scholarly journals An FF Domain-Dependent Protein Interaction Mediates a Signaling Pathway for Growth Factor-Induced Gene Expression

2005 ◽  
Vol 17 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Wei Jiang ◽  
Raffaella Sordella ◽  
Guang-Chao Chen ◽  
Shweta Hakre ◽  
Ananda L. Roy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Protein Interaction ◽  
Dependent Protein

scholarly journals Integrating Gene Expression and Protein Interaction Data for Signaling Pathway Prediction of Alzheimer’s Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Kong ◽  
Jingmao Zhang ◽  
Xiaoyang Mou ◽  
Yang Yang
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathway ◽  
Protein Interaction ◽  
Biological Information ◽  
Significant Advance ◽  
Protein Interaction Data ◽  
Transcriptional Level ◽  
Inflammatory Factor

Discovering the signaling pathway and regulatory network would provide significant advance in genome-wide understanding of pathogenesis of human diseases. Despite the rich transcriptome data, the limitation for microarray data is unable to detect changes beyond transcriptional level and insufficient in reconstructing pathways and regulatory networks. In our study, protein-protein interaction (PPI) data is introduced to add molecular biological information for predicting signaling pathway of Alzheimer’s disease (AD). Combining PPI with gene expression data, significant genes are selected by modified linear regression model firstly. Then, according to the biological researches that inflammation reaction plays an important role in the generation and deterioration of AD, NF-κB (nuclear factor-kappa B), as a significant inflammatory factor, has been selected as the beginning gene of the predicting signaling pathway. Based on that, integer linear programming (ILP) model is proposed to reconstruct the signaling pathway between NF-κB and AD virulence gene APP (amyloid precursor protein). The results identify 6 AD virulence genes included in the predicted inflammatory signaling pathway, and a large amount of molecular biological analysis shows the great understanding of the underlying biological process of AD.

scholarly journals Identification of Immune-Related Risk Signatures for the Prognostic Prediction in Oral Squamous Cell Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Chen Zou ◽  
Dahong Huang ◽  
Haigang Wei ◽  
Siyuan Wu ◽  
Jing Song ◽  
...  
Keyword(s):  
Gene Expression ◽  
Squamous Cell Carcinoma ◽  
Growth Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Signaling Pathway ◽  
Immune Cell ◽  
Risk Group ◽  
Growth Factor Receptor ◽  
Immune Cell Infiltration ◽  
Related Risk

Background. Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, which remains a major cause of morbidity and mortality in patients with head and neck cancers. However, the critical immune-related signatures and their prognostic values have rarely been investigated. Materials and Methods. Gene differential analysis was used to measure the differences of gene expression between the groups. Correlation analysis was used to assess the association between the gene expression levels and immune-related risk score/DNA methylation levels. The gene set enrichment analysis (GSEA) was used to identify the pathways or cell types enriched by those identified differentially expressed genes (DEGs). Results. In this study, we identified four immune-related gene signatures, including CTSG, TNFRSF4, LCORL, and PLAU, that were significantly associated with the overall survival in OSCC patients from the Cancer Genome Atlas (TCGA) OSCC cohort. Moreover, these four immune-related signatures were differentially expressed between the OSCC and nontumor tissues. The two groups (high and low risk) stratified by the immune-related risk scores had significantly different OS and mortality rates. The gene expression patterns and prognostic values of these immune-related signatures were also verified in two independent validation cohorts. Furthermore, the downregulated genes in the high-risk group (which were also upregulated in the low-risk group) were significantly enriched in the cell type-specific signatures of type 2 T helper cell (Th2), plasmacytoid dendritic cell (pDC), and memory B cell. In contrast, the upregulated genes in the high-score group were enriched in growth factor receptor-related signaling pathways, such as the VEGFA-VEGFR2 signaling pathway, PI3K-Akt signaling pathway, focal adhesion-PI3K-Akt-mTOR signaling pathway, and PDGF pathway, suggesting that those pathways were inversely correlated with immune cell infiltration. Conclusion. In summary, the immune-related signatures had the potential for predicting the risk of OSCC patients. Moreover, the present study also improved our understanding of the association between the growth factor receptor pathways and immune cell infiltration in OSCC.

scholarly journals Growth Factor-specific Signaling Pathway Stimulation and Gene Expression Mediated by ErbB Receptors

