CP Poly(A) RNA Binding Immunity via Outside-in Glycosyltransfer with MT of BTRC-Activating L12535 and PIN1 Subnetworks for Cognition in PFC|CD14

2020 ◽  
Author(s):  
Lin Wang ◽  
Qingchun Chen ◽  
Haitao Feng ◽  
Minghu Jiang ◽  
Juxiang Huang ◽  
...  
Keyword(s):  
Immune Response ◽  
Network Inference ◽  
Rna Binding ◽  
Biological Process ◽  
Cellular Component ◽  
Innate Immune ◽  
Molecular Function ◽  
Ubiquitin Protein Ligase ◽  
The Common ◽  
Cluster Of Differentiation

Abstract Background: Ras suppressor protein 1 (L12535) and peptidylprolyl cis/trans isomerase NIMA-interacting 1 (PIN1) common molecular and knowledge subnetworks containing microtubule associated protein 1B-MAP1B_1 (upstream) related to cognition by references were identified in human left hemisphere, based on our established significant high expression beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC)-activating downstream Gene (protein) reconstruction network inference (GRNInfer) and Database for Annotation, Visualization and Integrated Discovery (DAVID).Results: Our results show the common molecules exostosin-like glycosyltransferase 2 (EXTL2) interaction with MAP1B_1 both activating TERF1_1 with HSP90AB1 from BTRC-activating downstream GRNInfer database; The common biological process and molecular function of MAP1B_1, TERF1_1 as microtubule (MT) binding; HSP90AB1 as poly(A) RNA binding; BTRC, HSP90AB1, PIN1 as innate immune response from BTRC-activating downstream DAVID database; The common cellular component of EXTL2 at integral component of membrane; MAP1B_1, HSP90AB1, TERF1_1 at cytoplasm (CP); The common tissue distributions of L12535 and PIN1 in Prefrontal Cortex (PFC), PB cluster of differentiation (CD)14+Monocytes.Conclusions: We propose and mutual positively verify CP poly(A) RNA binding immunity via outside-in glycosyltransfer with MT of BTRC-activating L12535 and PIN1 subnetworks for cognition in PFC|CD14.

scholarly journals Transcriptomic inspection revealed a possible pathway regulating the formation of the high-quality brush hair in Chinese Haimen goat ( Capra hircus )

2018 ◽  
Vol 5 (1) ◽  
pp. 170907 ◽  
Author(s):  
Dejun Ji ◽  
Bo Yang ◽  
Yongjun Li ◽  
Miaoying Cai ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Biological Process ◽  
Kegg Pathway ◽  
Cellular Component ◽  
Biological Information ◽  
Capra Hircus ◽  
Molecular Function ◽  
High Quality ◽  
Type Iii ◽  
Kegg Pathways ◽  
Kegg Pathway Analysis

The high-quality brush hair, or Type III brush hair, is coarse hair but with a tip and little medulla, which uniquely grows in the cervical carina of Chinese Haimen goat ( Capra hircus ). To unveil the mechanism of the formation of Type III brush hair in Haimen goats, transcriptomic RNAseq technology was used for screening of differentially expressed genes (DEGs) in the skin samples of the Type III and the non-Type III hair goats, and these DEGs were analysed by KEGG pathway analysis. The results showed that a total of 295 DEGs were obtained, mainly from three main functional types: cellular component, molecular function and biological process. These DEGs were mainly enriched in three KEGG pathways, such as protein processing in endoplasmic reticulum, MAPK, and complement and coagulation cascades. These DEGs gave hints to a possible mechanism, under which heat stress possibly initiated the formation. The study provided some useful biological information, which could give a new view about the roles of certain factors in hair growth and give hints on the mechanism of the formation of the Type III brush hair in Chinese Haimen goat.

