The interaction of ASAH1 and NGF gene involving in neurotrophin signaling pathway contributes to schizophrenia susceptibility and psychopathology

2021 ◽  
Vol 104 ◽  
pp. 110015
Author(s):  
Yousong Su ◽  
Lu Yang ◽  
Zezhi Li ◽  
Weidi Wang ◽  
Mengjuan Xing ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neurotrophin Signaling ◽  
Schizophrenia Susceptibility ◽  
Ngf Gene

scholarly journals Identification of upregulated NF-κB inhibitor alpha and IRAK3 targeting lncRNA following intracranial aneurysm rupture-induced subarachnoid hemorrhage

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Leng ◽  
Dan Fan ◽  
Zhong Ren ◽  
Qiaoying Li
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Aneurysm ◽  
Signaling Pathway ◽  
Aneurysm Rupture ◽  
Cytokine Receptor ◽  
Gene Set Enrichment Analysis ◽  
Receptor Interaction ◽  
Regulatory Pathways ◽  
Ruptured Intracranial Aneurysm ◽  
Neurotrophin Signaling

Abstract Background This study was performed to identify genes and lncRNAs involved in the pathogenesis of subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysm (RIA). Methods Microarray GSE36791 was downloaded from Gene Expression Omnibus (GEO) database followed by the identification of significantly different expressed RNAs (DERs, including lncRNA and mRNA) between patients with SAH and healthy individuals. Then, the functional analyses of DEmRNAs were conducted and weighted gene co-expression network analysis (WGCNA) was also performed to extract the modules associated with SAH. Following, the lncRNA-mRNA co-expression network was constructed and the gene set enrichment analysis (GSEA) was performed to screen key RNA biomarkers involved in the pathogenesis of SAH from RIA. We also verified the results in a bigger dataset GSE7337. Results Totally, 561 DERs, including 25 DElncRNAs and 536 DEmRNAs, were identified. Functional analysis revealed that the DEmRNAs were mainly associated with immune response-associated GO-BP terms and KEGG pathways. Moreover, there were 6 modules significantly positive-correlated with SAH. The lncRNA-mRNA co-expression network contained 2 lncRNAs (LINC00265 and LINC00937) and 169 mRNAs. The GSEA analysis showed that these two lncRNAs were associated with three pathways (cytokine-cytokine receptor interaction, neurotrophin signaling pathway, and apoptosis). Additionally, IRAK3 and NFKBIA involved in the neurotrophin signaling pathway and apoptosis while IL1R2, IL18RAP and IL18R1 was associated with cytokine-cytokine receptor interaction pathway. The expression levels of these genes have the same trend in GSE36791 and GSE7337. Conclusion LINC00265 and LINC00937 may be implicated with the pathogenesis of SAH from RIA. They were involved in three important regulatory pathways. 5 mRNAs played important roles in the three pathways.

Identification of Potential Genes Associated with Vemurafenib Efficacy and Melanoma Prognosis

2021 ◽  
Vol 24 ◽  
Author(s):  
Yue Qi ◽  
GuiE Ma
Keyword(s):  
Signaling Pathway ◽  
Estrogen Signaling ◽  
Akt Signaling Pathway ◽  
Ppi Network ◽  
Hub Genes ◽  
Ampk Signaling ◽  
Melanoma Patients ◽  
Key Genes ◽  
Neurotrophin Signaling ◽  
Upregulated Genes

Objective: This work aimed to investigate the molecular mechanisms underlying the efficacy of vemurafenib as a treatment for melanoma. Methods: The GSE52882 dataset, which includes A375 and A2058 melanoma cell lines treated with vemurafenib and dimethyl sulfoxide (DMSO), and clinical information associated with melanoma patients, were acquired from the Gene Expression Omnibus (GEO) database and University of California Santa Cruz (UCSC), respectively. Functional enrichment analysis, protein-protein interaction (PPI) network construction, sub-module analysis, and transcriptional regulation analysis were performed on overlapping differentially expressed genes (DEGs) identified in both cell lines. Finally, we performed a survival analysis based on the genes identified. Results: A total of 447 consistently overlapping DEGs (176 up- and 271 down-regulated DEGs) were screened. Upregulated genes were enriched in pathways of neurotrophin signaling, estrogen signaling, and transcriptional misregulation in cancer. Downregulated DEGs played essential roles in melanogenesis, pathways of cancer, PI3K-Akt signaling pathway, and AMPK signaling pathway. Upregulated (MMP2, JUN, KAT28, and PIK3R3) and downregulated genes (CXCL8, CCND1, IGF1R, and ITGB3) were considered as hub genes in the PPI network. Additionally, PIK3R3 and LEF1 served as key genes in the regulatory network. The overexpression of MMP2 and CXCL8 was associated with a poor prognosis in melanoma patients. Results: A total of 447 consistently overlapping DEGs (176 up- and 271 down-regulated DEGs) were screened. Upregulated genes were enriched in pathways of neurotrophin signaling, estrogen signaling, and transcriptional misregulation in cancer. Downregulated DEGs played essential roles in melanogenesis, pathways of cancer, PI3K-Akt signaling pathway, and AMPK signaling pathway. Upregulated (MMP2, JUN, KAT28, and PIK3R3) and downregulated genes (CXCL8, CCND1, IGF1R, and ITGB3) were considered as hub genes in the PPI network. Additionally, PIK3R3 and LEF1 served as key genes in the regulatory network. The overexpression of MMP2 and CXCL8 was associated with a poor prognosis in melanoma patients. Conclusion: MMP2, CXCL8, PIK3R3, ITGB3, and LEF1 may play roles in the efficacy of vemurafenib treatment in melanoma; for example, MMP2 and PIK3R3 are likely associated with vemurafenib resistance. These findings will contribute to the development of novel therapies for melanoma.