2001 ◽  
Vol 276 (25) ◽  
pp. 22685-22698 ◽  
Author(s):  
Colleen Sweeney ◽  
Douglas Fambrough ◽  
Christine Huard ◽  
A. John Diamonti ◽  
Eric S. Lander ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Erbb Receptors ◽  
Specific Signaling Pathway

scholarly journals WNT signaling is required for peritoneal membrane angiogenesis

2018 ◽  
Vol 314 (6) ◽  
pp. F1036-F1045 ◽  
Author(s):  
Manreet Padwal ◽  
Genyang Cheng ◽  
Limin Liu ◽  
Felix Boivin ◽  
Azim S. Gangji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Wnt Signaling ◽  
Solute Transport ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Peritoneal Membrane ◽  
Peritoneal Fibrosis ◽  
Membrane Injury ◽  
Mesenchymal Transition

The wingless-type mouse mammary tumor virus integration site family (WNT) signaling pathway is involved in wound healing and fibrosis. We evaluated the WNT signaling pathway in peritoneal membrane injury. We assessed WNT1 protein expression in the peritoneal effluents of 54 stable peritoneal dialysis (PD) patients and WNT-related gene expression in ex vivo mesothelial cell cultures from 21 PD patients. In a transforming growth factor-β (TGF-β)-mediated animal model of peritoneal fibrosis, we evaluated regulation of the WNT pathway and the effect of WNT inhibition on peritoneal fibrosis and angiogenesis. WNT1 and WNT2 gene expression were positively correlated with peritoneal membrane solute transport in PD patients. In the mouse peritoneum, TGF-β-induced peritoneal fibrosis was associated with increased expression of WNT2 and WNT4. Peritoneal β-catenin protein was significantly upregulated after infection with adenovirus expressing TGF-β (AdTGF-β) along with elements of the WNT signaling pathway. Treatment with a β-catenin inhibitor (ICG-001) in mice with AdTGF-β-induced peritoneal fibrosis resulted in attenuation of peritoneal angiogenesis and reduced vascular endothelial growth factor. Similar results were also observed with the WNT antagonist Dickkopf-related protein (DKK)-1. In addition to this, DKK-1 blocked epithelial-mesenchymal transition and increased levels of the cell adhesion protein E-cadherin. We provide evidence that WNT signaling is active in the setting of experimental peritoneal fibrosis and WNT1 correlates with patient peritoneal membrane solute transport in PD patients. Intervention in this pathway is a possible therapy for peritoneal membrane injury.

scholarly journals Exercise-induced modification of the skeletal muscle transcriptome in Arabian horses

2017 ◽  
Vol 49 (6) ◽  
pp. 318-326 ◽  
Author(s):  
Katarzyna Ropka-Molik ◽  
Monika Stefaniuk-Szmukier ◽  
Kacper Z˙ukowski ◽  
Katarzyna Piórkowska ◽  
Monika Bugno-Poniewierska
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Fatty Acid ◽  
Growth Factor ◽  
Calcium Signaling ◽  
Signaling Pathway ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Skeletal Muscle Transcriptome

It has been found that Arabian and Thoroughbred horses differ in muscle fiber structure and thus in physiological changes occurring in muscles during exercise. The aim of the present study was to identify the global gene expression modifications that occur in skeletal muscle following a training regime to prepare for flat racing. Whole transcriptomes of muscle (gluteus medius) were compared between three time points of tissue collection: T0 (untrained horses), T1 (horses after intense gallop phase), and T2 (horses at the end of racing season), 23 samples in total. The numerous groups of exercise-regulated differentially expressed genes (DEGs) were related to muscle cell structure and signaling and included insulin-like growth factor 1 receptor ( IGF1R), insulin receptor ( INSR), transforming growth factor beta receptors 1 and 2 ( TGFBR1, TGFBR2), vascular endothelial growth factor B ( VEGFB); epidermal growth factor ( EGF), hepatocyte growth factor ( HGF), and vascular endothelial growth factor D ( FIGF). In Arabian horses, exercise modified the expression of genes belonging to the PPAR signaling pathway (e.g., PPARA, PPARD, and PLIN2), calcium signaling pathway, and pathways associated with metabolic processes (e.g., oxidative phosphorylation, fatty acid metabolism, glycolysis/gluconeogenesis, and citrate cycle). According to detected gene expression modifications, our results suggested that in Arabian horses, exercise switches energy generation toward fatty acid utilization and enhances glycogen transport and calcium signaling. The use of the RNA-Seq approach in analyzing the skeletal muscle transcriptome allowed for the proposal of a panel of new candidate genes potentially related to body homeostasis maintenance and racing performance in Arabian horses.

