Pub Date : 2003-07-22DOI: 10.1126/scisignal.1922003tw286
In vertebrate development, the Hox genes, which establish patterns and encode positional information, are found in groups of paralogs. Mutations in individual mouse Hox genes can perturb skeletal elements, but the variable expressivities and penetrance observed with mutations in paralogous Hox genes make it hard to distinguish whether these genes cause patterning at the global or local level. Wellik et al. now report targeted disruptions of all of the alleles of the Hox10 or Hox11 paralogous family to show that Hox genes act in globally patterning of the lumbosacral region of the axial skeleton and are integral in patterning principal elements of the limbs. D. M. Wellik, M. R. Capecchi, Hox10 and Hox11 genes are required to globally pattern the mammalian skeleton. Science 301, 363-367 (2003). [Abstract] [Full Text]
{"title":"Boning Up on Hox Genes","authors":"","doi":"10.1126/scisignal.1922003tw286","DOIUrl":"https://doi.org/10.1126/scisignal.1922003tw286","url":null,"abstract":"In vertebrate development, the Hox genes, which establish patterns and encode positional information, are found in groups of paralogs. Mutations in individual mouse Hox genes can perturb skeletal elements, but the variable expressivities and penetrance observed with mutations in paralogous Hox genes make it hard to distinguish whether these genes cause patterning at the global or local level. Wellik et al. now report targeted disruptions of all of the alleles of the Hox10 or Hox11 paralogous family to show that Hox genes act in globally patterning of the lumbosacral region of the axial skeleton and are integral in patterning principal elements of the limbs. D. M. Wellik, M. R. Capecchi, Hox10 and Hox11 genes are required to globally pattern the mammalian skeleton. Science 301, 363-367 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"136 1","pages":"TW286 - tw286"},"PeriodicalIF":0.0,"publicationDate":"2003-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72689034","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}
Pub Date : 2003-07-15DOI: 10.1126/scisignal.1912003tw279
Amino acid synthesis is tightly controlled in bacteria by a system in which the amino acids themselves, as well as their corresponding transfer RNAs (tRNAs), regulate production. For example, in Bacillus subtilis, the mechanism for regulating tryptophan (Trp) synthesis involves an antiterminator protein called TRAP, which is activated by Trp. However, TRAP activity is antagonized by a protein called anti-TRAP (AT), where the synthesis of AT is induced by uncharged tRNATrp. Chen and Yanofsky now show another level of regulation for the Trp operon in which uncharged tRNATrp also regulates the translation of AT through tandem Trp codons in a leader peptide coding sequence. This mechanism is somewhat reminiscent of the classical Trp attenuation system in Escherchia coli; however, the leader peptide in B. subtilis exerts its effect at the level of translation instead of transcription termination, as seen in E. coli. The authors term the B. subtilis system "regulatory sophistication" because it shows both transcriptional and translational regulation of AT in response to tRNATrp. G. Chen, C. Yanofsky, Tandem transcription and translation regulatory sensing of uncharged tryptophan tRNA. Science 301, 211-213 (2003). [Abstract] [Full Text]
{"title":"A Double Dose of Trp Regulation","authors":"","doi":"10.1126/scisignal.1912003tw279","DOIUrl":"https://doi.org/10.1126/scisignal.1912003tw279","url":null,"abstract":"Amino acid synthesis is tightly controlled in bacteria by a system in which the amino acids themselves, as well as their corresponding transfer RNAs (tRNAs), regulate production. For example, in Bacillus subtilis, the mechanism for regulating tryptophan (Trp) synthesis involves an antiterminator protein called TRAP, which is activated by Trp. However, TRAP activity is antagonized by a protein called anti-TRAP (AT), where the synthesis of AT is induced by uncharged tRNATrp. Chen and Yanofsky now show another level of regulation for the Trp operon in which uncharged tRNATrp also regulates the translation of AT through tandem Trp codons in a leader peptide coding sequence. This mechanism is somewhat reminiscent of the classical Trp attenuation system in Escherchia coli; however, the leader peptide in B. subtilis exerts its effect at the level of translation instead of transcription termination, as seen in E. coli. The authors term the B. subtilis system \"regulatory sophistication\" because it shows both transcriptional and translational regulation of AT in response to tRNATrp. G. Chen, C. Yanofsky, Tandem transcription and translation regulatory sensing of uncharged tryptophan tRNA. Science 301, 211-213 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"51 1","pages":"TW279 - tw279"},"PeriodicalIF":0.0,"publicationDate":"2003-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73275272","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}
