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Article: SARS-CoV-2 mutations altering regulatory properties: Deciphering host's and virus's perspectives.

Islam, Abul Bashar Mir Md Khademul / Khan, Md Abdullah-Al-Kamran

Gene reports

2021 Volume 24, Page(s) 101236

Abstract: Since the first recorded case of the SARS-CoV-2, it has acquired several mutations in its genome while spreading throughout the globe. In this study, we investigated the significance of these mutations by analyzing the host miRNA binding and virus's ... ...

Abstract	Since the first recorded case of the SARS-CoV-2, it has acquired several mutations in its genome while spreading throughout the globe. In this study, we investigated the significance of these mutations by analyzing the host miRNA binding and virus's internal ribosome entry site (IRES). Strikingly, we observed that due to the acquired mutations, five host miRNAs lost their affinity for targeting the viral genome, and another five can target the mutated viral genome. Moreover, functional enrichment analysis suggests that targets of both of these miRNAs might be involved in various host immune signaling pathways. Remarkably, we detected that three particular mutations in the IRES can disrupt its secondary structure which can consequently make the virus less functional. These results could be valuable in exploring the functional importance of the mutations of SARS-CoV-2 and could provide novel insights into the differences observed different parts of the world.
Language	English
Publishing date	2021-06-11
Publishing country	United States
Document type	Journal Article
ISSN	2452-0144
ISSN	2452-0144
DOI	10.1016/j.genrep.2021.101236
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Article ; Online: Computational analysis revealed miRNAs produced by Chikungunya virus target genes associated with antiviral immune responses and cell cycle regulation.

Islam, Md Sajedul / Khan, Md Abdullah-Al-Kamran

Computational biology and chemistry

2021 Volume 92, Page(s) 107462

Abstract: Chikungunya virus (CHIKV) that causes chikungunya fever, is an alphavirus that belongs to the Togaviridae family containing a single-stranded RNA genome. Mosquitoes of the Aedes species act as the vectors for this virus and can be found in the blood, ... ...

Abstract	Chikungunya virus (CHIKV) that causes chikungunya fever, is an alphavirus that belongs to the Togaviridae family containing a single-stranded RNA genome. Mosquitoes of the Aedes species act as the vectors for this virus and can be found in the blood, which can be passed from an infected person to a mosquito through mosquito bites. CHIKV has drawn much attention recently because of its potential of causing an epidemic. As the detailed mechanism of its pathogenesis inside the host system is still lacking, in this in silico research we have hypothesized that CHIKV might create miRNAs, which would target the genes associated with host cellular regulatory pathways, thereby providing the virus with prolonged refuge. Using bioinformatics approaches we found several putative miRNAs produced by CHIKV. Then we predicted the genes of the host targeted by these miRNAs. Functional enrichment analysis of these targeted genes shows the involvement of several biological pathways regulating antiviral immune stimulation, cellular proliferation, and cell cycle, thereby provide themselves with prolonged refuge and facilitate their pathogenesis, which in turn may lead to disease conditions. Finally, we analyzed a publicly available microarray dataset (GSE49985) to determine the altered expression levels of the targeted genes and found genes associated with pathways such as cell differentiation, phagocytosis, T-cell activation, response to cytokine, autophagy, Toll-like receptor signaling, RIG-I like receptor signaling and apoptosis. Our finding presents novel miRNAs and their targeted genes, which upon experimental validation could facilitate in developing new therapeutics to combat CHIKV infection and minimize CHIKV mediated diseases.
MeSH term(s)	Antiviral Agents/immunology ; Cell Cycle/genetics ; Cell Cycle/immunology ; Chikungunya virus/genetics ; Chikungunya virus/immunology ; Gene Regulatory Networks/genetics ; Gene Regulatory Networks/immunology ; MicroRNAs/analysis ; MicroRNAs/biosynthesis ; MicroRNAs/genetics
Chemical Substances	Antiviral Agents ; MicroRNAs
Language	English
Publishing date	2021-02-19
Publishing country	England
Document type	Journal Article
ISSN	1476-928X
ISSN (online)	1476-928X
DOI	10.1016/j.compbiolchem.2021.107462
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Article: SARS-CoV-2 Proteins Exploit Host's Genetic and Epigenetic Mediators for the Annexation of Key Host Signaling Pathways.

Khan, Md Abdullah-Al-Kamran / Islam, Abul Bashar Mir Md Khademul

Frontiers in molecular biosciences

2021 Volume 7, Page(s) 598583

Abstract: The constant rise of the death toll and cases of COVID-19 has made this pandemic a serious threat to human civilization. Understanding of host-SARS-CoV-2 interaction in viral pathogenesis is still in its infancy. In this study, we utilized a blend of ... ...

