIEZO1 upregulation.

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Cros, Nathalie, Jacky Muller, Sophie Bouju, Geneviève Piétu, Chantal Jacquet, Jean J. Léger, Jean-François Marini, and Claude A. Dechesne. "Upregulation of M-creatine kinase and glyceraldehyde3-phosphate dehydrogenase: two markers of muscle disuse." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 2 (February 1, 1999): R308—R316. http://dx.doi.org/10.1152/ajpregu.1999.276.2.r308.

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Muscle disuse induces substantial alterations in the highly plastic skeletal muscle tissues, which occur especially in antigravity slow muscles. We differentially screened a muscle cDNA array to identify modifications in gene profile expression induced in slow rat soleus muscle mechanically unloaded by hindlimb suspension as a model for muscle disuse. This study focused on muscle creatine kinase mRNA and protein and glyceraldehyde-3-phosphate dehydrogenase mRNA, which were found to be upregulated in unweighted muscles. These upregulations were analyzed over a 4-wk time course of hindlimb suspension and compared with variations in myosin heavy chain (MHC) isoforms while specifically focusing on type IIx MHC mRNA and protein. The two metabolic marker upregulations clearly preceded IIx MHC contractile protein upregulation. Muscle creatine kinase upregulation was shown to be an excellent, and the earliest, marker of muscle disuse at mRNA and protein levels.

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9

Falanga, Anna, Tiziano Barbui, and Frederick Rickles. "Hypercoagulability and Tissue Factor Gene Upregulation in Hematologic Malignancies." Seminars in Thrombosis and Hemostasis 34, no. 02 (March 2008): 204–10. http://dx.doi.org/10.1055/s-2008-1079262.

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10

Otterburn, David M., L. Grier Arthur, Shaheen J. Timmapuri, Suzanne M. McCahan, and Marshall Z. Schwartz. "Proteasome gene upregulation: a possible mechanism for intestinal adaptation." Journal of Pediatric Surgery 40, no. 2 (February 2005): 377–80. http://dx.doi.org/10.1016/j.jpedsurg.2004.10.024.

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11

Luo, Chunyan, Fan Wang, Subo Qin, Qiuyun Chen, and Qing K. Wang. "Coronary artery disease susceptibility gene ADTRP regulates cell cycle progression, proliferation, and apoptosis by global gene expression regulation." Physiological Genomics 48, no. 8 (August 1, 2016): 554–64. http://dx.doi.org/10.1152/physiolgenomics.00028.2016.

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The ADTRP gene encodes the androgen-dependent TFPI-regulating protein and is a susceptibility gene for contrary artery disease (CAD). We performed global gene expression profiling for ADTRP knock-down using microarrays in human HepG2 cells. Follow-up real-time RT-PCR analysis demonstrated that ADTRP knock-down regulates a diverse set of genes, including upregulation of seven histone genes, downregulation of multiple cell cycle genes ( CCND1, CDK4, and CDKN1A), and upregulation of apoptosis genes ( CASP7 and PDCD2) in HepG2 cells and endothelial cells. Consistently, ADTRP increases the number of S phase cells during cell cycle, promotes cell proliferation, and inhibits apoptosis. Our study provides novel insights into the function of ADTRP and biological pathways involving ADTRP, which may be involved in the pathogenesis of CAD.

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12

Shevchenko, Alexander I., Elena V. Dementyeva, Irina S. Zakharova, and Suren M. Zakian. "Diverse developmental strategies of X chromosome dosage compensation in eutherian mammals." International Journal of Developmental Biology 63, no. 3-4-5 (2019): 223–33. http://dx.doi.org/10.1387/ijdb.180376as.

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In eutherian mammals, dosage compensation arose to balance X-linked gene expression between sexes and relatively to autosomal gene expression in the evolution of sex chromosomes. Dosage compensation occurs in early mammalian development and comprises X chromosome upregulation and inactivation that are tightly coordinated epigenetic processes. Despite a uniform principle of dosage compensation, mechanisms of X chromosome inactivation and upregulation demonstrate a significant variability depending on sex, developmental stage, cell type, individual, and mammalian species. The review focuses on relationships between X chromosome inactivation and upregulation in mammalian early development.

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13

AYDOĞAN TÜRKOĞLU, Sümeyye, Gizem DAYI, and Feray KÖÇKAR. "Upregulation of PSMD4 gene by hypoxia in prostate cancer cells." TURKISH JOURNAL OF BIOLOGY 44, no. 5 (October 13, 2020): 275–83. http://dx.doi.org/10.3906/biy-2002-71.

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14

Xu, Song, Zhi-Fan Jia, Chunsheng Kang, Qiang Huang, Guangxiu Wang, Xiaozhi Liu, Xuan Zhou, Peng Xu, and Peiyu Pu. "Upregulation of SEPT7 Gene Inhibits Invasion of Human Glioma Cells." Cancer Investigation 28, no. 3 (November 16, 2009): 248–58. http://dx.doi.org/10.3109/07357900903179609.

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15

Kavsan, V. M., K. Shostak, O. Garifulin, G. Zehetner, and Yu Zozulya. "307 Upregulation of HC gp-39 gene in astrocytic gliomas." European Journal of Cancer Supplements 1, no. 5 (September 2003): S94. http://dx.doi.org/10.1016/s1359-6349(03)90340-5.

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16

Karam, Jose A., Sandra Huang, Jinhai Fan, Jennifer Stanfield, Roger A. Schultz, Rey-Chen Pong, Xiankai Sun, et al. "Upregulation of TRAG3 gene in urothelial carcinoma of the bladder." International Journal of Cancer 128, no. 12 (October 26, 2010): 2823–32. http://dx.doi.org/10.1002/ijc.25631.