Effects of the RNA-binding protein, KSRP, on innate immune response against Helicobacter pylori infection in mice

2018 ◽  
Vol 495 (2) ◽  
pp. 1573-1579 ◽  
Author(s):  
Ningzhe Li ◽  
Mei Cao ◽  
Sijun Yi ◽  
Juan Cheng ◽  
Lei Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Innate Immune Response ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Innate Immune ◽  
Helicobacter Pylori Infection

scholarly journals Multi-Level Analyses of Genome-Wide Association Study to Reveal Significant Risk Genes and Pathways in Neuromyelitis Optica Spectrum Disorder

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting Li ◽  
He Li ◽  
Yue Li ◽  
Shu-An Dong ◽  
Ming Yi ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Biological Process ◽  
Susceptibility Gene ◽  
Susceptibility Genes ◽  
Cellular Component ◽  
Molecular Function ◽  
Risk Genes ◽  
Kegg Pathways ◽  
Gene Sets ◽  
Genome Wide

BackgroundNeuromyelitis optica spectrum disorder (NMOSD) is an inflammatory disease of the central nervous system and it is understandable that environmental and genetic factors underlie the etiology of NMOSD. However, the susceptibility genes and associated pathways of NMOSD patients who are AQP4-Ab positive and negative have not been elucidated.MethodsSecondary analysis from a NMOSD Genome-wide association study (GWAS) dataset originally published in 2018 (215 NMOSD cases and 1244 controls) was conducted to identify potential susceptibility genes and associated pathways in AQP4-positive and negative NMOSD patients, respectively (132 AQP4-positive and 83 AQP4-negative).ResultsIn AQP4-positive NMOSD cases, five shared risk genes were obtained at chromosome 6 in AQP4-positive NMOSD cases by using more stringent p-Values in both methods (p < 0.05/16,532), comprising CFB, EHMT2, HLA-DQA1, MSH5, and SLC44A4. Fifty potential susceptibility gene sets were determined and 12 significant KEGG pathways were identified. Sixty-seven biological process pathways, 32 cellular-component pathways, and 29 molecular-function pathways with a p-Value of <0.05 were obtained from the GO annotations of the 128 pathways identified. In the AQP4 negative NMOSD group, no significant genes were obtained by using more stringent p-Values in both methods (p < 0.05/16,485). The 22 potential susceptibility gene sets were determined. There were no shared potential susceptibility genes between the AQP4-positive and negative groups, furthermore, four significant KEGG pathways were also identified. Of the GO annotations of the 165 pathways identified, 99 biological process pathways, 37 cellular-component pathways, and 29 molecular-function pathways with a p-Value of <0.05 were obtained.ConclusionThe potential molecular mechanism underlying NMOSD may be related to proteins encoded by these novel genes in complements, antigen presentation, and immune regulation. The new results may represent an improved comprehension of the genetic and molecular mechanisms underlying NMOSD.

scholarly journals Tristetraprolin prevents gastric metaplasia in mice by suppressing pathogenic inflammation

2021 ◽  
Author(s):  
Jonathan T. Busada ◽  
Stuti Kadka ◽  
Kylie N. Peterson ◽  
Deborah J. Stumpo ◽  
Lecong Zhou ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Immune Activation ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Innate Immune ◽  
Cancer Development ◽  
Expression Of Genes ◽  
Gastric Metaplasia ◽  
Spasmolytic Polypeptide

AbstractAberrant immune activation is associated with numerous inflammatory and autoimmune diseases and contributes to cancer development and progression. Within the stomach, inflammation drives a well-established sequence from gastritis to metaplasia, eventually resulting in adenocarcinoma. Unfortunately, the processes that regulate gastric inflammation and prevent carcinogenesis remain unknown. Tristetraprolin (TTP) is an RNA-binding protein that promotes the turnover of numerous pro-inflammatory and oncogenic mRNAs. Here, we utilized a TTP-overexpressing model, the TTPΔARE mouse, to examine whether TTP can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM). We found that TTPΔARE mice were completely protected from ADX-induced gastric inflammation and SPEM. RNA sequencing revealed that TTP overexpression suppressed the expression of genes associated with the innate immune response. Finally, we show that protection from gastric inflammation was only partially due to suppression of Tnf, a well-known TTP target. Our results demonstrate that TTP exerts broad anti-inflammatory effects in the stomach and suggest that therapies that increase TTP expression may be effective treatments of pro-neoplastic gastric inflammation.

