Identification of an interaction network of Arabidopsis transcription factors and MAP kinases involved in chitin signaling and pathogen defense

2012 ◽  
Author(s):  
Geon Hui Son
Keyword(s):  
Transcription Factors ◽  
Map Kinases ◽  
Interaction Network ◽  
Pathogen Defense

scholarly journals Transcriptome Analysis of Hypertrophic Heart Tissues from Murine Transverse Aortic Constriction and Human Aortic Stenosis Reveals Key Genes and Transcription Factors Involved in Cardiac Remodeling Induced by Mechanical Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Peng Yu ◽  
Baoli Zhang ◽  
Ming Liu ◽  
Ying Yu ◽  
Ji Zhao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Aortic Stenosis ◽  
Mechanical Stress ◽  
Cardiac Remodeling ◽  
Interaction Network ◽  
Cytokine Signaling ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Genomic Changes

Background. Mechanical stress-induced cardiac remodeling that results in heart failure is characterized by transcriptional reprogramming of gene expression. However, a systematic study of genomic changes involved in this process has not been performed to date. To investigate the genomic changes and underlying mechanism of cardiac remodeling, we collected and analyzed DNA microarray data for murine transverse aortic constriction (TAC) and human aortic stenosis (AS) from the Gene Expression Omnibus database and the European Bioinformatics Institute. Methods and Results. The differential expression genes (DEGs) across the datasets were merged. The Venn diagrams showed that the number of intersections for early and late cardiac remodeling was 74 and 16, respectively. Gene ontology and protein–protein interaction network analysis showed that metabolic changes, cell differentiation and growth, cell cycling, and collagen fibril organization accounted for a great portion of the DEGs in the TAC model, while in AS patients’ immune system signaling and cytokine signaling displayed the most significant changes. The intersections between the TAC model and AS patients were few. Nevertheless, the DEGs of the two species shared some common regulatory transcription factors (TFs), including SP1, CEBPB, PPARG, and NFKB1, when the heart was challenged by applied mechanical stress. Conclusions. This study unravels the complex transcriptome profiles of the heart tissues and highlighting the candidate genes involved in cardiac remodeling induced by mechanical stress may usher in a new era of precision diagnostics and treatment in patients with cardiac remodeling.

scholarly journals Targeting of p38 Mitogen-Activated Protein Kinases to MEF2 Transcription Factors

1999 ◽  
Vol 19 (6) ◽  
pp. 4028-4038 ◽  
Author(s):  
Shen-Hsi Yang ◽  
Alex Galanis ◽  
Andrew D. Sharrocks
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activation ◽  
Cellular Response ◽  
Map Kinases ◽  
Biological Response ◽  
Extracellular Signals ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

ABSTRACT Mitogen-activated protein (MAP) kinase-mediated signalling to the nucleus is an important event in the conversion of extracellular signals into a cellular response. However, the existence of multiple MAP kinases which phosphorylate similar phosphoacceptor motifs poses a problem in maintaining substrate specificity and hence the correct biological response. Both the extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) subfamilies of MAP kinases use a second specificity determinant and require docking to their transcription factor substrates to achieve maximal substrate activation. In this study, we demonstrate that among the different MAP kinases, the MADS-box transcription factors MEF2A and MEF2C are preferentially phosphorylated and activated by the p38 subfamily members p38α and p38β2. The efficiency of phosphorylation in vitro and transcriptional activation in vivo of MEF2A and MEF2C by these p38 subtypes requires the presence of a kinase docking domain (D-domain). Furthermore, the D-domain from MEF2A is sufficient to confer p38 responsiveness on different transcription factors, and reciprocal effects are observed upon the introduction of alternative D-domains into MEF2A. These results therefore contribute to our understanding of signalling to MEF2 transcription factors and demonstrate that the requirement for substrate binding by MAP kinases is an important facet of three different subclasses of MAP kinases (ERK, JNK, and p38).

scholarly journals MicroRNA-based regulation of genomics and transcriptomics of inflammatory cytokines in COVID-19

2021 ◽  
Author(s):  
Manoj Khokhar ◽  
Sojit Tomo ◽  
Purvi Purohit
Keyword(s):  
Transcription Factors ◽  
Inflammatory Response ◽  
In Silico ◽  
Wide Spectrum ◽  
Interaction Network ◽  
In Silico Analysis ◽  
Enrichment Analysis ◽  
Microarray Dataset ◽  
Therapeutic Strategies ◽  
Protein Protein Interaction

Background: Coronavirus disease 2019 is characterized by the elevation of a wide spectrum of inflammatory mediators which are associated with poor disease outcomes. We aimed at an in-silico analysis of regulatory microRNA and their transcription factors (TF) for these inflammatory genes that may help to devise potential therapeutic strategies in the future. Methods: The cytokine regulating immune-expressed genes (CRIEG) were sorted from literature and GEO microarray dataset and their co-differentially expressed miRNA and transcription factors were predicted from publicly available databases. Enrichment analysis was done through mienturnet, MiEAA, and Gene Ontology, and pathways predicted by KEGG and Reactome pathways. The functional and regulatory features were analyzed and visualized through Cytoscape. Results: Sixteen CRIEG were observed to have a significant protein-protein interaction network. The ontological analysis revealed significantly enriched pathways for biological processes, molecular functions, and cellular components. The search performed in the miRNA database yielded 10 miRNAs that are significantly involved in the regulation of these genes and their transcription factors. Conclusion: An In-Silico representation of a network involving miRNAs, CRIEGs, and TF which take part in the inflammatory response in COVID-19 has been elucidated. These regulatory factors may have potentially critical roles in the inflammatory response in COVID-19 and may be explored further for the development of targeted therapeutic strategies and mechanistic validation.

