A mouse model for SARS-CoV-2-induced acute respiratory distress syndrome

Hong, Weiqi; Yang, Jingyun; Bi, Zhenfei; He, C.; Hong, Lei; Wu, Yu; Yang, Yun; Fan, Chen; Lu, Shuaiyao; Peng, Xiaozhong; Wei, Xiawei

doi:10.1038/s41392-020-00451-w

Cited by 513 publications

(107 citation statements)

References 5 publications

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“…Since the first three-dimensional (3D) crystal structure of rhodopsin purified from bovine eyes was characterized in 2000 [ 159 ], tremendous progresses have made on understanding the structure–function relationships between ligand molecules and GPCR, which facilitated drug development at a remarkable speed [ 160 ]. As knowledge of interaction between GPCRs and their ligand molecules supports understanding their own biological and physiological functions, the research progress would reinforce the drug design.…”

Section: Gene Expression and Functional Characterization Of The Gpcrs In Insectsmentioning

confidence: 99%

G-Protein Coupled Receptors (GPCRs): Signaling Pathways, Characterization, and Functions in Insect Physiology and Toxicology

Liu

Wang

et al. 2021

IJMS

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G-protein-coupled receptors (GPCRs) are known to play central roles in the physiology of many organisms. Members of this seven α-helical transmembrane protein family transduce the extracellular signals and regulate intracellular second messengers through coupling to heterotrimeric G-proteins, adenylate cyclase, cAMPs, and protein kinases. As a result of the critical function of GPCRs in cell physiology and biochemistry, they not only play important roles in cell biology and the medicines used to treat a wide range of human diseases but also in insects’ physiological functions. Recent studies have revealed the expression and function of GPCRs in insecticide resistance, improving our understanding of the molecular complexes governing the development of insecticide resistance. This article focuses on the review of G-protein coupled receptor (GPCR) signaling pathways in insect physiology, including insects’ reproduction, growth and development, stress responses, feeding, behaviors, and other physiological processes. Hormones and polypeptides that are involved in insect GPCR regulatory pathways are reviewed. The review also gives a brief introduction of GPCR pathways in organisms in general. At the end of the review, it provides the recent studies on the function of GPCRs in the development of insecticide resistance, focusing in particular on our current knowledge of the expression and function of GPCRs and their downstream regulation pathways and their roles in insecticide resistance and the regulation of resistance P450 gene expression. The latest insights into the exciting technological advances and new techniques for gene expression and functional characterization of the GPCRs in insects are provided.

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Section: Gene Expression and Functional Characterization Of The Gpcrs In Insectsmentioning

confidence: 99%

G-Protein Coupled Receptors (GPCRs): Signaling Pathways, Characterization, and Functions in Insect Physiology and Toxicology

Liu

Wang

et al. 2021

IJMS

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“…It has been shown that ABCB5 can keep melanoma-initiating cells by a pro-inflammatory cytokine signaling pathway [ 126 ]. Overexpression of ABCG2 has also been reported in head and neck, lung, brain, osteosarcoma, melanoma, and prostate CSCs [ 127 ]. Some studies reported overexpression of ABC transporters also has been identified in side population (SP) of CSCs cells that indicate a stemness phenotype and can be used as candidates for the identification of CSCs [ 15 , 125 , 128 ].…”

Section: Drug Resistance Mechanisms Of Cscsmentioning

confidence: 99%

Current understanding of epigenetics mechanism as a novel target in reducing cancer stem cells resistance

