Current Protocols in Pharmacology最新文献_第10页

Overview of Genetically Engineered Mouse Models of Papillary and Anaplastic Thyroid Cancers: Enabling Translational Biology for Patient Care Improvement 乳头状癌和间变性甲状腺癌基因工程小鼠模型综述:促进转化生物学改善患者护理

Current Protocols in Pharmacology Pub Date : 2015-06-01 DOI: 10.1002/0471141755.ph1433s69

Roch-Philippe Charles

引用次数: 1

Murine Models of Helicobacter (pylori or felis)-associated Gastric Cancer 幽门螺杆菌相关胃癌的小鼠模型

Current Protocols in Pharmacology Pub Date : 2015-06-01 DOI: 10.1002/0471141755.ph1434s69

Carrie A. Duckworth, Michael D. Burkitt, Jonathan M. Williams, Bryony N. Parsons, Joseph M.F. Tang, D. Mark Pritchard

{"title":"Murine Models of Helicobacter (pylori or felis)-associated Gastric Cancer","authors":"Carrie A. Duckworth, Michael D. Burkitt, Jonathan M. Williams, Bryony N. Parsons, Joseph M.F. Tang, D. Mark Pritchard","doi":"10.1002/0471141755.ph1434s69","DOIUrl":"10.1002/0471141755.ph1434s69","url":null,"abstract":"Gastric adenocarcinoma is the fifth most common cancer and third most common cause of cancer-related death in the world. The majority of these cancers develop in genetically susceptible individuals who are chronically infected with the Gram-negative bacterium Helicobacter pylori. Often these individuals have also been exposed to certain environmental factors that increase susceptibility, such as dietary components. Murine models of Helicobacter-induced gastric cancer are valuable tools for investigating the mechanisms responsible for the stepwise pathological changes of chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric adenocarcinoma. Helicobacter felis colonization greatly accelerates the development of gastric neoplasia in mice, and causes pathologies similar to those observed with Helicobacter pylori-associated gastric carcinogenesis in humans. These mouse models are therefore useful for investigating genetic and environmental factors that may be involved in the pathogenesis and treatment of gastric cancer. Detailed in these protocols are procedures for inducing Helicobacter-associated carcinogenesis in mice as well as the histological analysis and interpretation of gastric pathology in these animals. © 2015 by John Wiley & Sons, Inc.","PeriodicalId":10871,"journal":{"name":"Current Protocols in Pharmacology","volume":"69 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/0471141755.ph1434s69","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34152420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Determination of GPCR Phosphorylation Status: Establishing a Phosphorylation Barcode. 测定GPCR磷酸化状态:建立磷酸化条形码。

Current Protocols in Pharmacology Pub Date : 2015-06-01 DOI: 10.1002/0471141755.ph0213s69

Rudi Prihandoko, Sophie J Bradley, Andrew B Tobin, Adrian J Butcher

{"title":"Determination of GPCR Phosphorylation Status: Establishing a Phosphorylation Barcode.","authors":"Rudi Prihandoko, Sophie J Bradley, Andrew B Tobin, Adrian J Butcher","doi":"10.1002/0471141755.ph0213s69","DOIUrl":"https://doi.org/10.1002/0471141755.ph0213s69","url":null,"abstract":"G protein-coupled receptors (GPCRs) are rapidly phosphorylated following agonist occupation in a process that mediates receptor uncoupling from its cognate G protein, a process referred to as desensitization. In addition, this process provides a mechanism by which receptors can engage with arrestin adaptor molecules and couple to downstream signaling pathways. The importance of this regulatory process has been highlighted recently by the understanding that ligands can direct receptor signaling along one pathway in preference to another, the phenomenon of signaling bias that is partly mediated by the phosphorylation status or phosphorylation barcode of the receptor. Methods to determine the phosphorylation status of a GPCR in vitro and in vivo are necessary to understand not only the physiological mechanisms involved in GPCR signaling, but also to fully examine the signaling properties of GPCR ligands. This unit describes detailed methods for determining the overall phosphorylation pattern on a receptor (the phosphorylation barcode), as well as mass spectrometry approaches that can define the precise sites that become phosphorylated. These techniques, coupled with the generation and characterization of receptor phosphorylation-specific antibodies, provide a full palate of techniques necessary to determine the phosphorylation status of any given GPCR subtype.","PeriodicalId":10871,"journal":{"name":"Current Protocols in Pharmacology","volume":"69 ","pages":"2.13.1-2.13.26"},"PeriodicalIF":0.0,"publicationDate":"2015-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/0471141755.ph0213s69","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34152421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21