Abstract	The constant rise of the death toll and cases of COVID-19 has made this pandemic a serious threat to human civilization. Understanding of host-SARS-CoV-2 interaction in viral pathogenesis is still in its infancy. In this study, we utilized a blend of computational and knowledgebase approaches to model the putative virus-host interplay in host signaling pathways by integrating the experimentally validated host interactome proteins and differentially expressed host genes in SARS-CoV-2 infection. While searching for the pathways in which viral proteins interact with host proteins, we discovered various antiviral immune response pathways such as hypoxia-inducible factor 1 (HIF-1) signaling, autophagy, retinoic acid-inducible gene I (RIG-I) signaling, Toll-like receptor signaling, fatty acid oxidation/degradation, and IL-17 signaling. All these pathways can be either hijacked or suppressed by the viral proteins, leading to improved viral survival and life cycle. Aberration in pathways such as HIF-1 signaling and relaxin signaling in the lungs suggests the pathogenic lung pathophysiology in COVID-19. From enrichment analysis, it was evident that the deregulated genes in SARS-CoV-2 infection might also be involved in heart development, kidney development, and AGE-RAGE signaling pathway in diabetic complications. Anomalies in these pathways might suggest the increased vulnerability of COVID-19 patients with comorbidities. Moreover, we noticed several presumed infection-induced differentially expressed transcription factors and epigenetic factors, such as miRNAs and several histone modifiers, which can modulate different immune signaling pathways, helping both host and virus. Our modeling suggests that SARS-CoV-2 integrates its proteins in different immune signaling pathways and other cellular signaling pathways for developing efficient immune evasion mechanisms while leading the host to a more complicated disease condition. Our findings would help in designing more targeted therapeutic interventions against SARS-CoV-2.
Language	English
Publishing date	2021-01-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2020.598583
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Article ; Online: Lung transcriptome of a COVID-19 patient and systems biology predictions suggest impaired surfactant production which may be druggable by surfactant therapy.

Islam, Abul Bashar Mir Md Khademul / Khan, Md Abdullah-Al-Kamran

Scientific reports

2020 Volume 10, Issue 1, Page(s) 19395

Abstract: An incomplete understanding of the molecular mechanisms behind impairment of lung pathobiology by COVID-19 complicates its clinical management. In this study, we analyzed the gene expression pattern of cells obtained from biopsies of COVID-19-affected ... ...

Abstract	An incomplete understanding of the molecular mechanisms behind impairment of lung pathobiology by COVID-19 complicates its clinical management. In this study, we analyzed the gene expression pattern of cells obtained from biopsies of COVID-19-affected patient and compared to the effects observed in typical SARS-CoV-2 and SARS-CoV-infected cell-lines. We then compared gene expression patterns of COVID-19-affected lung tissues and SARS-CoV-2-infected cell-lines and mapped those to known lung-related molecular networks, including hypoxia induced responses, lung development, respiratory processes, cholesterol biosynthesis and surfactant metabolism; all of which are suspected to be downregulated following SARS-CoV-2 infection based on the observed symptomatic impairments. Network analyses suggest that SARS-CoV-2 infection might lead to acute lung injury in COVID-19 by affecting surfactant proteins and their regulators SPD, SPC, and TTF1 through NSP5 and NSP12; thrombosis regulators PLAT, and EGR1 by ORF8 and NSP12; and mitochondrial NDUFA10, NDUFAF5, and SAMM50 through NSP12. Furthermore, hypoxia response through HIF-1 signaling might also be targeted by SARS-CoV-2 proteins. Drug enrichment analysis of dysregulated genes has allowed us to propose novel therapies, including lung surfactants, respiratory stimulants, sargramostim, and oseltamivir. Our study presents a distinct mechanism of probable virus induced lung damage apart from cytokine storm.
MeSH term(s)	COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/genetics ; Coronavirus Infections/immunology ; Coronavirus Infections/metabolism ; Epigenesis, Genetic ; Gene Expression Profiling ; Humans ; Lung/drug effects ; Lung/metabolism ; Molecular Targeted Therapy ; Organ Specificity ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/genetics ; Pneumonia, Viral/immunology ; Pneumonia, Viral/metabolism ; Pulmonary Surfactants/metabolism ; Systems Biology ; Viral Proteins/metabolism
Chemical Substances	Pulmonary Surfactants ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-11-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-76404-8
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Article ; Online: Cutting Edge: PDGF-DD Binding to NKp44 Costimulates TLR9 Signaling and Proinflammatory Cytokine Secretion in Human Plasmacytoid Dendritic Cells.