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17

Amini Nik, Saeid, Peter Hohenstein, Ali Jadidizadeh, Kim Van Dam, Adriana Bastidas, Rachel L. Berry, Charles E. Patek, Bernadette Van der Schueren, Jean‐Jacques Cassiman, and Sabine Tejpar. "Upregulation of Wilms' tumor gene 1 ( WT1 ) in desmoid tumors." International Journal of Cancer 114, no. 2 (November 11, 2004): 202–8. http://dx.doi.org/10.1002/ijc.20717.

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18

Wilhelm, Scott M., Michael S. Simonson, Ann V. Robinson, Nicholas T. Stowe, and James A. Schulak. "Cold Ischemia Induces Endothelin Gene Upregulation in the Preserved Kidney." Journal of Surgical Research 85, no. 1 (July 1999): 101–8. http://dx.doi.org/10.1006/jsre.1999.5662.

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19

Wang, Lijuan, Odysseus Zis, Guixian Ma, Zhixin Shan, Xiong Zhang, Shuo Wang, Chengbo Dai, et al. "Upregulation of Macrophage Migration Inhibitory Factor Gene Expression in Stroke." Stroke 40, no. 3 (March 2009): 973–76. http://dx.doi.org/10.1161/strokeaha.108.530535.

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20

Coosemans, A., S. Amini Nik, S. Caluwaerts, S. Lambin, G. Verbist, R. Van Bree, V. Schelfhout, et al. "Upregulation of Wilms’ tumour gene 1 (WT1) in uterine sarcomas." European Journal of Cancer 43, no. 10 (July 2007): 1630–37. http://dx.doi.org/10.1016/j.ejca.2007.04.008.

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21

MICHISHITA, E., G. GARCES, J. BARRETT, and I. HORIKAWA. "Upregulation of the KIAA1199 gene is associated with cellular mortality." Cancer Letters 239, no. 1 (July 28, 2006): 71–77. http://dx.doi.org/10.1016/j.canlet.2005.07.028.

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22

Tian, Jing, Anita Smith, John Nechtman, Robert Podolsky, Saurabh Aggarwal, Connie Snead, Sanjiv Kumar, et al. "Effect of PPARγ inhibition on pulmonary endothelial cell gene expression: gene profiling in pulmonary hypertension." Physiological Genomics 40, no. 1 (December 2009): 48–60. http://dx.doi.org/10.1152/physiolgenomics.00094.2009.

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Peroxisome proliferator-activated receptor type gamma (PPARγ) is a subgroup of the PPAR transcription factor family. Recent studies indicate that loss of PPARγ is associated with the development of pulmonary hypertension (PH). We hypothesized that the endothelial dysfunction associated with PPARγ inhibition may play an important role in the disease process by altering cellular gene expression and signaling cascades. We utilized microarray analysis to determine if PPARγ inhibition induced changes in gene expression in pulmonary arterial endothelial cells (PAEC). We identified 100 genes and expressed sequence tags (ESTs) that were upregulated by >1.5-fold and 21 genes and ESTs that were downregulated by >1.3-fold ( P < 0.05) by PPARγ inhibition. The upregulated genes can be broadly classified into four functional groups: cell cycle, angiogenesis, ubiquitin system, and zinc finger proteins. The genes with the highest fold change in expression: hyaluronan-mediated motility receptor (HMMR), VEGF receptor 2 (Flk-1), endothelial PAS domain protein 1 (EPAS1), basic fibroblast growth factor (FGF-2), and caveolin-1 in PAEC were validated by real time RT-PCR. We further validated the upregulation of HMMR, Flk-1, FGF2, and caveolin-1 by Western blot analysis. In keeping with the microarray results, PPARγ inhibition led to re-entry of cell cycle at G1/S phase and cyclin C upregulation. PPARγ inhibition also exacerbated VEGF-induced endothelial barrier disruption. Finally we confirmed the downregulation of PPARγ and the upregulation of HMMR, Flk-1, FGF2, and Cav-1 proteins in the peripheral lung tissues of an ovine model of PH. In conclusion, we have identified an array of endothelial genes modulated by attenuated PPARγ signaling that may play important roles in the development of PH.

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Han, Seung-Woo, Byung-Kwon Jung, So-Hyun Park, and Kwon-Yul Ryu. "Reversible Regulation of Polyubiquitin Gene UBC via Modified Inducible CRISPR/Cas9 System." International Journal of Molecular Sciences 20, no. 13 (June 28, 2019): 3168. http://dx.doi.org/10.3390/ijms20133168.

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Ubiquitin is required under both normal and stress conditions. Under stress conditions, upregulation of the polyubiquitin gene UBC is essential to meet the requirement of increased ubiquitin levels to confer stress resistance. However, UBC upregulation is usually observed only under stress conditions and not under normal conditions. Therefore, it has not been possible to upregulate UBC under normal conditions to study the effect of excess ubiquitin on cellular machinery. Recently, the CRISPR/Cas9 system has been widely used in biological research as a useful tool to study gene disruption effects. In this study, using an inducible CRISPR/Cas9 variant, a dCas9–VP64 fusion protein, combined with a single guide RNA (sgRNA) containing MS2 aptamer loops and MS2-p65-HSF1, we developed a system to increase the ubiquitin pool via upregulation of UBC. Although it is challenging to upregulate the expression of a gene that is already expressed at high levels, the significance of our system is that UBC upregulation can be induced in an efficient, reversible manner that is compatible with cellular processes, even under normal conditions. This system can be used to study ubiquitin pool dynamics and it will be a useful tool in identifying the role of ubiquitin under normal and stress conditions.

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Suzuki, Atsuo, Yuhri Miyawaki, Eriko Okuyama, Moe Murata, Ando Yumi, Io Kato, Yuki Takagi, et al. "Ribavirin-Induced Intracellular GTP Depletion Upregulates Factor VII Expression." Blood 120, no. 21 (November 16, 2012): 1113. http://dx.doi.org/10.1182/blood.v120.21.1113.1113.

