Co-expression Networks Identify DHX15 RNA Helicase as a B Cell Regulatory Factor

Detanico, Thiago; Virgen-Slane, Richard; Steen-Fuentes, Seth; Lin, Wai Wai; Rhode-Kurnow, Antje; Chappell, Elizabeth; Correa, Ricardo G.; DiCandido, Michael J; Mbow, Moustapha; Li, Jun; Ware, Carl F.

doi:10.3389/fimmu.2019.02903

Cited by 10 publications

(11 citation statements)

References 38 publications

(48 reference statements)

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“…In recent years, RNA helicases have gained notoriety due to their role in cell maintenance, controlling many biological processes, including cell differentiation and apoptosis 9 . Also, several groups have linked the defects in helicase functioning with cancer, infectious diseases, immune response, and neurodegenerative disorders 2,10 . For instance, recent studies have shown that the deregulated expression of an increasing number of these enzymes usually appears in many types of tumors 11,12 , hence being related to carcinogenesis and cancer progression [13][14][15][16][17] .…”

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confidence: 99%

The loss of DHX15 impairs endothelial energy metabolism, lymphatic drainage and tumor metastasis in mice

et al. 2021

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DHX15 is a downstream substrate for Akt1, which is involved in key cellular processes affecting vascular biology. Here, we explored the vascular regulatory function of DHX15. Homozygous DHX15 gene deficiency was lethal in mouse and zebrafish embryos. DHX15—/— zebrafish also showed downregulation of VEGF-C and reduced formation of lymphatic structures during development. DHX15+/− mice depicted lower vascular density and impaired lymphatic function postnatally. RNAseq and proteome analysis of DHX15 silenced endothelial cells revealed differential expression of genes involved in the metabolism of ATP biosynthesis. The validation of these results demonstrated a lower activity of the Complex I in the mitochondrial membrane of endothelial cells, resulting in lower intracellular ATP production and lower oxygen consumption. After injection of syngeneic LLC1 tumor cells, DHX15+/− mice showed partially inhibited primary tumor growth and reduced lung metastasis. Our results revealed an important role of DHX15 in vascular physiology and pave a new way to explore its potential use as a therapeutical target for metastasis treatment.

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confidence: 99%

The loss of DHX15 impairs endothelial energy metabolism, lymphatic drainage and tumor metastasis in mice

et al. 2021

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“…The fundamental idea behind this analysis was to shed some light into gene-gene interactions underpinning MS disease with regard to cause and effect ( 36 ). In this study, we reused GSE17048 experiment data which contained the profiled mRNA expression for all known genes in whole blood from 144 health individuals, 99 with MS (43 PPMS, 36 RRMS, and 20 SPMS).…”

Section: Resultsmentioning

confidence: 99%

“…The results were analyzed using the 2 − Ct method (35). In this study, beta-actin gene (as a reference gene) and S100A6, TUBA1C, and LASP1 genes [as target genes (TRG)] and CT data from real-time expression of TUBA1C, LASP1, and S100A6 were statistically analyzed (P < 0.05) by REST 2009 software.…”

Section: Quantitative Real Time Pcr Analysismentioning

confidence: 99%

Gene network reveals LASP1, TUBA1C, and S100A6 are likely playing regulatory roles in multiple sclerosis

Karimi

Motovali-Bashi²,

Ghaderi–Zefrehei³

2023

Front. Neurol.

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IntroductionMultiple sclerosis (MS), a non-contagious and chronic disease of the central nervous system, is an unpredictable and indirectly inherited disease affecting different people in different ways. Using Omics platforms genomics, transcriptomics, proteomics, epigenomics, interactomics, and metabolomics database, it is now possible to construct sound systems biology models to extract full knowledge of the MS and recognize the pathway to uncover the personalized therapeutic tools.MethodsIn this study, we used several Bayesian Networks in order to find the transcriptional gene regulation networks that drive MS disease. We used a set of BN algorithms using the R add-on package bnlearn. The BN results underwent further downstream analysis and were validated using a wide range of Cytoscape algorithms, web based computational tools and qPCR amplification of blood samples from 56 MS patients and 44 healthy controls. The results were semantically integrated to improve understanding of the complex molecular architecture underlying MS, distinguishing distinct metabolic pathways and providing a valuable foundation for the discovery of involved genes and possibly new treatments.ResultsResults show that the LASP1, TUBA1C, and S100A6 genes were most likely playing a biological role in MS development. Results from qPCR showed a significant increase (P < 0.05) in LASP1 and S100A6 gene expression levels in MS patients compared to that in controls. However, a significant down regulation of TUBA1C gene was observed in the same comparison.ConclusionThis study provides potential diagnostic and therapeutic biomarkers for enhanced understanding of gene regulation underlying MS.

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“…The fundamental idea behind this analysis was to shed some light into gene-gene interactions underpinning MS disease with regard to cause and effect. The bnlearn package was used to nd the gene regulatory network behind this disease [22]. The results of comparison of the network structures determined from various algorithms, including Hill Climbing, Tabu Search, Max-Min Hill Climbing, and Restricted Maximize algorithms with different scoring functions, are shown in Table 2.…”

Section: Resultsmentioning

confidence: 99%

Gene Networks Reveal LASP1, TUBA1C, and S100A6 as Likely Drivers of Multiple Sclerosis (MS)

Karimi

Bashi

Ghaderi–Zefrehei

2021

Preprint

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Background: Multiple sclerosis (MS), a non-contagious and chronic disease of the central nervous system, is an unpredictable and indirectly inherited disease affecting different people in different ways.Using Omics platforms data i.e. genomics, transcriptomics, proteomics, epigenomics, interactomics, and metabolomics it is now possible to construct sound systems biology models to extract full knowledge of the MS and path the way to likely construct personalized and therapeutic tools.Methods: In this study, we learned many Bayesian Networks in order to find the transcriptional gene regulation networks that drive MS disease. We used a set of BN algorithms using the R add-on package bnlearn. The BN results underwent further downstream analysis and were validated using a wide range of Cytoscape algorithms, web based computational tools and qPCR amplification of blood samples from 56 MS patients and 44 healthy controls. The results were semantically integrated to come up with improved understanding of the complex molecular architecture underlying MS, distinguishing distinct metabolic pathways and providing a valuable foundation for the discovery of deriven genes and possibly new treatments. Results: Results show that the LASP1, TUBA1C, and S100A6 genes were most significant and likely playing a biological role in MS development. Results from qPCR showed a significant increase (P <0.05) in LASP1 and S100A6 gene expression levels in MS patients compared to controls. However, a significant down regulation of TUBA1C was observed in the same comparison. Conclusion: This study provides potential diagnostic and therapeutic biomarkers for increasing understanding of gene regulation underlying MS.

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Co-expression Networks Identify DHX15 RNA Helicase as a B Cell Regulatory Factor

Cited by 10 publications

References 38 publications

The loss of DHX15 impairs endothelial energy metabolism, lymphatic drainage and tumor metastasis in mice

The loss of DHX15 impairs endothelial energy metabolism, lymphatic drainage and tumor metastasis in mice

Gene network reveals LASP1, TUBA1C, and S100A6 are likely playing regulatory roles in multiple sclerosis

Gene Networks Reveal LASP1, TUBA1C, and S100A6 as Likely Drivers of Multiple Sclerosis (MS)

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