scholarly journals Genome-Wide Identification, Expression Analysis, and Subcellular Localization of Carthamus tinctorius bHLH Transcription Factors

2019 ◽  
Vol 20 (12) ◽  
pp. 3044 ◽  
Author(s):  
Yingqi Hong ◽  
Naveed Ahmad ◽  
Yuanyuan Tian ◽  
Jianyu Liu ◽  
Liyan Wang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Subcellular Localization ◽  
Expression Analysis ◽  
Interaction Network ◽  
Carthamus Tinctorius ◽  
Protein Motifs ◽  
Quantitative Expression ◽  
Helix Loop Helix ◽  
Genome Wide ◽  
Bhlh Genes

The basic helix–loop–helix (bHLH) family is the second largest superfamily of transcription factors that belongs to all three eukaryotic kingdoms. The key function of this superfamily is the regulation of growth and developmental mechanisms in plants. However, the bHLH gene family in Carthamus tinctorius has not yet been studied. Here, we identified 41 bHLH genes in Carthamus tinctorius that were classified into 23 subgroups. Further, we conducted a phylogenetic analysis and identified 10 conserved protein motifs found in the safflower bHLH family. We comprehensively analyzed a group of bHLH genes that could be associated with flavonoid biosynthesis in safflower by gene expression analysis, gene ontology annotation, protein interaction network prediction, subcellular localization of the candidate CtbHLH40 gene, and real-time quantitative expression analysis. This study provides genome-wide identification of the genes related to biochemical and physiological processes in safflower.

MAP kinases and the adaptive response to hypertonicity: functional preservation from yeast to mammals

2004 ◽  
Vol 287 (6) ◽  
pp. F1102-F1110 ◽  
Author(s):  
David Sheikh-Hamad ◽  
Michael C. Gustin
Keyword(s):  
Transcription Factors ◽  
Signaling Pathways ◽  
Adaptive Response ◽  
Mammalian Cells ◽  
Map Kinases ◽  
Current Knowledge ◽  
Cis Elements ◽  
P38 Kinase ◽  
Functional Preservation ◽  
Multiple Signaling

The adaptation to hypertonicity in mammalian cells is driven by multiple signaling pathways that include p38 kinase, Fyn, the catalytic subunit of PKA, ATM, and JNK2. In addition to the well-characterized tonicity enhancer (TonE)-TonE binding protein interaction, other transcription factors (and their respective cis elements) can potentially respond to hypertonicity. This review summarizes the current knowledge about the signaling pathways that regulate the adaptive response to osmotic stress and discusses new insights from yeast that could be relevant to the osmostress response in mammals.

scholarly journals Signaling through P2X7 Receptor in Human T Cells Involves p56lck, MAP Kinases, and Transcription Factors AP-1 and NF-κB

2002 ◽  
Vol 278 (3) ◽  
pp. 1549-1560 ◽  
Author(s):  
Vadim Budagian ◽  
Elena Bulanova ◽  
Luba Brovko ◽  
Zane Orinska ◽  
Raja Fayad ◽  
...  
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
P2x7 Receptor ◽  
Map Kinases ◽  
Human T Cells

scholarly journals Identification of hydatidosis-related modules and key regulatory genes

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9280
Author(s):  
Jijun Song ◽  
Mingxin Song
Keyword(s):  
Transcription Factors ◽  
Signaling Pathway ◽  
Target Genes ◽  
Expression Profiles ◽  
Differential Expression Analysis ◽  
Interaction Network ◽  
Enrichment Analysis ◽  
Bmp Signaling ◽  
Differentially Expressed ◽  
Regulatory Effects