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Abstract Abstract 1113 In this study, we investigated the molecular basis of upregulation of factor VII (FVII) gene expression by ribavirin, and found that intracellular GTP depletion induced by ribavirin activated FVII gene transcription and modulated transcription elongation. In 2006, Yamamoto et al. reported that anti-hepatitis C virus (HCV) agent ribavirin elevated the activity of FVII in HCV-infected hemophilia patients; however, the precise mechanisms were still unknown. In addition, the anti-HCV mechanisms of ribavirin were not yet fully elucidated, although the extended studies have been done. We investigated the effects of ribavirin in vitro and confirmed the approximately 4-fold upregulation of FVII mRNA by ribavirin treatment in HepG2 cells. FVII mRNA was increased in a dose-dependent manner up to 100μg/mL of ribavirin at a lower concentration than therapeutic concentration of 150μg/mL. FVII mRNA induction by ribavirin was also observed in a time-dependent manner from 24 h to 72 h after treatment. Ribavirin metabolite ribavirin 5'-monophosphate is one of the IMP dehydrogenase (IMPDH) inhibitors, and the other IMPDH inhibitors mycophenolic acid (MPA) and 6-mercaptupurine (6-MP) also induced FVII upregulation. It is well known that inhibition of IMPDH causes intracellular GTP depletion, and guanosine supplementation to salvage GTP could reverse FVII mRNA increase in ribavirin-treated cells. These results indicated that cellular GTP reduction associated with FVII gene upregulation. The mechanisms of gene upregulation by GTP depletion were not elucidated. The promoter activities and mRNA stability of FVII were analyzed under ribavirin treatment. The FVII gene promoter activity was enhanced up to 1.5-fold by ribavirin treatment; however the activation did not reach 4-fold induction of FVII mRNA increase. There was no significant change of FVII mRNA half-life in ribavirin-treated cells. Since the promoter activation might display transcription initiation capacity, the contribution of transcription elongation stage was further investigated. Transcription elongation was regulated by phosphorylation of carbo-terminal domain (CTD) of RNA polymerase II (PolII). Transcription elongation factor P-TEFb (positive-transcription elongation factor b), which consists as a complex of CDK9 and cyclin T, phosphorylates Ser of PolII CTD. The kinase activity of P-TEFb could be inhibited by 5,6-dichlorobenzimidazole 1-b-D-ribofuranoside (DRB). In FVII gene upregulation, DRB completely canceled ribavirin-induced FVII mRNA increase. We also performed nuclear run-on assay to verify the potential transcription elongation capacity of paused PolII, and observed a dramatic increase of FVII mRNA in ribavirin-treated cells. These results suggested that ribavirin-induced FVII gene upregulation was caused not only by transcription initiation but also by accelerated transcription elongation rate. There are various transcription factor associated with transcription elongation in addition to P-TEFb, such as elongin, ELL (eleven nineteen-lysine rich leukemia). We found that ELL3, a member of ELL family protein, was upregulated by ribavirin treatment. A ELL3 mRNA increase occurred prior to FVII mRNA upregulation, and the ELL3 upregulation was also canceled by guanosine supplementation. These results indicated ELL3 induction by ribavirin was also a response to cellular GTP depletion. To confirm the contribution of ELL3 protein to FVII gene transcription elongation, we used siRNAs specific to ELL3 and as expected, knockdown of ELL3 resulted in diminished FVII upregulation. A chromatin immunoprecipitation (ChIP) revealed ELL3 recruitment to the FVII gene, and the recruitments of PolII and CDK9 were also enhanced by ribavirin treatment. Taken together, FVII gene upregulation by ribavirin was associated with intracellular GTP depletion. The GTP reduction mainly modulates transcription elongation rate rather than transcription initiation, though the relationships between cellular GTP depletion and enhanced transcription elongation must be investigated. This study uncovered candidate mechanisms of ribavirin and the other IMPDH inhibitors and highlights a development of novel pharmaceutical therapies for hemophilia. Disclosures: No relevant conflicts of interest to declare.

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25

Tigani, Wendalina, Moira Pinzan Rossi, Osvaldo Artimagnella, Manuela Santo, Rossana Rauti, Teresa Sorbo, Francesco Paolo Ulloa Severino, et al. "Foxg1 Upregulation Enhances Neocortical Activity." Cerebral Cortex 30, no. 9 (May 7, 2020): 5147–65. http://dx.doi.org/10.1093/cercor/bhaa107.

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Abstract Foxg1 is an ancient transcription factor gene orchestrating a number of neurodevelopmental processes taking place in the rostral brain. In this study, we investigated its impact on neocortical activity. We found that mice overexpressing Foxg1 in neocortical pyramidal cells displayed an electroencephalography (EEG) with increased spike frequency and were more prone to kainic acid (KA)-induced seizures. Consistently, primary cultures of neocortical neurons gain-of-function for Foxg1 were hyperactive and hypersynchronized. That reflected an unbalanced expression of key genes encoding for ion channels, gamma aminobutyric acid and glutamate receptors, and was likely exacerbated by a pronounced interneuron depletion. We also detected a transient Foxg1 upregulation ignited in turn by neuronal activity and mediated by immediate early genes. Based on this, we propose that even small changes of Foxg1 levels may result in a profound impact on pyramidal cell activity, an issue relevant to neuronal physiology and neurological aberrancies associated to FOXG1 copy number variations.

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26

Carrier, Ewa, Shermila Kausal, and Anand S. Srivastava. "Gene Regulation during the Erythrocytic Differentiation of Embryonic Stem Cells." Blood 106, no. 11 (November 16, 2005): 4255. http://dx.doi.org/10.1182/blood.v106.11.4255.4255.