The Platelet Glycoprotein Ib-IX Axis In Murine Polymicrobial Sepsis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2274-2274
Author(s):  
Adam Corken ◽  
Susan Russell ◽  
Judith Dent ◽  
Steven Post ◽  
Jerry Ware
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Polymicrobial Sepsis ◽  
Platelet Glycoprotein ◽  
Wild Type ◽  
Platelet Receptor ◽  
The Common ◽  
Leucine Rich Repeats

Abstract The platelet glycoprotein (GP) Ib-IX receptor complex is expressed exclusively on the surface of platelets and is well characterized as a primary adhesion receptor supporting normal hemostasis and pathologic thrombosis. Beyond hemostasis and thrombosis, platelets can also participate in the innate immune response and inflammation. While the platelet as a contributor to the immune continuum is recognized, many aspects of the molecular mechanisms whereby platelets influence the immune response are still undefined. Here, we report studies using a murine model of GP Ib-IX deficiency linking GP Ib-IX to the immune response associated with polymicrobial sepsis, as modeled by cecal ligation and puncture (CLP). In the CLP model, genetic absence of the major GP Ib-IX hemostatic ligand, von Willebrand factor (VWF), improves survival following CLP when compared to control wild-type animals (p= 0.003, Logrank analysis). This suggests a VWF role in thrombosis contributes to survival outcome following CLP. In contrast, genetic absence of the VWF platelet receptor, GP Ib-IX, does not improve survival with no statistical difference comparing wild-type animals to GPIb-IX deficient animals. The molecular basis to explain improved survival in VWF-deficient (ligand deficient) but not GPIb-IX deficient (receptor deficient) animals was pursued. We tested the hypothesis GPIb-IX has normal physiologic and pathophysiologic functions beyond platelet adhesion influencing infection and an inflammatory response. Indeed, GPIb-IX influencing the innate immune response is not completely unexpected since a hallmark structural feature of each subunit of the GPIb-IX receptor is leucine rich repeats, the common motif to all members of the toll like receptor family (TLRs). Whether structural similarities are a consequence of ancestral origins for GPIb-IX and TLRs is unknown. We first documented in the absence of murine platelet GP Ib-IX there are reduced platelet-neutrophil and platelet-monocyte interactions under normal conditions and following CLP in whole blood. Whether there are physiologic consequences for disrupting a platelet/monocyte and/or platelet/neutrophil axis was determined via multianalyte profiling of circulating cytokine levels on a Luminex analyzer following CLP. In the absence of GP Ib-IX there is a robust and statistically significant increase 24 hrs following CLP in some of the major proinflammatory cytokines produced by monocytes and macrophages, including TNFα, MCP-1, MIP-β, IL-6, and IL-15. Increases in cytokines, such as IL-5 and IL-13, associated with other immune cells were also observed. These results highlight a coagulation/inflammation interface where the platelet, and specifically GP Ib-IX, contributes to the pathophysiology of CLP. On the one hand, absence of platelet GPIb-IX reduces thrombotic potential, but it occurs at the expense of upregulation of inflammatory cytokine release leading to a reduced survival in CLP. Clearly, survival outcomes in CLP reflect a complex dysregulation of coagulation and inflammation where platelet GPIb-IX likely contributes to both processes with physiologic consequences. Understanding dysregulation of the coagulation/ inflammation interface and identifying a platelet receptor (GPIb-IX) critical to both adds new information to this complex set of pathophysiologic events Sharing the common structural motifs, leucine rich repeats, with the well characterized family of toll-like receptors, platelet GPIb-IX should now be considered an active participant in the inflammatory cascade. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Innate Immune Response of Human Plasmacytoid Dendritic Cells to Poxvirus Infection Is Subverted by Vaccinia E3 via Its Z-DNA/RNA Binding Domain

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e36823 ◽  
Author(s):  
Hua Cao ◽  
Peihong Dai ◽  
Weiyi Wang ◽  
Hao Li ◽  
Jianda Yuan ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Rna Binding ◽  
Plasmacytoid Dendritic Cells ◽  
Binding Domain ◽  
Innate Immune ◽  
Rna Binding Domain ◽  
Z Dna

scholarly journals The RNA-binding protein LUC7L2 mediates MITA/STING intron retention to negatively regulate innate antiviral response

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chen Li ◽  
Lu Feng ◽  
Wei-Wei Luo ◽  
Cao-Qi Lei ◽  
Mi Li ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Adaptor Protein ◽  
Antiviral Response ◽  
Innate Immune ◽  
Innate Antiviral Response ◽  
Hsv 1