Barrow, Alexander David / Cella, Marina / Edeling, Melissa Anne / Khan, Md Abdullah-Al-Kamran / Cervantes-Barragan, Luisa / Bugatti, Mattia / Schmedt, Christian / Vermi, William / Colonna, Marco

Journal of immunology (Baltimore, Md. : 1950)

2024 Volume 212, Issue 3, Page(s) 369–374

Abstract: NKp44 is a human receptor originally found on activated NK cells, group 1 and group 3 innate lymphoid cells that binds dimers of platelet-derived growth factor D (PDGF-DD). NKp44 is also expressed on tissue plasmacytoid dendritic cells (PDCs), but NKp44- ... ...

Abstract	NKp44 is a human receptor originally found on activated NK cells, group 1 and group 3 innate lymphoid cells that binds dimers of platelet-derived growth factor D (PDGF-DD). NKp44 is also expressed on tissue plasmacytoid dendritic cells (PDCs), but NKp44-PDGF-DD interaction on PDCs remains unstudied. Engagement of NKp44 with PDGF-DD in vitro enhanced PDC secretion of IFN-α, TNF, and IL-6 in response to the TLR9 ligand CpG-ODN, but not TLR7/8 ligands. In tissues, PDCs were found in close contact with PDGF-DD-expressing cells in the high endothelial venules and epithelium of tonsils, melanomas, and skin lesions infected with Molluscum contagiosum. Recombinant PDGF-DD enhanced the serum IFN-α response to systemic HSV-1 infection in a humanized mouse model. We conclude that NKp44 integrates with TLR9 signaling to enhance PDC cytokine production. These findings may have bearings for immune responses to TLR9-based adjuvants, therapy for tumors expressing PDGF-DD, and infections with DNA viruses that induce PDGF-DD expression to enhance viral spread.
MeSH term(s)	Animals ; Mice ; Humans ; Immunity, Innate ; Toll-Like Receptor 9/metabolism ; Interferon-alpha/metabolism ; Dendritic Cells ; Killer Cells, Natural
Chemical Substances	Toll-Like Receptor 9 ; Interferon-alpha ; TLR9 protein, human
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2200496
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Article ; Online: SARS-CoV-2 Proteins Exploit Host’s Genetic and Epigenetic Mediators for the Annexation of Key Host Signaling Pathways

Md. Abdullah-Al-Kamran Khan / Abul Bashar Mir Md. Khademul Islam

Frontiers in Molecular Biosciences, Vol

2021 Volume 7

Abstract	The constant rise of the death toll and cases of COVID-19 has made this pandemic a serious threat to human civilization. Understanding of host-SARS-CoV-2 interaction in viral pathogenesis is still in its infancy. In this study, we utilized a blend of computational and knowledgebase approaches to model the putative virus-host interplay in host signaling pathways by integrating the experimentally validated host interactome proteins and differentially expressed host genes in SARS-CoV-2 infection. While searching for the pathways in which viral proteins interact with host proteins, we discovered various antiviral immune response pathways such as hypoxia-inducible factor 1 (HIF-1) signaling, autophagy, retinoic acid-inducible gene I (RIG-I) signaling, Toll-like receptor signaling, fatty acid oxidation/degradation, and IL-17 signaling. All these pathways can be either hijacked or suppressed by the viral proteins, leading to improved viral survival and life cycle. Aberration in pathways such as HIF-1 signaling and relaxin signaling in the lungs suggests the pathogenic lung pathophysiology in COVID-19. From enrichment analysis, it was evident that the deregulated genes in SARS-CoV-2 infection might also be involved in heart development, kidney development, and AGE-RAGE signaling pathway in diabetic complications. Anomalies in these pathways might suggest the increased vulnerability of COVID-19 patients with comorbidities. Moreover, we noticed several presumed infection-induced differentially expressed transcription factors and epigenetic factors, such as miRNAs and several histone modifiers, which can modulate different immune signaling pathways, helping both host and virus. Our modeling suggests that SARS-CoV-2 integrates its proteins in different immune signaling pathways and other cellular signaling pathways for developing efficient immune evasion mechanisms while leading the host to a more complicated disease condition. Our findings would help in designing more targeted therapeutic interventions against SARS-CoV-2.
Keywords	host-virus interactions ; COVID-19 ; SARS-CoV-2 ; immune evasion ; epigenetic regulation ; host immune response ; Biology (General) ; QH301-705.5
Subject code	570 ; 572
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Computational engineering the binding affinity of Adalimumab monoclonal antibody for designing potential biosimilar candidate.

