Bioscience Reports最新文献_第9页

Dengue virus: pathogenesis and potential for small molecule inhibitors. 登革热病毒：发病机制和潜在的小分子抗病毒药物。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR20240134

Navya Chauhan, Kishan Kumar Gaur, Tejeswara Rao Asuru, Prasenjit Guchhait

{"title":"Dengue virus: pathogenesis and potential for small molecule inhibitors.","authors":"Navya Chauhan, Kishan Kumar Gaur, Tejeswara Rao Asuru, Prasenjit Guchhait","doi":"10.1042/BSR20240134","DOIUrl":"10.1042/BSR20240134","url":null,"abstract":"Dengue, caused by dengue virus (DENV), is now endemic in nearly 100 countries and infection incidence is reported in another 30 countries. Yearly an estimated 400 million cases and 2200 deaths are reported. Effective vaccines against DENV are limited and there has been significant focus on the development of effective antiviral against the disease. The World Health Organization has initiated research programs to prioritize the development and optimization of antiviral agents against several viruses including Flaviviridae. A significant effort has been taken by the researchers to develop effective antivirals against DENV. Several potential small-molecule inhibitors like efavirenz, tipranavir and dasabuvir have been tested against envelope and non-structural proteins of DENV, and are in clinical trials around the world. We recently developed one small molecule, namely 7D, targeting the host PF4-CXCR3 axis. 7D inhibited all 4 serotypes of DENV in vitro and specifically DENV2 infection in two different mice models. Although the development of dengue vaccines remains a high priority, antibody cross reactivity among the serotypes and resulting antibody-dependent enhancement (ADE) of infection are major concerns that have limited the development of effective vaccine against DENV. Therefore, there has been a significant emphasis on the development of antiviral drugs against dengue. This review article describes the rescue effects of some of the small molecule inhibitors to viral/host factors associated with DENV pathogenesis.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11327219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction: Nucleus pulposus cell senescence is alleviated by resveratrol through regulating the ROS/NF-κB pathway under high-magnitude compression. 撤回：在高强度挤压下，白藜芦醇可通过调节 ROS/NF-κB 通路缓解髓核细胞衰老。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2018-0670_RET

引用次数: 0

Retraction: Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway. 撤回：白藜芦醇通过激活 ROS 介导的 PI3K/Akt 通路减轻高糖诱导的髓核细胞凋亡和衰老。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2017-1454_RET

引用次数: 0

Retraction: Resveratrol attenuates mechanical compression-induced nucleus pulposus cell apoptosis through regulating the ERK1/2 signaling pathway in a disc organ culture. 撤回：在椎间盘器官培养中，白藜芦醇通过调节ERK1/2信号通路减轻机械压缩诱导的髓核细胞凋亡

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2017-1703_RET

引用次数: 0

Characterization of human aquaporin ion channels in a yeast expression system as a tool for novel ion channel discovery. 在酵母表达系统中表征人类 Aquaporin 离子通道，作为发现新型离子通道的工具。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR20240542

Saeed Nourmohammadi, Sam W Henderson, Sunita A Ramesh, Andrea J Yool

{"title":"Characterization of human aquaporin ion channels in a yeast expression system as a tool for novel ion channel discovery.","authors":"Saeed Nourmohammadi, Sam W Henderson, Sunita A Ramesh, Andrea J Yool","doi":"10.1042/BSR20240542","DOIUrl":"10.1042/BSR20240542","url":null,"abstract":"Aquaporin (AQP) channels found in all domains of life are transmembrane proteins which mediate passive transport of water, glycerol, signaling molecules, metabolites, and charged solutes. Discovery of new classes of ion-conducting AQP channels has been slow, likely reflecting time- and labor-intensive methods required for traditional electrophysiology. Work here defines a sensitive mass-throughput system for detecting AQP ion channels, identified by rescue of cell growth in the K+-transport-defective yeast strain CY162 following genetic complementation with heterologously expressed cation-permeable channels, using the well characterized human AQP1 channel for proof of concept. Results showed AQP1 conferred transmembrane permeability to cations which rescued survival in CY162 yeast. Comprehensive testing showed that growth response properties fully recapitulated AQP1 pharmacological agonist and antagonist profiles for activation, inhibition, dose-dependence, and structure-function relationships, demonstrating validity of the yeast screening tool for AQP channel identification and drug discovery efforts. This method also provided new information on divalent cation blockers of AQP1, pH sensitivity of antagonists, and ion permeability of human AQP6. Site-directed mutagenesis of AQP1 channel regulatory domains confirmed that yeast growth rescue was mediated by the introduced channels. Optical monitoring with a lithium-sensitive photoswitchable probe in living cells independently demonstrated monovalent cation permeability of AQP1 channels in yeast plasma membrane. Ion channel properties of AQP1 expressed in yeast were consistent with those of AQP1 expressed in Xenopus laevis oocyte and K+-transport defective Escherichia coli. Outcomes here establish a powerful new approach for efficient screening of phylogenetically diverse AQPs for yet untested functions as cation channels.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction: Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway. 撤回：机械生长因子通过抑制 p38 MAPK 通路减轻机械过载诱导的髓核细胞凋亡。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2018-2462_RET

引用次数: 0

Retraction: Nucleus pulposus cell apoptosis is attenuated by CDMP-2 through regulating oxidative damage under the hyper-osmotic environment. 撤回：CDMP-2通过调节高渗透环境下的氧化损伤来减轻髓核细胞凋亡。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2018-1176_RET

引用次数: 0

Retraction: Osteogenic protein-1 attenuates nucleus pulposus cell apoptosis through activating the PI3K/Akt/mTOR pathway in a hyperosmotic culture. 撤回：骨生成蛋白-1在高渗培养中通过激活PI3K/Akt/mTOR途径减轻髓核细胞凋亡

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2018-1708_RET