scholarly journals Network of microRNA, transcription factors, target genes and host genes in human mesothelioma

2017 ◽  
Vol 13 (6) ◽  
pp. 3039-3046 ◽  
Author(s):  
Guanhua Zhang ◽  
Zhiwen Xu ◽  
Ning Wang
Keyword(s):  
Transcription Factors ◽  
Target Genes ◽  
Host Genes

scholarly journals The network of microRNAs, transcription factors, target genes and host genes in human renal cell carcinoma

2014 ◽  
Vol 9 (1) ◽  
pp. 498-506 ◽  
Author(s):  
CHENGLU SONG ◽  
ZHIWEN XU ◽  
YUE JIN ◽  
MINGHUI ZHU ◽  
KUNHAO WANG ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Transcription Factors ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Target Genes ◽  
Human Renal Cell Carcinoma ◽  
Host Genes

scholarly journals Network analysis of microRNAs, transcription factors, target genes and host genes in human anaplastic astrocytoma

2016 ◽  
Vol 12 (1) ◽  
pp. 437-444 ◽  
Author(s):  
LUCHEN XUE ◽  
ZHIWEN XU ◽  
KUNHAO WANG ◽  
NING WANG ◽  
XIAOXU ZHANG ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Network Analysis ◽  
Anaplastic Astrocytoma ◽  
Target Genes ◽  
Host Genes

scholarly journals Regulatory Network of MicroRNAs, Target Genes, Transcription Factors and Host Genes in Endometrial Cancer

2015 ◽  
Vol 16 (2) ◽  
pp. 475-483 ◽  
Author(s):  
Lu-Chen Xue ◽  
Zhi-Wen Xu ◽  
Kun-Hao Wang ◽  
Ning Wang ◽  
Xiao-Xu Zhang ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Transcription Factors ◽  
Regulatory Network ◽  
Target Genes ◽  
Host Genes

scholarly journals Network analysis of microRNAs, transcription factors, target genes and host genes in nasopharyngeal carcinoma

2016 ◽  
Vol 11 (6) ◽  
pp. 3821-3828 ◽  
Author(s):  
HAO WANG ◽  
ZHIWEN XU ◽  
MENGYAO MA ◽  
NING WANG ◽  
KUNHAO WANG
Keyword(s):  
Transcription Factors ◽  
Network Analysis ◽  
Nasopharyngeal Carcinoma ◽  
Target Genes ◽  
Host Genes

scholarly journals Regulatory Network Analysis in Estradiol-Treated Human Endothelial Cells

2021 ◽  
Vol 22 (15) ◽  
pp. 8193
Author(s):  
Daniel Pérez-Cremades ◽  
Ana B. Paes ◽  
Xavier Vidal-Gómez ◽  
Ana Mompeón ◽  
Carlos Hermenegildo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Regulatory Network ◽  
Mirna Target ◽  
Target Genes ◽  
Functional Characterization ◽  
Human Endothelial Cells ◽  
Mrna Targets ◽  
Canonical Pathways

Background/Aims: Estrogen has been reported to have beneficial effects on vascular biology through direct actions on endothelium. Together with transcription factors, miRNAs are the major drivers of gene expression and signaling networks. The objective of this study was to identify a comprehensive regulatory network (miRNA-transcription factor-downstream genes) that controls the transcriptomic changes observed in endothelial cells exposed to estradiol. Methods: miRNA/mRNA interactions were assembled using our previous microarray data of human umbilical vein endothelial cells (HUVEC) treated with 17β-estradiol (E2) (1 nmol/L, 24 h). miRNA–mRNA pairings and their associated canonical pathways were determined using Ingenuity Pathway Analysis software. Transcription factors were identified among the miRNA-regulated genes. Transcription factor downstream target genes were predicted by consensus transcription factor binding sites in the promoter region of E2-regulated genes by using JASPAR and TRANSFAC tools in Enrichr software. Results: miRNA–target pairings were filtered by using differentially expressed miRNAs and mRNAs characterized by a regulatory relationship according to miRNA target prediction databases. The analysis identified 588 miRNA–target interactions between 102 miRNAs and 588 targets. Specifically, 63 upregulated miRNAs interacted with 295 downregulated targets, while 39 downregulated miRNAs were paired with 293 upregulated mRNA targets. Functional characterization of miRNA/mRNA association analysis highlighted hypoxia signaling, integrin, ephrin receptor signaling and regulation of actin-based motility by Rho among the canonical pathways regulated by E2 in HUVEC. Transcription factors and downstream genes analysis revealed eight networks, including those mediated by JUN and REPIN1, which are associated with cadherin binding and cell adhesion molecule binding pathways. Conclusion: This study identifies regulatory networks obtained by integrative microarray analysis and provides additional insights into the way estradiol could regulate endothelial function in human endothelial cells.

scholarly journals Role of Satb1 and Satb2 Transcription Factors in the Glutamate Receptors Expression and Ca2+ Signaling in the Cortical Neurons In Vitro

2021 ◽  
Vol 22 (11) ◽  
pp. 5968
Author(s):  
Egor A. Turovsky ◽  
Maria V. Turovskaya ◽  
Evgeniya I. Fedotova ◽  
Alexey A. Babaev ◽  
Viktor S. Tarabykin ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Nmda Receptor ◽  
Cortical Neurons ◽  
Target Genes ◽  
Cortical Cell ◽  
Inhibitory System ◽  
Selective Agonist ◽  
Genes Encoding ◽  
Deficient Mice

Transcription factors Satb1 and Satb2 are involved in the processes of cortex development and maturation of neurons. Alterations in the expression of their target genes can lead to neurodegenerative processes. Molecular and cellular mechanisms of regulation of neurotransmission by these transcription factors remain poorly understood. In this study, we have shown that transcription factors Satb1 and Satb2 participate in the regulation of genes encoding the NMDA-, AMPA-, and KA- receptor subunits and the inhibitory GABA(A) receptor. Deletion of gene for either Satb1 or Satb2 homologous factors induces the expression of genes encoding the NMDA receptor subunits, thereby leading to higher amplitudes of Ca2+-signals in neurons derived from the Satb1-deficient (Satb1fl/+ * NexCre/+) and Satb1-null mice (Satb1fl/fl * NexCre/+) in response to the selective agonist reducing the EC50 for the NMDA receptor. Simultaneously, there is an increase in the expression of the Gria2 gene, encoding the AMPA receptor subunit, thus decreasing the Ca2+-signals of neurons in response to the treatment with a selective agonist (5-Fluorowillardiine (FW)). The Satb1 deletion increases the sensitivity of the KA receptor to the agonist (domoic acid), in the cortical neurons of the Satb1-deficient mice but decreases it in the Satb1-null mice. At the same time, the Satb2 deletion decreases Ca2+-signals and the sensitivity of the KA receptor to the agonist in neurons from the Satb1-null and the Satb1-deficient mice. The Satb1 deletion affects the development of the inhibitory system of neurotransmission resulting in the suppression of the neuron maturation process and switching the GABAergic responses from excitatory to inhibitory, while the Satb2 deletion has a similar effect only in the Satb1-null mice. We show that the Satb1 and Satb2 transcription factors are involved in the regulation of the transmission of excitatory signals and inhibition of the neuronal network in the cortical cell culture.

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