Pub Date : 2003-07-01DOI: 10.1126/scisignal.1892003tw252
Neurons target and concentrate voltage-dependent sodium channels in microdomains of the axonal membrane. These sodium channels are clustered at the axonal initial segment, where action potentials are generated, and in the nodes of Ranvier of myelinated axons. How are these components selectively sorted to these domains? Garrido et al. show that a 27-amino acid motif contained in one of the intracellular linkers of the pore-forming subunit can target and concentrate the sodium channel within the initial segment of the axon. This peptide motif was sufficient to direct and to concentrate different proteins to the initial segment. In addition, the overexpression of a cytosolic chimeric protein containing the motif disorganized endogenous sodium channels. J. J. Garrido, P. Giraud, E. Carlier, F. Fernandes, A. Moussif, M.-P. Fache, D. Debanne, B. Dargent, A targeting motif involved in sodium channel clustering at the axonal initial segment. Science 300, 2091-2094 (2003). [Abstract] [Full Text]
神经元在轴突膜的微域内靶向和集中电压依赖性钠通道。这些钠离子通道聚集在产生动作电位的轴突起始段和有髓鞘轴突的兰维尔结。这些组件是如何选择性地排序到这些域的?Garrido等人的研究表明，一个包含27个氨基酸的基序包含在孔隙形成亚基的一个细胞内连接体中，可以靶向并集中轴突初始段内的钠通道。这个肽基序足以引导和集中不同的蛋白质到初始片段。此外，含有基序的细胞质嵌合蛋白的过表达扰乱了内源性钠通道。J. J. Garrido, P. Giraud, E. Carlier, F. Fernandes, A. Moussif, m . p。法希，D. Debanne, B. Dargent，一种涉及钠通道在轴突初始段聚集的靶向基序。科学通报，2003,20(5):444 - 444。【摘要】【全文】
{"title":"How to Concentrate Sodium Channels","authors":"","doi":"10.1126/scisignal.1892003tw252","DOIUrl":"https://doi.org/10.1126/scisignal.1892003tw252","url":null,"abstract":"Neurons target and concentrate voltage-dependent sodium channels in microdomains of the axonal membrane. These sodium channels are clustered at the axonal initial segment, where action potentials are generated, and in the nodes of Ranvier of myelinated axons. How are these components selectively sorted to these domains? Garrido et al. show that a 27-amino acid motif contained in one of the intracellular linkers of the pore-forming subunit can target and concentrate the sodium channel within the initial segment of the axon. This peptide motif was sufficient to direct and to concentrate different proteins to the initial segment. In addition, the overexpression of a cytosolic chimeric protein containing the motif disorganized endogenous sodium channels. J. J. Garrido, P. Giraud, E. Carlier, F. Fernandes, A. Moussif, M.-P. Fache, D. Debanne, B. Dargent, A targeting motif involved in sodium channel clustering at the axonal initial segment. Science 300, 2091-2094 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"2 1","pages":"TW252 - tw252"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75902627","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}
Pub Date : 2003-06-03DOI: 10.1126/scisignal.1852003tw211
The evidence for adaptive mutation in response to environmental stress has been obtained from laboratory strains of organisms that tend to be more homologous than the wild type. Bjedov et al. (see the Perspective by Rosenberg and Hastings) collected about 800 natural isolates of the bacterium Escherichia coli and found that the majority display stress-inducible (or stationary-phase) elevation of mutation in response to growth-limiting conditions. Their analysis shows that carbon starvation is the physiologically relevant trigger and that removing oxygen largely eliminated enhanced mutation in aging colonies. Genetic analysis of a single natural isolate revealed the roles of the carbon-sensing genetic regulators, the stationary-phase and stress-response regulon, the RecA protein, high-fidelity DNA polymerase II, and compromised mismatch repair. Computer simulations showed that the remarkably high frequency of aging colony mutators in natural isolates could be accounted for by the indirect selective advantage of increased genetic variability. I. Bjedov, O. Tenaillon, B. Gérard, V. Souza, E. Denamur, M. Radman, F. Taddei, I. Matic. Stress-induced mutagenesis in bacteria. Science 300, 1404-1409 (2003). [Abstract] [Full Text] S. M. Rosenberg, P. J. Hastings, Modulating mutation rates in the wild. Science 300, 1382-1383 (2003). [Summary] [Full Text]
对环境胁迫的适应性突变的证据已经从生物的实验室菌株中获得，这些菌株往往比野生型更具同源性。Bjedov等人(参见Rosenberg和Hastings的观点)收集了大约800株天然分离的大肠杆菌，发现大多数大肠杆菌在生长限制条件下表现出应力诱导(或静止期)突变的升高。他们的分析表明，碳饥饿是生理上相关的触发因素，去除氧气在很大程度上消除了衰老菌落中增强的突变。单个天然分离物的遗传分析揭示了碳敏感遗传调控因子、静止期和应激反应调控因子、RecA蛋白、高保真DNA聚合酶II和受损错配修复的作用。计算机模拟表明，自然分离株中老化菌落突变体的显著高频率可能是遗传变异性增加的间接选择优势造成的。I. Bjedov, O. Tenaillon, B. gsamrard, V. Souza, E. Denamur, M. Radman, F. Taddei, I. Matic。应激诱导的细菌诱变。科学300,1404-1409(2003)。[摘要]S. M. Rosenberg, P. J. Hastings，调节野生基因突变率。科学通报，2003,19(3)。【摘要】【全文】