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Abstract We have studied the in vitro differentiation of murine embryonic stem cells (ES cells) towards erythropoiesis and expression of genes during this process. It has been reported that dexamethasone directs ES cells towards erythrocytic differentiation but the mechanism of gene regulation induced by dexamethasone is not well understood. We hypothesized that dexamethasone induces upregulation of erythropoietic genes such as GATA-1, FLK-1, EPO-R and directs ES cells towards erythropoietic differentiation. Murine ES cells (129 CCE) obtained from Dr. Nagy laboratory, Canada (Nagy et al., Histochem Cell Biol., 2001; 115:49–58) were subjected to the in vitro primary hematopoietic differentiation media containing methylcellulose, IMDM, IL -3, IL-6 and SCF (stem cell factor) without LIF (leukemia inhibitory factor) to promote embryoid body (EB) formation. Total RNA was collected on day 3, 5 and 9 EBs for gene expression studies using RT-PCR. On day 9 EBs were subjected to secondary differentiation using three different cytokines and growth factors combination 1) SCF, EPO, dexamethasone, IGF, 2) SCF, IL-3, IL-6, TPO, 3) SCF IL-3, IL-6, TPO, EPO. Total RNA from day12 of secondary differentiated ES cells was collected to study cytokines and growth factors dependent erythrocytic differentiation and gene regulation, using RT-PCR. Our results demonstrate upregulation of Gata-1, Flk-1, HoxB-4, Epo-R and globin genes (α-globin, BH-1 globin, β-major globin, e -globin and z-globin) in the 9 days old EBs, whereas, RNA collected from 5 days old EBs showed expression of HoxB-4, e-globin, γ-globin, BH1-globin and FLK-1. Three days old EBs showed only HoxB-4 and FLK-1 gene expression and lack of expression of globin genes, indicating that erythtropoiesis-specific genes activate later. Gene expression studies of RNA collected from secondary differentiated ES cells and media containing dexamethasone showed downregulation of GATA-3 and upregulation of GATA-1, Flk-1 and Epo-R in comparison to the two other cytokines and growth factors media combination. These results confirm our hypothesis that dexamethasome induces erythropoiesis by down regulating GATA -3 and upregulating erythropoietic-related genes such as GATA-1, Flk-1 and Epo-R. The morphological characteristics of cells after secondary differentiation showed enhanced production of erythrocytic precursors in dexamethasone containing media, which corresponded with molecular studies. Further studies will address the role of wnt/β-catenin and E-cadherin in this process.

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Ullah, H. M. Arif, A. K. Elfadl, SunYoung Park, Yong Deuk Kim, Myung-Jin Chung, Ji-Yoon Son, Hyun-Ho Yun, et al. "Nogo-A Is Critical for Pro-Inflammatory Gene Regulation in Myocytes and Macrophages." Cells 10, no. 2 (January 31, 2021): 282. http://dx.doi.org/10.3390/cells10020282.

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Nogo-A (Rtn 4A), a member of the reticulon 4 (Rtn4) protein family, is a neurite outgrowth inhibitor protein that is primarily expressed in the central nervous system (CNS). However, previous studies revealed that Nogo-A was upregulated in skeletal muscles of Amyotrophic lateral sclerosis (ALS) patients. Additionally, experiments showed that endoplasmic reticulum (ER) stress marker, C/EBP homologous protein (CHOP), was upregulated in gastrocnemius muscle of a murine model of ALS. We therefore hypothesized that Nogo-A might relate to skeletal muscle diseases. According to our knocking down and overexpression results in muscle cell line (C2C12), we have found that upregulation of Nogo-A resulted in upregulation of CHOP, pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, while downregulation of Nogo-A led to downregulation of CHOP, IL-6 and TNF-α. Immunofluorescence results showed that Nogo-A and CHOP were expressed by myofibers as well as tissue macrophages. Since resident macrophages share similar functions as bone marrow-derived macrophages (BMDM), we therefore, isolated macrophages from bone marrow to study the role of Nogo-A in activation of these cells. Lipopolysaccharide (LPS)-stimulated BMDM in Nogo-KO mice showed low mRNA expression of CHOP, IL-6 and TNF-α compared to BMDM in wild type (WT) mice. Interestingly, Nogo knockout (KO) BMDM exhibited lower migratory activity and phagocytic ability compared with WT BMDM after LPS treatment. In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-α in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-α. Furthermore, upregulation of Nogo-A in dystrophin-deficient (mdx) murine model, myopathy and Duchenne muscle dystrophy (DMD) clinical biopsies was associated with upregulation of CHOP, IL-6 and TNF-α. To the best of our knowledge, this is the first study to demonstrate Nogo-A as a regulator of inflammation in diseased muscle and bone marrow macrophages and that deletion of Nogo-A alleviates muscle inflammation and it can be utilized as a therapeutic target for improving muscle diseases.

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Ali, Hirowati, Coyza Prana, and Ellyza Nasrul. "Upregulation of SCUBE1 in Dengue Virus Infection." Open Access Macedonian Journal of Medical Sciences 7, no. 10 (May 29, 2019): 1602–7. http://dx.doi.org/10.3889/oamjms.2019.352.