Rodent Models of Amyotrophic Lateral Sclerosis. 肌萎缩侧索硬化症啮齿动物模型。

Current Protocols in Pharmacology Pub Date : 2015-06-01 DOI: 10.1002/0471141755.ph0567s69

Thomas Philips, Jeffrey D Rothstein

{"title":"Rodent Models of Amyotrophic Lateral Sclerosis.","authors":"Thomas Philips, Jeffrey D Rothstein","doi":"10.1002/0471141755.ph0567s69","DOIUrl":"https://doi.org/10.1002/0471141755.ph0567s69","url":null,"abstract":"Amyotrophic Lateral Sclerosis (ALS) is a motor neuron disease affecting upper and lower motor neurons in the central nervous system. Patients with ALS develop extensive muscle wasting and atrophy leading to paralysis and death 3 to 5 years after disease onset. The condition may be familial (fALS 10%) or sporadic ALS (sALS, 90%). The large majority of fALS cases are due to genetic mutations in the Superoxide dismutase 1 gene (SOD1, 15% of fALS) and repeat nucleotide expansions in the gene encoding C9ORF72 (∼40% to 50% of fALS and ∼10% of sALS). Studies suggest that ALS is mediated through aberrant protein homeostasis (i.e., ER stress and autophagy) and/or changes in RNA processing (as in all non‐SOD1‐mediated ALS). In all of these cases, animal models suggest that the disorder is mediated non‐cell autonomously, i.e., not only motor neurons are involved, but glial cells including microglia, astrocytes, and oligodendrocytes, and other neuronal subpopulations are also implicated in the pathogenesis. Provided in this unit is a review of ALS rodent models, including discussion of their relative advantages and disadvantages. Emphasis is placed on correlating the model phenotype with the human condition and the utility of the model for defining the disease process. Information is also presented on RNA processing studies in ALS research, with particular emphasis on the newest ALS rodent models. © 2015 by John Wiley & Sons, Inc.","PeriodicalId":10871,"journal":{"name":"Current Protocols in Pharmacology","volume":"69 ","pages":"5.67.1-5.67.21"},"PeriodicalIF":0.0,"publicationDate":"2015-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/0471141755.ph0567s69","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34049084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 161

Single-Channel Analysis of Glutamate Receptors 谷氨酸受体的单通道分析

Current Protocols in Pharmacology Pub Date : 2015-03-02 DOI: 10.1002/0471141755.ph1117s68

Chris Shelley

引用次数: 0

Arrestin-3-Dependent Activation of c-Jun N-Terminal Kinases (JNKs) c-Jun n-末端激酶(JNKs)依赖性的arrestin -3激活

Current Protocols in Pharmacology Pub Date : 2015-03-02 DOI: 10.1002/0471141755.ph0212s68

Xuanzhi Zhan, Seunghyi Kook, Tamer S. Kaoud, Kevin N. Dalby, Eugenia V. Gurevich, Vsevolod V. Gurevich