scholarly journals Identification of the possible therapeutic targets in the insulin-like growth factor 1 receptor pathway in a cohort of Egyptian hepatocellular carcinoma complicating chronic hepatitis C type 4

2020 ◽  
Vol 14 (1) ◽  
pp. 1-11
Author(s):  
Nada M.K. Mabrouk ◽  
Dalal M. Elkaffash ◽  
Mona Abdel-Hadi ◽  
Salah-ElDin Abdelmoneim ◽  
Sameh Saad ElDeen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pathway Analysis ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Insulin Like Growth Factor ◽  
Tumor Characteristics

Background: Molecular targeted drugs are the first line of treatment of advanced hepatocellular carcinoma (HCC) due to its chemo- and radioresistant nature. HCC has several well-documented etiologic factors that drive hepatocarcinogenesis through different molecular pathways. Currently, hepatitis C virus (HCV) is a leading cause of HCC. Therefore, we included a unified cohort of HCV genotype 4-related HCCs to study the expression levels of genes involved in the insulin-like growth factor 1 receptor (IGF1R) pathway, which is known to be involved in all aspects of cancer growth and progression. Aim: Determine the gene expression patterns of IGF1R pathway genes in a cohort of Egyptian HCV-related HCCs. Correlate them with different patient/tumor characteristics. Determine the activity status of involved pathways. Methods: Total ribonucleic acid (RNA) was extracted from 32 formalin-fixed paraffin-embedded tissues of human HCV-related HCCs and 6 healthy liver donors as controls. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) using RT2 Profiler PCR Array for Human Insulin Signaling Pathway was done to determine significantly up- and downregulated genes with identification of most frequently coregulated genes, followed by correlation of gene expression with different patient/tumor characteristics. Finally, canonical pathway analysis was performed using the Ingenuity Pathway Analysis software. Results: Six genes – AEBP1, AKT2, C-FOS, PIK3R1, PRKCI, SHC1 – were significantly overexpressed. Thirteen genes – ADRB3, CEBPA, DUSP14, ERCC1, FRS3, IGF2, INS, IRS1, JUN, MTOR, PIK3R2, PPP1CA, RPS6KA1 – were significantly underexpressed. Several differentially expressed genes were related to different tumor/patient characteristics. Nitric oxide and reactive oxygen species production pathway was significantly activated in the present cohort, while the growth hormone signaling pathway was inactive. Conclusions: The gene expression patterns identified in this study may serve as possible therapeutic targets in HCV-related HCCs. The most frequently coregulated genes may serve to guide combined molecular targeted therapies. The IGF1R pathway showed evidence of inactivity in the present cohort of HCV-related HCCs, so targeting this pathway in therapy may not be effective.

scholarly journals Dexamethasone-induced intrauterine growth restriction impacts the placental prolactin family, insulin-like growth factor-II and the Akt signaling pathway

2005 ◽  
Vol 185 (2) ◽  
pp. 253-263 ◽  
Author(s):  
Rupasri Ain ◽  
Lindsey N Canham ◽  
Michael J Soares
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Intrauterine Growth Restriction ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Placental Development ◽  
Junctional Zone ◽  
Intrauterine Growth ◽  
Factor Ii

Intrauterine growth restriction (IUGR) is a major cause of perinatal death and neonatal morbidity and mortality. There are numerous causes of IUGR. Glucocorticoid-induced IUGR is highly relevant because administration of synthetic glucocorticoids, principally dexamethasone, to women threatened by premature labor is widely used in clinical practice. Fetal growth is directly related to placental growth and development. In this report, we analyzed the effect of dexamethasone on placental development in the rat. Dexamethasone administered between days 13 and 20 of pregnancy not only induced IUGR but also decreased placental mass by approximately 50%. Impaired placental development was associated with dysregulated placental prolactin (PRL) family and insulin-like growth factor-II (IGF-II) gene expression. Furthermore, there was a significant decrease in the activation of Akt/protein kinase B in the junctional zone of the placenta, as assessed by the phosphorylation status of Akt and the pro-apoptotic protein BAD, a downstream target of the Akt signaling pathway. Such changes are consistent with increases in indices of apoptosis, including increased cleavage of poly(ADP-ribose) polymerase (PARP) in the junctional zone of the placenta of dexamethasone-treated rats. In summary, dexamethasone-induced IUGR is associated with placental insufficiency, including dysregulated placental hormone/cytokine gene expression and down-regulation of the IGF-II/Akt signaling pathway resulting in increases in indices of placental apoptosis.

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