USF1 Promotes Lung Adenocarcinoma Progression by Regulating Neurotrophin Signaling Pathway

2021 ◽  
Author(s):  
Yu Wang ◽  
Yunxia Zhao ◽  
Xiangwei Zhang ◽  
Yuanzhu Jiang ◽  
Wei Ma ◽  
...  
Keyword(s):  
Mouse Model ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Expression Level ◽  
Migration And Invasion ◽  
Cellular Viability ◽  
Invasion Potential ◽  
Clinical Records ◽  
Neurotrophin Signaling ◽  
Related Proteins

Abstract Background: We aimed at investigation of the effect and the underlying neurotrophin signaling pathway of the upstream transcription factor 1 (USF1) in lung adenocarcinoma (LUAD).Methods: The Cancer Genome Atlas (TCGA) database was used to analyze USF1 expression data and to extract patients’ clinical records. Immunohistochemical assay and Western blotting (WB) were used to determine the expression levels of USF1 in LUAD. The neurotrophin signaling pathway was analyzed by bioinformatic analysis while the expression of all related proteins was determined by WB. In addition cellular viability, proliferation, migration and invasion potential were investigated by the CCK-8, colony formation, wound healing and transwell. Meanwhile, the effect of USF1 in LUAD progression was investigated in a mouse model. The link between USF1 and UGT1A3 (UDP Glucuronosyltransferase Family 1 Member A3) was studied by the dual-luciferase reporter assay. Results: We have detected a high expression level of USF1 in LUAD, which was associated with advanced tumor stage, nodal metastasis, and poor patient’s survival rate. The knockdown of USF1 inhibited cellular viability, proliferation, migration and invasion. Meanwhile, USF1 knockdown inhibited tumor growth in a mouse model. Besides, USF1 targeted UGT1A3, which was proven by the fact that the USF1 knockdown decreased the expression level of UGT1A3, whereas the upregulated expression of UGT1A3 increased cellular viability and proliferation. We have proved that the neurotrophin signaling pathway in LUAD was activated by USF1 and UGT1A3. The expression of the related proteins was also inhibited by the USF1 knockdown, while the overexpression of IRAK increased cancer cells’ migration and invasion potential.Conclusion: USF1 was highly expressed in LUAD and promoted LUAD progression by regulating the neurotrophin signaling pathway. These findings provide a new theoretical data that could serve as a good foundation for the treatment of LUAD.

scholarly journals Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders

2008 ◽  
Vol 17 (9) ◽  
pp. 1234-1244 ◽  
Author(s):  
Josep Maria Mercader ◽  
Ester Saus ◽  
Zaida Agüera ◽  
Mònica Bayés ◽  
Claudette Boni ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Signaling Pathway ◽  
Neurotrophin Signaling

BDNF-trkB signaling in late life cognitive decline and Alzheimer’s disease

2011 ◽  
Vol 2 (2) ◽  
Author(s):  
Hoau-Yan Wang ◽  
Andres Stucky ◽  
Chang-Gyu Hahn ◽  
Robert Wilson ◽  
David Bennett ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Signaling Pathway ◽  
Neurofibrillary Tangle ◽  
Anterior Cingulate ◽  
Postmortem Brain ◽  
Downstream Signaling ◽  
Postmortem Brain Tissue ◽  
Neurotrophin Signaling ◽  
Neurodegenerative Dementias ◽  
Stimulation Paradigm

AbstractExpression levels of BDNF and trkB, primary components of an important neurotrophin signaling pathway, have been reported to be abnormal in neurodegenerative dementias. Here, we used a novel postmortem brain tissue stimulation paradigm to examine BDNF-induced trkB signaling in participants of the Religious Orders Study, a large longitudinal clinicopathological study of aging and cognition. Thawed slices of anterior cingulate cortex were incubated in BDNF and changes in phosphorylated trkB and downstream signaling molecules ERK2 and Akt were measured, as well as the association of NMDA receptors with trkB. We found that stimulation with BDNF induced much greater activity of the BDNF-trkB signaling pathway in brain tissues of people with cognitive decline and AD, as evidenced by significantly more phosphorylation of trkB (pY-trkB), ERK2 (pY/pT-ERK2), Akt (pS-Akt), and greater BDNF-induced coupling of trKB with NMDAR2A/B. These findings were independent of PHFtau neurofibrillary tangle and amyloid-b plaque densities and other potentially confounding variables. Regression analyses with clinical features further characterized significant relationships between measures of BDNF-trkB activation and domains of cognition and emotional functioning. Increased BDNF-trkB signaling with cognitive decline could reflect a primary derangement of pathway functioning or a compensatory neuroplastic response to counteract neural injury associated with neurodegenerative processes.

Sign in / Sign up

Export Citation Format

Share Document