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BACKGROUND: Dengue is a major communicable disease in tropical areas, with an increasing prevalence every year. Thrombocytopenia is one of the commonly used laboratory parameters for predicting the severity of the disease. It is detected on day 6 or day 7 after the febrile stage, and its presence indicates that the disease has become potentially fatal. Therefore, it is necessary to identify a marker for the early recognition of dengue virus infection during the febrile stage before the detection of thrombocytopenia on day 6 to prevent severe disease outcomes. Signal peptide-CUB- (complement C1r/C1s)-EGF (epidermal growth factor)-like domain-containing protein 1 (SCUBE1) is secreted in activated platelets under inflammatory conditions and enhances platelet-platelet adhesion and agglutination. This gene was first identified in human vascular endothelium, but its biological role in platelets remains unknown. AIM: This study aims to identify SCUBE1 expression during the febrile stage of dengue virus infection and examine the correlation of its expression with thrombocytopenia occurrence on day 6. MATERIAL AND METHODS: Blood samples were collected from 17 patients infected with dengue virus on day-3 fever and from 16 healthy controls who met the inclusion and exclusion criteria for dengue virus infection according to the World Health Organization (WHO) classification for dengue virus infection. All samples were subjected to SCUBE1 gene analysis using real-time reverse transcription quantitative PCR (RT-PCR). RESULTS: The results showed that upregulation of SCUBE1 gene in infected patients (8.9 ± 3.1-fold) compared to that in healthy controls, indicating SCUBE1 involvement in dengue virus infection. Furthermore, we analysed the laboratory parameters of infected patients on day 3 and day 6, when thrombocytopenia is usually detected. Platelet count was found to be significantly decreased from day 3 until day 6 in the infected patients. Unfortunately, our results showed no correlation between SCUBE1 expression in the febrile stage and the occurrence of thrombocytopenia on day 6. CONCLUSION: The conclusion of this study is SCUBE1 might play a role in dengue virus infection but does not correlate with thrombocytopenia on day-6 fever.

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Palacios, Génesis, Raquel Diaz-Solano, Basilio Valladares, Roberto Dorta-Guerra, and Emma Carmelo. "Early Transcriptional Liver Signatures in Experimental Visceral Leishmaniasis." International Journal of Molecular Sciences 22, no. 13 (July 2, 2021): 7161. http://dx.doi.org/10.3390/ijms22137161.

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Transcriptional analysis of complex biological scenarios has been used extensively, even though sometimes the results of such analysis may prove imprecise or difficult to interpret due to an overwhelming amount of information. In this study, a large-scale real-time qPCR experiment was coupled to multivariate statistical analysis in order to describe the main immunological events underlying the early L. infantum infection in livers of BALB/c mice. High-throughput qPCR was used to evaluate the expression of 223 genes related to immunological response and metabolism 1, 3, 5, and 10 days post infection. This integrative analysis showed strikingly different gene signatures at 1 and 10 days post infection, revealing the progression of infection in the experimental model based on the upregulation of particular immunological response patterns and mediators. The gene signature 1 day post infection was not only characterized by the upregulation of mediators involved in interferon signaling and cell chemotaxis, but also the upregulation of some inhibitory markers. In contrast, at 10 days post infection, the upregulation of many inflammatory and Th1 markers characterized a more defined gene signature with the upregulation of mediators in the IL-12 signaling pathway. Our results reveal a significant connection between the expression of innate immune response and metabolic and inhibitory markers in early L. infantum infection of the liver.

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Pan, Ya-Jing, Si-Jia Zhou, Jin Feng, Qiong Bai, La-Ta A, and Ai-Hua Zhang. "Urotensin II Induces Mice Skeletal Muscle Atrophy Associated with Enhanced Autophagy and Inhibited Irisin Precursor (Fibronectin Type III Domain Containing 5) Expression in Chronic Renal Failure." Kidney and Blood Pressure Research 44, no. 4 (2019): 479–95. http://dx.doi.org/10.1159/000499880.

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Background/Aims: Skeletal muscle atrophy is one of the main manifestations of protein energy wasting. We hypothesized that urotensin II (UII) can lead to skeletal muscle atrophy through upregulating autophagy and affecting Irisin precursor fibronectin type III domain containing 5 (FNDC5) expressions. Methods: Three animal models (the sham operation, wild-type C57BL/6 mice with 5/6 nephrectomy, UII receptor (UT) gene knockout (UTKO) mice with 5/6 nephrectomy) were designed. Skeletal muscle weight, cross-sectional area (CSA) along with UII, FNDC5, LC3, and p62 expression were investigated. C2C12 cells were differentiated for up to 4 days into myotubes. These cells were then exposed to different UII concentrations (10–5 to 10–7 M) for 6–12 h and analyzed for the expressions of autophagic markers. These cells were also exposed to the same predetermined UII concentrations for 48–72 h and analyzed for the FNDC5 expression. Myotube diameter was measured. Results: Upregulation of UII expression in skeletal muscle tissue was accompanied by reduced muscle weight and skeletal muscle CSA in the 2 posterior limbs, upregulated autophagy markers expression, and downregulated FNDC5 expression in 5/6 nephrectomy mice. The decrease of skeletal muscle weight, skeletal muscle CSA, downregulation of FNDC5 expression, and the upregulation of autophagy markers were inhibited in UTKO with 5/6 nephrectomy mice. Our in vitrostudy showed that UII could directly decrease myotube diameter, induce autophagy markers upregulation, and inhibit expression of FNDC5. When UII receptor gene was interfered by UT-specific siRNA, UII induced autophagy markers upregulation and FNDC5 downregulation were inhibited. Conclusion: We are the first to verify UII induces mice skeletal muscle atrophy associated with enhanced skeletal muscle autophagy and inhibited FNDC5 expression in chronic renal failure.

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Videla, Luis, A. "Thyroid hormone calorigenesis and mitochondrial redox signaling: upregulation of gene expression." Frontiers in Bioscience 12, no. 1 (2007): 1220. http://dx.doi.org/10.2741/2140.