Background Echinococcosis caused by larval of Echinococcus is prevalent all over the world. Although clinical experience showed that the presence of tapeworms could not be found in liver lesions, the repeated infection and aggravation of lesions still occur in the host. Here, this study constructed a multifactor-driven disease-related dysfunction network to explore the potential molecular pathogenesis mechanism in different hosts after E.multilocularis infection. Method First, iTRAQ sequencing was performed on human liver infected with E.multilocularis. Second, obtained microRNAs(miRNAs) expression profiles of humans and canine infected with Echinococcus from the GEO database. In addition, we also performed differential expression analysis, protein interaction network analysis, enrichment analysis, and crosstalk analysis to obtain genes and modules related to E.multilocularis infection. Pivot analysis is used to calculate the potential regulatory effects of multiple factors on the module and identify related non-coding RNAs(ncRNAs) and transcription factors(TFs). Finally, we screened the target genes of miRNAs of Echinococcus to further explore its infection mechanism. Results A total of 267 differentially expressed proteins from humans and 3,635 differentially expressed genes from canine were obtained. They participated in 16 human-related dysfunction modules and five canine-related dysfunction modules, respectively. Both human and canine dysfunction modules are significantly involved in BMP signaling pathway and TGF-beta signaling pathway. In addition, pivot analysis found that 1,129 ncRNAs and 110 TFs significantly regulated human dysfunction modules, 158 ncRNAs and nine TFs significantly regulated canine dysfunction modules. Surprisingly, the Echinococcus miR-184 plays a role in the pathogenicity regulation by targeting nine TFs and one ncRNA in humans. Similarly, miR-184 can also cause physiological dysfunction by regulating two transcription factors in canine. Conclusion The results show that the miRNA-184 of Echinococcus can regulate the pathogenic process through various biological functions and pathways. The results laid a solid theoretical foundation for biologists to further explore the pathogenic mechanism of Echinococcosis.

scholarly journals Expression Patterns of MYB (V-myb Myeloblastosis Viral Oncogene Homolog) Gene Family in Resistant and Susceptible Tung Trees Responding to Fusarium Wilt Disease

Forests ◽  
2019 ◽  
Vol 10 (2) ◽  
pp. 193
Author(s):  
Xue Wang ◽  
Qiyan Zhang ◽  
Ming Gao ◽  
Liwen Wu ◽  
Yangdong Wang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Fusarium Wilt ◽  
Expression Patterns ◽  
Interaction Network ◽  
Wilt Disease ◽  
Tung Oil ◽  
Viral Oncogene ◽  
Fusarium Wilt Disease ◽  
High Interaction ◽  
Viral Oncogene Homolog

Vernicia fordii (tung oil tree) is famous in the world for its production of tung oil. Unfortunately, it was infected by the soil-borne fungus Fusarium oxysporum f. sp. fordii 1 (Fof-1) and suffered serious wilt disease. Conversely, its sister species V. montana is highly resistant to Fof-1. The MYB (v-myb myeloblastosis viral oncogene homolog) transcription factors were activated during the pathogen Fof-1 infection according to our previous comparative transcriptomic results. Depending on whether the sequence has a complete MYB-DNA-binding domain, a total of 75 VfMYB and 77 VmMYB genes were identified in susceptible V. fordii and resistant V. montana, respectively. In addition, we detected 49 pairs of one-to-one orthologous Vf/VmMYB genes with the reciprocal-best BLAST-hits (RBH)method. In order to investigate the expression modes and the internal network of MYB transcription factors in the two species responding to Fusarium wilt disease, the expressions of Vf/VmMYBs were then investigated and we found that most orthologous Vf/VmMYB genes exhibited similar expression patterns during the Fof-1 infection. However, four pairs of Vf/VmMYB genes, annotated as unknown proteins and mediator of root architecture, demonstrated absolute opposite expression patterns in the two Vernicia species responding to Fof-1. The interaction network of VmMYB genes were further constructed using weighted gene co-expression network analysis (WGCNA) method and four hub genes showing extremely high interaction with the other 1157 genes were identified. RT-qPCR result verified the opposite expression pattern of the hub gene VmMYB011 and VmMYB041 in two Vernicia species. In summary, co-expression network of the Vf/VmMYBs and significantly opposite related pairs of genes in resistant and susceptible Vernicia species provided knowledge for understanding the molecular basis of Vernicia responding to Fusarium wilt disease.

scholarly journals Network Analysis Identifies Gene Regulatory Network Indicating the Role of RUNX1 in Human Intervertebral Disc Degeneration

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 771 ◽  
Author(s):  
Nazir M. Khan ◽  
Martha E Diaz-Hernandez ◽  
Steven M. Presciutti ◽  
Hicham Drissi
Keyword(s):  
Transcription Factors ◽  
Network Analysis ◽  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Regulatory Network ◽  
Interaction Network ◽  
Functional Enrichment ◽  
Network Cluster ◽  
Chemokine Signaling

Intervertebral disc (IVD) degeneration (IDD) is a multifactorial physiological process which is often associated with lower back pain. Previous studies have identified some molecular markers associated with disc degeneration, which despite their significant contributions, have provided limited insight into the etiology of IDD. In this study, we utilized a network medicine approach to uncover potential molecular mediators of IDD. Our systematic analyses of IDD associated with 284 genes included functional annotation clustering, interaction networks, network cluster analysis and Transcription factors (TFs)-target gene network analysis. The functional enrichment and protein–protein interaction network analysis highlighted the role of inflammatory genes and cytokine/chemokine signaling in IDD. Moreover, sub-network analysis identified significant clusters possessing organized networks of 24 cytokine and chemokine genes, which may be considered as key modulators for IDD. The expression of these genes was validated in independent microarray datasets. In addition, the regulatory network analysis identified the role of multiple transcription factors, with RUNX1 being a master regulator in the pathogenesis of IDD. Our analyses highlighted the role of cytokine genes and interacting pathways in IDD and further improved our understanding of the genetic mechanisms underlying IDD.

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