Khan, Md Abdullah-Al-Kamran / Turjya, Rafeed Rahman / Islam, Abul Bashar Mir Md Khademul

Journal of molecular graphics & modelling

2020 Volume 102, Page(s) 107774

Abstract: Amongst the anti-TNF-α therapy for rheumatoid arthritis and other autoimmune diseases, Adalimumab mAb is one of the best candidates. However, several risk factors are found to be associated with higher doses. Improvement of the binding properties will ... ...

Abstract	Amongst the anti-TNF-α therapy for rheumatoid arthritis and other autoimmune diseases, Adalimumab mAb is one of the best candidates. However, several risk factors are found to be associated with higher doses. Improvement of the binding properties will therefore significantly increase its therapeutic efficacy, reduce the dosage requirements, and ultimately the associated toxicity and treatment cost. Here, we proposed a systematic in silico approach of finding newer mAb variants with improved binding properties. Using various bioinformatics tools, we have identified the significant amino acid residues on Adalimumab mAb. Next, we searched for the suitability of the other residues for mutating the significant residues and from the combinations of suitable mutations, variants were designed. To find the most significant ones, binding properties of the variants were compared with the wild type Adalimumab mAb using molecular docking scrutiny and molecular dynamics simulation. Finally, structural properties between the variant and wild type were analyzed. We have identified the six most significant residues on Adalimumab mAb involved in the antigen-antibody interactions. Using the suitable mutations replacing each of these residues, we have modeled 143 variants. From several docking analyses, we have found five significant variants and after molecular dynamics simulation, one most significant variant with improved binding affinity was identified whose structural properties are similar to the wild type Adalimumab mAb. Designed variant from this study, may provide newer insights on the structure-based affinity improvements of monoclonal antibodies and likewise modifications of the Fc region will also improve the therapeutic effector functions of antibodies too.
MeSH term(s)	Adalimumab ; Antibodies, Monoclonal ; Biosimilar Pharmaceuticals ; Molecular Docking Simulation ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha
Chemical Substances	Antibodies, Monoclonal ; Biosimilar Pharmaceuticals ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha ; Adalimumab (FYS6T7F842)
Language	English
Publishing date	2020-10-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1396450-1
ISSN	1873-4243 ; 1093-3263
ISSN (online)	1873-4243
ISSN	1093-3263
DOI	10.1016/j.jmgm.2020.107774
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Article ; Online: Bidirectional promoters: an enigmatic genome architecture and their roles in cancers.

Ahmad, Sheikh Shafin / Samia, Nure Sharaf Nower / Khan, Auroni Semonti / Turjya, Rafeed Rahman / Khan, Md Abdullah-Al-Kamran

Molecular biology reports

2021 Volume 48, Issue 9, Page(s) 6637–6644

Abstract: Bidirectional promoters are the transcription regulatory regions of genes positioned head-to-head on opposite strands. Specific sequence signals, chromatin modifications and three-dimensional structures of the transcription site facilitate the ... ...

Abstract	Bidirectional promoters are the transcription regulatory regions of genes positioned head-to-head on opposite strands. Specific sequence signals, chromatin modifications and three-dimensional structures of the transcription site facilitate the unconventional yet tightly regulated transcription proceeding in both directions from these promoters. Mutations or aberrant epigenetic changes can lead to abnormal enhanced or reduced expression from either of the bidirectionally transcribed genes resulting in tumorigenesis. Moreover, bidirectionally transcribed genes might also contribute towards the immune regulation in tumor microenvironment. In this review, we aimed to expound the characteristic features of bidirectional promoters alongside their transcriptional regulations, and ultimately, the association of these enigmatic genomic elements in different cancers.
MeSH term(s)	Cell Transformation, Neoplastic/genetics ; CpG Islands/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Humans ; Neoplasms/genetics ; Promoter Regions, Genetic/genetics ; Transcription, Genetic ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Language	English
Publishing date	2021-08-10
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-021-06612-6
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Article ; Online: Aberration of the modulatory functions of intronic microRNA hsa-miR-933 on its host gene ATF2 results in type II diabetes mellitus and neurodegenerative disease development.

Islam, Abul Bashar Mir Md Khademul / Mohammad, Eusra / Khan, Md Abdullah-Al-Kamran

Human genomics

2020 Volume 14, Issue 1, Page(s) 34

Abstract: Background: MicroRNAs are ~ 22-nucleotide-long biological modifiers that act as the post-transcriptional modulator of gene expression. Some of them are identified to be embedded within the introns of protein-coding genes, these miRNAs are called the ... ...