{"title":"Arrestin-3-Dependent Activation of c-Jun N-Terminal Kinases (JNKs)","authors":"Xuanzhi Zhan, Seunghyi Kook, Tamer S. Kaoud, Kevin N. Dalby, Eugenia V. Gurevich, Vsevolod V. Gurevich","doi":"10.1002/0471141755.ph0212s68","DOIUrl":"10.1002/0471141755.ph0212s68","url":null,"abstract":"Only one out of four mammalian arrestin subtypes, arrestin-3, facilitates the activation of JNK family kinases. Here we describe two different protocols used for elucidating the mechanisms involved. One is based on reconstitution of signaling modules from purified proteins: arrestin-3, MKK4, MKK7, JNK1, JNK2, and JNK3. The main advantage of this method is that it unambiguously establishes which effects are direct because only intended purified proteins are present in these assays. The key drawback is that the upstream-most kinases of these cascades, ASK1 or other MAPKKKs, are not available in purified form, limiting reconstitution to incomplete two-kinase modules. The other approach is used for analyzing the effects of arrestin-3 on JNK activation in intact cells. In this case, signaling modules include ASK1 and/or other MAPKKKs. However, as every cell expresses thousands of different proteins their possible effects on the readout cannot be excluded. Nonetheless, the combination of in vitro reconstitution from purified proteins and cell-based assays makes it possible to elucidate the mechanisms of arrestin-3-dependent activation of JNK family kinases. © 2015 by John Wiley & Sons, Inc.","PeriodicalId":10871,"journal":{"name":"Current Protocols in Pharmacology","volume":"68 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/0471141755.ph0212s68","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33102481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Generation of Human Acute Lymphoblastic Leukemia Xenografts for Use in Oncology Drug Discovery 用于肿瘤药物发现的人类急性淋巴细胞白血病异种移植物的产生

Current Protocols in Pharmacology Pub Date : 2015-03-02 DOI: 10.1002/0471141755.ph1432s68

Linda Holmfeldt, Charles G. Mullighan

引用次数: 6

Single-Channel Recording of Glutamate Receptors 谷氨酸受体的单通道记录

Current Protocols in Pharmacology Pub Date : 2015-03-02 DOI: 10.1002/0471141755.ph1116s68

Chris Shelley

引用次数: 1

Overview of Different Mechanisms of Arrestin-Mediated Signaling 阻滞蛋白介导的信号传导不同机制综述

Current Protocols in Pharmacology Pub Date : 2014-12-01 DOI: 10.1002/0471141755.ph0210s67

Vsevolod V. Gurevich, Eugenia V. Gurevich

{"title":"Overview of Different Mechanisms of Arrestin-Mediated Signaling","authors":"Vsevolod V. Gurevich, Eugenia V. Gurevich","doi":"10.1002/0471141755.ph0210s67","DOIUrl":"10.1002/0471141755.ph0210s67","url":null,"abstract":"Arrestins are characterized by their ability to selectively bind active, phosphorylated GPCRs and suppress (arrest) receptor coupling to G proteins. Nonvisual arrestins are also signaling proteins in their own right, activating a variety of cellular pathways. Arrestins are highly flexible proteins that can assume many distinct conformations. In their receptor-bound conformation, arrestins have higher affinity for a subset of partners. This explains how receptor activation regulates certain branches of arrestin-dependent signaling via arrestin recruitment to GPCRs. However, free arrestins are also active molecular entities that act in other pathways and localize signaling proteins to particular subcellular compartments, such as cytoskeleton. These functions are regulated by the enhancement or reduction of arrestin affinity for target proteins by other binding partners and by proteolytic cleavage. Recent findings suggest that the two visual arrestins, arrestin-1 and arrestin-4, which are expressed in photoreceptor cells, do not regulate signaling solely via binding to photopigments but also interact with a variety of nonreceptor partners, critically affecting the health and survival of photoreceptor cells. Detailed in this overview are GPCR-dependent and independent modes of arrestin-mediated regulation of cellular signaling pathways. © 2014 by John Wiley & Sons, Inc.","PeriodicalId":10871,"journal":{"name":"Current Protocols in Pharmacology","volume":"67 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/0471141755.ph0210s67","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10468442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 40

Guinea Pig Models of Asthma 豚鼠哮喘模型

Current Protocols in Pharmacology Pub Date : 2014-12-01 DOI: 10.1002/0471141755.ph0526s67

Alice E. McGovern, Stuart B. Mazzone

引用次数: 1