et al. 2021

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At present, after extensive studies in the field of cancer, cancer stem cells (CSCs) have been proposed as a major factor in tumor initiation, progression, metastasis, and recurrence. CSCs are a subpopulation of bulk tumors, with stem cell-like properties and tumorigenic capabilities, having the abilities of self-renewal and differentiation, thereby being able to generate heterogeneous lineages of cancer cells and lead to resistance toward anti-tumor treatments. Highly resistant to conventional chemo- and radiotherapy, CSCs have heterogeneity and can migrate to different organs and metastasize. Recent studies have demonstrated that the population of CSCs and the progression of cancer are increased by the deregulation of different epigenetic pathways having effects on gene expression patterns and key pathways connected with cell proliferation and survival. Further, epigenetic modifications (DNA methylation, histone modifications, and RNA methylations) have been revealed to be key drivers in the formation and maintenance of CSCs. Hence, identifying CSCs and targeting epigenetic pathways therein can offer new insights into the treatment of cancer. In the present review, recent studies are addressed in terms of the characteristics of CSCs, the resistance thereof, and the factors influencing the development thereof, with an emphasis on different types of epigenetic changes in genes and main signaling pathways involved therein. Finally, targeted therapy for CSCs by epigenetic drugs is referred to, which is a new approach in overcoming resistance and recurrence of cancer.

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“…STAT3 in particular is upregulated in EBV-positive nasopharyngeal carcinoma cell lines [ 97 , 98 ]. Additionally, in EBV-induced nasopharyngeal carcinoma, LMP1 facilitates increased interactions between MYC and the MYC target genes HK2 and IDH2 , which encode enzymes in glycolysis and the TCA cycle, respectively [ 99 , 100 , 101 ]. This MYC stabilization occurs through an LMP1 signaling pathway that involves PI3K/AKT/GSK3β and FBXW7 signaling [ 100 , 101 ].…”

Section: Regulation Of Myc By Dna Tumor Virus Oncoproteinsmentioning

confidence: 99%

“…Additionally, in EBV-induced nasopharyngeal carcinoma, LMP1 facilitates increased interactions between MYC and the MYC target genes HK2 and IDH2 , which encode enzymes in glycolysis and the TCA cycle, respectively [ 99 , 100 , 101 ]. This MYC stabilization occurs through an LMP1 signaling pathway that involves PI3K/AKT/GSK3β and FBXW7 signaling [ 100 , 101 ]. The importance of the LMP1-mediated MYC activation pathway was emphasized by a study in which the histone deacetylase inhibitor romidepsin was found to be cytotoxic to an EBV-positive diffuse large B-cell lymphoma in both a cell culture and a mouse xenograft model by reducing the expression of both LMP1 and MYC [ 102 ].…”

Section: Regulation Of Myc By Dna Tumor Virus Oncoproteinsmentioning

confidence: 99%

Metabolic Control by DNA Tumor Virus-Encoded Proteins

Prusinkiewicz

Mymryk

2021

Pathogens

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Viruses co-opt a multitude of host cell metabolic processes in order to meet the energy and substrate requirements for successful viral replication. However, due to their limited coding capacity, viruses must enact most, if not all, of these metabolic changes by influencing the function of available host cell regulatory proteins. Typically, certain viral proteins, some of which can function as viral oncoproteins, interact with these cellular regulatory proteins directly in order to effect changes in downstream metabolic pathways. This review highlights recent research into how four different DNA tumor viruses, namely human adenovirus, human papillomavirus, Epstein–Barr virus and Kaposi’s associated-sarcoma herpesvirus, can influence host cell metabolism through their interactions with either MYC, p53 or the pRb/E2F complex. Interestingly, some of these host cell regulators can be activated or inhibited by the same virus, depending on which viral oncoprotein is interacting with the regulatory protein. This review highlights how MYC, p53 and pRb/E2F regulate host cell metabolism, followed by an outline of how each of these DNA tumor viruses control their activities. Understanding how DNA tumor viruses regulate metabolism through viral oncoproteins could assist in the discovery or repurposing of metabolic inhibitors for antiviral therapy or treatment of virus-dependent cancers.

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A mouse model for SARS-CoV-2-induced acute respiratory distress syndrome

Cited by 513 publications

References 5 publications

G-Protein Coupled Receptors (GPCRs): Signaling Pathways, Characterization, and Functions in Insect Physiology and Toxicology

G-Protein Coupled Receptors (GPCRs): Signaling Pathways, Characterization, and Functions in Insect Physiology and Toxicology

Current understanding of epigenetics mechanism as a novel target in reducing cancer stem cells resistance

Metabolic Control by DNA Tumor Virus-Encoded Proteins

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