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Vaez, Farin, Ali Farazmand, Sarvenaz Shaaheen, Shayan Mostafaei, Ahmadreza Jamshidi, Mahdi Vojdanian, Ashkan Asadollahbaik, and Mahdi Mahmoudi. "Upregulation of transforming growth factor-B1 gene in ankylosing spondylitis patients." Rheumatology Research 2, no. 3 (May 3, 2017): 103–7. http://dx.doi.org/10.22631/rr.2017.69997.1026.

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Ehrlich, Melanie, and Michelle Lacey. "DNA methylation and differentiation: silencing, upregulation and modulation of gene expression." Epigenomics 5, no. 5 (October 2013): 553–68. http://dx.doi.org/10.2217/epi.13.43.

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Tran, Katherine L., Xiangru Lu, Ming Lei, Qingping Feng, and Qingyu Wu. "Upregulation of corin gene expression in hypertrophic cardiomyocytes and failing myocardium." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (October 2004): H1625—H1631. http://dx.doi.org/10.1152/ajpheart.00298.2004.

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High levels of plasma atrial natriuretic peptides (ANP) are associated with pathological conditions such as congestive heart failure (CHF). Recently, we have identified a cardiac serine protease, corin, that is the pro-ANP convertase. In this study, we examined the regulation of corin gene expression in cultured hypertrophic cardiomyocytes and in the left ventricular (LV) myocardium of a rat model of heart failure. Quantitative RT-PCR analysis showed that both corin and ANP mRNA levels were significantly increased in phenylephrine (PE)-stimulated rat neonatal cardiomyocytes in culture. The increase in corin mRNA correlated closely with the increase in cell size and ANP mRNA expression in the PE-treated cells ( r = 0.95, P < 0.01; r = 0.92, P < 0.01, respectively). The PE-treated cardiomyocytes had an increased activity in converting recombinant human pro-ANP to biologically active ANP, as determined by a pro-ANP processing assay and a cell-based cGMP assay. In a rat model of heart failure induced by ligation of the left coronary artery, corin mRNA expression in the noninfarcted LV myocardium was significantly higher than that of control heart tissues from sham-operated animals, when examined by Northern blot analysis and RT-PCR at 8 wk. These results indicate that the corin gene is upregulated in hypertrophic cardiomyocytes and failing myocardium. Increased corin expression may contribute to elevation of ANP in the setting of cardiac hypertrophy and heart failure.

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Deramaudt, Bertrand M. J. M., P. Remy, and N. G. Abraham. "Upregulation of human heme oxygenase gene expression by Ets-family proteins." Journal of Cellular Biochemistry 72, no. 3 (March 1, 1999): 311–21. http://dx.doi.org/10.1002/(sici)1097-4644(19990301)72:3<311::aid-jcb1>3.0.co;2-g.

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Wang, Yaping, Ning Sun, Chao Lu, Yibing Bei, Ruizhe Qian, and Luchun Hua. "Upregulation of circadian gene 'hClock' contribution to metastasis of colorectal cancer." International Journal of Oncology 50, no. 6 (May 8, 2017): 2191–99. http://dx.doi.org/10.3892/ijo.2017.3987.

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Nickenig, Georg, Jörg Röling, Kerstin Strehlow, Petra Schnabel, and Michael Böhm. "Insulin Induces Upregulation of Vascular AT1Receptor Gene Expression by Posttranscriptional Mechanisms." Circulation 98, no. 22 (December 1998): 2453–60. http://dx.doi.org/10.1161/01.cir.98.22.2453.

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Kim, Jeongeun, Huijeong Ahn, Sangjung Yu, Jae-Hee Ahn, Hyun-Jeong Ko, Mi-Na Kweon, Eui-Ju Hong, Beum-Soo An, Eunsong Lee, and Geun-Shik Lee. "IκBζ controls NLRP3 inflammasome activation via upregulation of the Nlrp3 gene." Cytokine 127 (March 2020): 154983. http://dx.doi.org/10.1016/j.cyto.2019.154983.

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Hardin-Pouzet, H., P. Giraudon, M. F. Belin, and M. Didier-Bazes. "Glucocorticoid upregulation of glutamate dehydrogenase gene expression in vitro in astrocytes." Molecular Brain Research 37, no. 1-2 (April 1996): 324–28. http://dx.doi.org/10.1016/0169-328x(95)00327-o.

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SHAO, HONGWEI, DONGMING LAN, ZHAOHUI DUAN, ZEHUAN LIU, JUN MIN, LICHUN ZHANG, JIAN HUANG, JING SU, SHANGWU CHEN, and ANLONG XU. "Upregulation of Mitochondrial Gene Expression in PBMC from Convalescent SARS Patients." Journal of Clinical Immunology 26, no. 6 (October 6, 2006): 546–54. http://dx.doi.org/10.1007/s10875-006-9046-y.

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Charytonowicz, Elizabeth, Igor Matushansky, Josep Domingo-Doménech, Mireia Castillo-Martín, Marc Ladanyi, Carlos Cordon-Cardo, and Mel Ziman. "PAX7-FKHR fusion gene inhibits myogenic differentiation via NF-kappaB upregulation." Clinical and Translational Oncology 14, no. 3 (March 2012): 197–206. http://dx.doi.org/10.1007/s12094-012-0784-4.

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Sakai, Hidekazu, Artit Jinawath, Shoji Yamaoka, and Yasuhito Yuasa. "Upregulation of MUC6 mucin gene expression by NFκB and Sp factors." Biochemical and Biophysical Research Communications 333, no. 4 (August 2005): 1254–60. http://dx.doi.org/10.1016/j.bbrc.2005.06.037.

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Kolla, Venkatadri, and Gerald Litwack. "Upregulation of Mineralocorticoid- and Glucocorticoid-Receptor Gene Expression by Sp-I." Molecular Cell Biology Research Communications 1, no. 1 (April 1999): 44–47. http://dx.doi.org/10.1006/mcbr.1999.0110.