Abstract	Background: MicroRNAs are ~ 22-nucleotide-long biological modifiers that act as the post-transcriptional modulator of gene expression. Some of them are identified to be embedded within the introns of protein-coding genes, these miRNAs are called the intronic miRNAs. Previous findings state that these intronic miRNAs are co-expressed with their host genes. This co-expression is necessary to maintain the robustness of the biological system. Till to date, only a few experiments are performed discretely to elucidate the functional relationship between few co-expressed intronic miRNAs and their associated host genes. Results: In this study, we have interpreted the underlying modulatory mechanisms of intronic miRNA hsa-miR-933 on its target host gene ATF2 and found that aberration can lead to several disease conditions. A protein-protein interaction network-based approach was adopted, and functional enrichment analysis was performed to elucidate the significantly over-represented biological functions and pathways of the common targets. Our approach delineated that hsa-miR-933 might control the hyperglycemic condition and hyperinsulinism by regulating ATF2 target genes MAP4K4, PRKCE, PEA15, BDNF, PRKACB, and GNAS which can otherwise lead to the development of type II diabetes mellitus. Moreover, we showed that hsa-miR-933 can regulate a target of ATF2, brain-derived neurotrophic factor (BDNF), to modulate the optimal expression of ATF2 in neuron cells to render neuroprotection for the inhibition of neurodegenerative diseases. Conclusions: Our in silico model provides interesting resources for experimentations in a model organism or cell line for further validation. These findings may extend the common perception of gene expression analysis with new regulatory functionality.
MeSH term(s)	Activating Transcription Factor 2/genetics ; Activating Transcription Factor 2/metabolism ; Cell Line ; Chromogranins/genetics ; Chromogranins/metabolism ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/genetics ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; GTP-Binding Protein alpha Subunits, Gs/genetics ; GTP-Binding Protein alpha Subunits, Gs/metabolism ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Gene Ontology ; Gene Regulatory Networks ; Humans ; Hyperglycemia/genetics ; Hyperglycemia/metabolism ; Hyperinsulinism/genetics ; Hyperinsulinism/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Introns/genetics ; MicroRNAs/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Protein Kinase C-epsilon/genetics ; Protein Kinase C-epsilon/metabolism ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism
Chemical Substances	ATF2 protein, human ; Activating Transcription Factor 2 ; Chromogranins ; Intracellular Signaling Peptides and Proteins ; MicroRNAs ; MAP4K4 protein, human (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits (EC 2.7.11.11) ; PRKACB protein, human (EC 2.7.11.11) ; PRKCE protein, human (EC 2.7.11.13) ; Protein Kinase C-epsilon (EC 2.7.11.13) ; GNAS protein, human (EC 3.6.1.-) ; GTP-Binding Protein alpha Subunits, Gs (EC 3.6.5.1)
Language	English
Publishing date	2020-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2147618-4
ISSN	1479-7364 ; 1479-7364
ISSN (online)	1479-7364
ISSN	1479-7364
DOI	10.1186/s40246-020-00285-1
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Article: Epigenetic Regulator miRNA Pattern Differences Among SARS-CoV, SARS-CoV-2, and SARS-CoV-2 World-Wide Isolates Delineated the Mystery Behind the Epic Pathogenicity and Distinct Clinical Characteristics of Pandemic COVID-19.

Khan, Md Abdullah-Al-Kamran / Sany, Md Rabi Us / Islam, Md Shafiqul / Islam, Abul Bashar Mir Md Khademul

Frontiers in genetics

2020 Volume 11, Page(s) 765

Abstract: A detailed understanding of the molecular mechanism of SARS-CoV-2 pathogenesis is still elusive, and there is a need to address its deadly nature and to design effective therapeutics. Here, we present a study that elucidates the interplay between the ... ...

Abstract	A detailed understanding of the molecular mechanism of SARS-CoV-2 pathogenesis is still elusive, and there is a need to address its deadly nature and to design effective therapeutics. Here, we present a study that elucidates the interplay between the SARS-CoV and SARS-CoV-2 viruses' and host's miRNAs, an epigenetic regulator, as a mode of pathogenesis; and we explored how the SARS-CoV and SARS-CoV-2 infections differ in terms of their miRNA-mediated interactions with the host and the implications this has in terms of disease complexity. We have utilized computational approaches to predict potential host and viral miRNAs and their possible roles in different important functional pathways. We have identified several putative host antiviral miRNAs that can target the SARS viruses and also predicted SARS viruses-encoded miRNAs targeting host genes.
Keywords	covid19
Language	English
Publishing date	2020-07-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.00765
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