AbstractMITA (also known as STING) is an ER-located adaptor protein, which mediates DNA-triggered innate immune response and is critically involved in autoimmune diseases and tumorigenesis. MITA is regulated by post-translational modifications, but how post-transcriptional mechanisms are involved in the regulation of MITA is still largely unknown. Here, we identified the RNA-binding protein LUC7L2 as a negative regulator of DNA virus-triggered innate immune response. LUC7L2-deficient mice exhibited resistance to lethal herpes simplex virus 1 (HSV-1) infection and reduced HSV-1 loads in the brain. Mechanistically, LUC7L2 directly bound to intron 3 of MITA precursor messenger RNA, inhibited its splicing and promoted its nonsense-mediated decay, leading to its downregulation at protein level. LUC7L2-deficient cells had markedly increased MITA level, leading to heightened innate antiviral response. Finally, LUC7L2 was induced following HSV-1 infection. Our findings reveal a feedback negative post-transcriptional regulatory mechanism for regulation of MITA-mediated innate immune response to viral and aberrant cellular DNA.

scholarly journals NUDT1-Knockdown Inhibits Proliferation, Invasion and Migration of CAL27

2020 ◽  
Author(s):  
Qiusheng Shan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Biological Process ◽  
Cellular Component ◽  
Expression Level ◽  
Molecular Function ◽  
Invasion And Migration ◽  
And Migration

Abstract Background: The high level of reactive oxygen species (ROS) in cancer could oxidize guanine into 8-oxoG resulting in A: T changed into G: C or G: C into A: T. Nudix hydrolase 1 (NUDT1) overexpressed in many kind of cancers could hydrolyze the 8-oxo-dGTP into 8-oxo-dGMP or pyrophosphate to prevent the DNA damage or gene mutation. However, the role and function of NUDT1 in oral squamous cell carcinoma (OSCC) has not been investigated.Methods: Firstly, the bioinformatics methods were used to predict the biological process, cellular component and molecular function of NUDT1 and to confirm the mRNA and protein expression level of NUDT1 in OSCC. Furthermore, the MTT assay, Flow Cytometry, Transwell (Invasion), Scratch Test and Transwell (Migration) were used to test the effect of NUDT1 inhibitor on the proliferation, cell apoptosis, invasion and migration of CAL27. In addition, western blot was used to exam the expression level of NUDT1 and cleaved caspase-3 in different groups. Finally, the laser scanning microscope (LSM) was used to test the invadopodia formation level in different groups.Results: The bioinformatics analysis suggested that both mRNA and protein of NUDT1 overexpressed in head and neck squamous cell carcinoma (HNSCC) and OSCC. Furthermore, the biological process of NUDT1 mainly enriched in response to oxidative stress, aging, response to cadmium ion and male gonad development in OSCC. the cellular component of NUDT1 mainly enriched in extracellular exosome, cytoplasm, plasma membrane and nucleus in OSCC. The molecular function of NUDT1 mainly enriched in protein binding in OSCC. Finally, the biological experiments confirmed that NUDT1-knockdown could inhibit the proliferation, invasion, migration and promote cell apoptosis of CAL27.Conclusion: The overexpressed NUDT1 is positively associated with the progression of OSCC which has much potential to be new target in targeted therapy of OSCC.

scholarly journals Semantic Annotation for Biological Information Retrieval System

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Mohamed Marouf Z. Oshaiba ◽  
Enas M. F. El Houby ◽  
Akram Salah
Keyword(s):  
Query Expansion ◽  
Retrieval System ◽  
Biological Process ◽  
Semantic Annotation ◽  
Information Retrieval System ◽  
Cellular Component ◽  
Biological Information ◽  
Molecular Function ◽  
Problem Finding ◽  
Biological Domain

Online literatures are increasing in a tremendous rate. Biological domain is one of the fast growing domains. Biological researchers face a problem finding what they are searching for effectively and efficiently. The aim of this research is to find documents that contain any combination of biological process and/or molecular function and/or cellular component. This research proposes a framework that helps researchers to retrieve meaningful documents related to their asserted terms based on gene ontology (GO). The system utilizes GO by semantically decomposing it into three subontologies (cellular component, biological process, and molecular function). Researcher has the flexibility to choose searching terms from any combination of the three subontologies. Document annotation is taking a place in this research to create an index of biological terms in documents to speed the searching process. Query expansion is used to infer semantically related terms to asserted terms. It increases the search meaningful results using the term synonyms and term relationships. The system uses a ranking method to order the retrieved documents based on the ranking weights. The proposed system achieves researchers’ needs to find documents that fit the asserted terms semantically.

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