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Yasuhara, Kazuyuki, Yoshitaka Ohno, Atsushi Kojima, Kenji Uehara, Moroe Beppu, Takao Sugiura, Mitsuaki Fujimoto, et al. "Absence of heat shock transcription factor 1 retards the regrowth of atrophied soleus muscle in mice." Journal of Applied Physiology 111, no. 4 (October 2011): 1142–49. http://dx.doi.org/10.1152/japplphysiol.00471.2011.

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Effects of heat shock transcription factor 1 (HSF1) gene on the regrowth of atrophied mouse soleus muscles were studied. Both HSF1-null and wild-type mice were subjected to continuous hindlimb suspension for 2 wk followed by 4 wk of ambulation recovery. There was no difference in the magnitude of suspension-related decrease of muscle weight, protein content, and the cross-sectional area of muscle fibers between both types of mice. However, the regrowth of atrophied soleus muscle in HSF1-null mice was slower compared with that in wild-type mice. Lower baseline expression level of HSP25, HSC70, and HSP72 were noted in soleus muscle of HSF1-null mice. Unloading-associated downregulation and reloading-associated upregulation of HSP25 and HSP72 mRNA were observed not only in wild-type mice but also in HSF1-null mice. Reloading-associated upregulation of HSP72 and HSP25 during the regrowth of atrophied muscle was observed in wild-type mice. Minor and delayed upregulation of HSP72 at mRNA and protein levels was also seen in HSF1-null mice. Significant upregulations of HSF2 and HSF4 were observed immediately after the suspension in HSF1-null mice, but not in wild-type mice. Therefore, HSP72 expression in soleus muscle might be regulated by the posttranscriptional level, but not by the stress response. Evidence from this study suggested that the upregulation of HSPs induced by HSF1-associated stress response might play, in part, important roles in the mechanical loading (stress)-associated regrowth of skeletal muscle.

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Mirakhorli, Tahereh, Zahra Oraghi Ardebili, Alireza Ladan-Moghadam, and Elham Danaee. "Bulk and nanoparticles of zinc oxide exerted their beneficial effects by conferring modifications in transcription factors, histone deacetylase, carbon and nitrogen assimilation, antioxidant biomarkers, and secondary metabolism in soybean." PLOS ONE 16, no. 9 (September 8, 2021): e0256905. http://dx.doi.org/10.1371/journal.pone.0256905.

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Nanoscience paves the way for producing highly potent fertilizers and pesticides to meet farmer’s expectations. This study investigated the physiological and molecular responses of soybean seedlings to the long-time application of zinc oxide nanoparticles (ZnO NPs) and their bulk type (BZnO) at 5 mg L-1 under the two application methods (I- foliar application; II- soil method). The ZnO NPs/BZnO treatments in a substance type- and method-dependent manner improved plant growth performance and yield. ZnO NPs transactionally upregulated the EREB gene. However, the expression of the bHLH gene displayed a contrary downward trend in response to the supplements. ZnO NPs moderately stimulated the transcription of R2R3MYB. The HSF-34 gene was also exhibited a similar upward trend in response to the nano-supplements. Moreover, the ZnONP treatments mediated significant upregulation in the WRKY1 transcription factor. Furthermore, the MAPK1 gene displayed a similar upregulation trend in response to the supplements. The foliar application of ZnONP slightly upregulated transcription of the HDA3 gene, while this gene showed a contrary slight downregulation trend in response to the supplementation of nutrient solution. The upregulation in the CAT gene also resulted from the nano-supplements. The concentrations of photosynthetic pigments exhibited an increasing trend in the ZnONP-treated seedlings. The applied treatments contributed to the upregulation in the activity of nitrate reductase and the increase in the proline concentrations. ZnO NPs induced the activity of antioxidant enzymes, including peroxidase and catalase by averages of 48.3% and 41%, respectively. The utilization of ZnO NPs mediated stimulation in the activity of phenylalanine ammonia-lyase and increase in soluble phenols. The findings further underline this view that the long-time application of ZnO NPs at low concentrations is a safe low-risk approach to meet agricultural requirements.

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Han, Eun-Soo, Florian L. Muller, Viviana I. Pérez, Wenbo Qi, Huiyun Liang, Liang Xi, Chunxiao Fu, et al. "The in vivo gene expression signature of oxidative stress." Physiological Genomics 34, no. 1 (June 2008): 112–26. http://dx.doi.org/10.1152/physiolgenomics.00239.2007.

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How higher organisms respond to elevated oxidative stress in vivo is poorly understood. Therefore, we measured oxidative stress parameters and gene expression alterations (Affymetrix arrays) in the liver caused by elevated reactive oxygen species induced in vivo by diquat or by genetic ablation of the major antioxidant enzymes CuZn-superoxide dismutase ( Sod1) and glutathione peroxidase-1 ( Gpx1). Diquat (50 mg/kg) treatment resulted in a significant increase in oxidative damage within 3–6 h in wild-type mice without any lethality. In contrast, treatment of Sod1−/− or Gpx1−/− mice with a similar concentration of diquat resulted in a significant increase in oxidative damage within an hour of treatment and was lethal, i.e., these mice are extremely sensitive to the oxidative stress generated by diquat. The expression response to elevated oxidative stress in vivo does not involve an upregulation of classic antioxidant genes, although long-term oxidative stress in Sod1−/− mice leads to a significant upregulation of thiol antioxidants (e.g., Mt1, Srxn1, Gclc, Txnrd1), which appears to be mediated by the redox-sensitive transcription factor Nrf2. The main finding of our study is that the common response to elevated oxidative stress with diquat treatment in wild-type, Gpx1−/−, and Sod1−/− mice and in untreated Sod1−/− mice is an upregulation of p53 target genes ( p21, Gdf15, Plk3, Atf3, Trp53inp1, Ddit4, Gadd45a, Btg2, Ndrg1). A retrospective comparison with previous studies shows that induction of these p53 target genes is a conserved expression response to oxidative stress, in vivo and in vitro, in different species and different cells/organs.

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Ghalaei, Abolfazl, Maryam Kay, Shiva Zarrinfam, Parisa Hoseinpour, Mehrdad Behmanesh, and Bahram M. Soltani. "Overexpressed in colorectal carcinoma gene (OCC-1) upregulation and APPL2 gene downregulation in breast cancer specimens." Molecular Biology Reports 45, no. 6 (September 14, 2018): 1889–95. http://dx.doi.org/10.1007/s11033-018-4336-z.

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Golalipour, Masoud, Frouzandeh Mahjoubi, and Mohammad Hossein Sanati. "Gene Dosage Is Not Responsible for the Upregulation of MRP1 Gene Expression in Adult Leukemia Patients." Archives of Medical Research 38, no. 3 (April 2007): 297–304. http://dx.doi.org/10.1016/j.arcmed.2006.10.016.

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Avdic, Selmir, Brian P. McSharry, Megan Steain, Emma Poole, John Sinclair, Allison Abendroth, and Barry Slobedman. "Human Cytomegalovirus-Encoded Human Interleukin-10 (IL-10) Homolog Amplifies Its Immunomodulatory Potential by Upregulating Human IL-10 in Monocytes." Journal of Virology 90, no. 8 (January 20, 2016): 3819–27. http://dx.doi.org/10.1128/jvi.03066-15.

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ABSTRACTThe human cytomegalovirus (HCMV) gene UL111A encodes cytomegalovirus-encoded human interleukin-10 (cmvIL-10), a homolog of the potent immunomodulatory cytokine human interleukin 10 (hIL-10). This viral homolog exhibits a range of immunomodulatory functions, including suppression of proinflammatory cytokine production and dendritic cell (DC) maturation, as well as inhibition of major histocompatibility complex (MHC) class I and class II. Here, we present data showing that cmvIL-10 upregulates hIL-10, and we identify CD14+monocytes and monocyte-derived macrophages and DCs as major sources of hIL-10 secretion in response to cmvIL-10. Monocyte activation was not a prerequisite for cmvIL-10-mediated upregulation of hIL-10, which was dose dependent and controlled at the transcriptional level. Furthermore, cmvIL-10 upregulated expression of tumor progression locus 2 (TPL2), which is a regulator of the positive hIL-10 feedback loop, whereas expression of a negative regulator of the hIL-10 feedback loop, dual-specificity phosphatase 1 (DUSP1), remained unchanged. Engagement of the hIL-10 receptor (hIL-10R) by cmvIL-10 led to upregulation of heme oxygenase 1 (HO-1), an enzyme linked with suppression of inflammatory responses, and this upregulation was required for cmvIL-10-mediated upregulation of hIL-10. We also demonstrate an important role for both phosphatidylinositol 3-kinase (PI3K) and STAT3 in the upregulation of HO-1 and hIL-10 by cmvIL-10. In addition to upregulating hIL-10, cmvIL-10 could exert a direct immunomodulatory function, as demonstrated by its capacity to upregulate expression of cell surface CD163 when hIL-10 was neutralized. This study identifies a mechanistic basis for cmvIL-10 function, including the capacity of this viral cytokine to potentially amplify its immunosuppressive impact by upregulating hIL-10 expression.IMPORTANCEHuman cytomegalovirus (HCMV) is a large, double-stranded DNA virus that causes significant human disease, particularly in the congenital setting and in solid-organ and hematopoietic stem cell transplant patients. A prominent feature of HCMV is the wide range of viral gene products that it encodes which function to modulate host defenses. One of these is cmvIL-10, which is a homolog of the potent immunomodulatory cytokine human interleukin 10 (hIL-10). In this study, we report that, in addition to exerting a direct biological impact, cmvIL-10 upregulates the expression of hIL-10 by primary blood-derived monocytes and that it does so by modulating existing cellular pathways. This capacity of cmvIL-10 to upregulate hIL-10 represents a mechanism by which HCMV may amplify its immunomodulatory impact during infection.

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Su, Dongmei, Sun Jing, Lina Guan, Qian Li, Huiling Zhang, Xiaobo Gao, and Xu Ma. "Role of Nodal–PITX2C signaling pathway in glucose-induced cardiomyocyte hypertrophy." Biochemistry and Cell Biology 92, no. 3 (June 2014): 183–90. http://dx.doi.org/10.1139/bcb-2013-0124.

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Pathological cardiac hypertrophy is a major cause of morbidity and mortality in cardiovascular disease. Recent studies have shown that cardiomyocytes, in response to high glucose (HG) stimuli, undergo hypertrophic growth. While much work still needs to be done to elucidate this important mechanism of hypertrophy, previous works have showed that some pathways or genes play important roles in hypertrophy. In this study, we showed that sublethal concentrations of glucose (25 mmol/L) could induce cardiomyocyte hypertrophy with an increase in the cellular surface area and the upregulation of the atrial natriuretic peptide (ANP) gene, a hypertrophic marker. High glucose (HG) treatments resulted in the upregulation of the Nodal gene, which is under-expressed in cardiomyocytes. We also determined that the knockdown of the Nodal gene resisted HG-induced cardiomyocyte hypertrophy. The overexpression of Nodal was able to induce hypertrophy in cardiomyocytes, which was associated with the upregulation of the PITX2C gene. We also showed that increases in the PITX2C expression, in response to Nodal, were mediated by the Smad4 signaling pathway. This study is highly relevant to the understanding of the effects of the Nodal–PITX2C pathway on HG-induced cardiomyocyte hypertrophy, as well as the related molecular mechanisms.

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