{"title":"The Wild Side of Adaptive Mutation","authors":"","doi":"10.1126/scisignal.1852003tw211","DOIUrl":"https://doi.org/10.1126/scisignal.1852003tw211","url":null,"abstract":"The evidence for adaptive mutation in response to environmental stress has been obtained from laboratory strains of organisms that tend to be more homologous than the wild type. Bjedov et al. (see the Perspective by Rosenberg and Hastings) collected about 800 natural isolates of the bacterium Escherichia coli and found that the majority display stress-inducible (or stationary-phase) elevation of mutation in response to growth-limiting conditions. Their analysis shows that carbon starvation is the physiologically relevant trigger and that removing oxygen largely eliminated enhanced mutation in aging colonies. Genetic analysis of a single natural isolate revealed the roles of the carbon-sensing genetic regulators, the stationary-phase and stress-response regulon, the RecA protein, high-fidelity DNA polymerase II, and compromised mismatch repair. Computer simulations showed that the remarkably high frequency of aging colony mutators in natural isolates could be accounted for by the indirect selective advantage of increased genetic variability. I. Bjedov, O. Tenaillon, B. Gérard, V. Souza, E. Denamur, M. Radman, F. Taddei, I. Matic. Stress-induced mutagenesis in bacteria. Science 300, 1404-1409 (2003). [Abstract] [Full Text] S. M. Rosenberg, P. J. Hastings, Modulating mutation rates in the wild. Science 300, 1382-1383 (2003). [Summary] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"37 1","pages":"TW211 - tw211"},"PeriodicalIF":0.0,"publicationDate":"2003-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90656948","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}
Pub Date : 2003-06-03DOI: 10.1126/scisignal.1852003tw212
Cellular morphogenesis is particularly important in plant development, because these cells do not migrate but remain where they are formed. The highly patterned formation of root hairs from some (but not all) epidermal cells of the growing root in Arabidopsis offers an opportunity to study tissue patterning as well as cellular morphogenesis. Ohashi et al. searched for the genes downstream of the group of transcription factors that regulate whether a root hair develops. Beginning with GLABRA2, the furthest downstream of the transcription factors, the authors identified a phospholipase D gene as its direct target. Experimental alterations of the phospholipase D gene expression indicate that phospholipid signaling contributes to cellular morphogenic choices. Y. Ohashi, A. Oka, R. Rodrigues-Pousada, M. Possenti, I. Ruberti, G. Morelli, T. Aoyama, Modulation of phospholipid signaling by GLABRA2 in root-hair pattern formation. Science 300, 1427-1430 (2003). [Abstract] [Full Text]
{"title":"Phospholipid Signaling in Plant Development","authors":"","doi":"10.1126/scisignal.1852003tw212","DOIUrl":"https://doi.org/10.1126/scisignal.1852003tw212","url":null,"abstract":"Cellular morphogenesis is particularly important in plant development, because these cells do not migrate but remain where they are formed. The highly patterned formation of root hairs from some (but not all) epidermal cells of the growing root in Arabidopsis offers an opportunity to study tissue patterning as well as cellular morphogenesis. Ohashi et al. searched for the genes downstream of the group of transcription factors that regulate whether a root hair develops. Beginning with GLABRA2, the furthest downstream of the transcription factors, the authors identified a phospholipase D gene as its direct target. Experimental alterations of the phospholipase D gene expression indicate that phospholipid signaling contributes to cellular morphogenic choices. Y. Ohashi, A. Oka, R. Rodrigues-Pousada, M. Possenti, I. Ruberti, G. Morelli, T. Aoyama, Modulation of phospholipid signaling by GLABRA2 in root-hair pattern formation. Science 300, 1427-1430 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"191 1","pages":"TW212 - tw212"},"PeriodicalIF":0.0,"publicationDate":"2003-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75019654","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}
Pub Date : 2003-05-27DOI: 10.1126/scisignal.1842003tw203
Jonathan Rigelsford
Capsaicin, a natural compound in chili peppers that produces a burning sensation in the mouth, acts through a pain receptor in the mammalian peripheral nervous system, the TRPV1 ion channel. Neurons expressing TRPV1 also perceive pain associated with stimuli such as high temperature and acidity. TRPV1 is activated by the hydrolysis of a membrane phospholipid called phosphatidylinositol 4,5-bisphosphate (PIP2). Prescott and Julius have identified a direct binding site on TRPV1 for PIP2 and show that the strength of this interaction determines the activation threshold of the channel. E. D. Prescott, D. Julius, A modular PIP2 binding site as a determinant of capsaicin receptor sensitivity. Science 300, 1284-1288 (2003). [Abstract] [Full Text]
辣椒素是辣椒中的一种天然化合物，能在口腔中产生灼烧感，它通过哺乳动物外周神经系统中的疼痛感受器TRPV1离子通道起作用。表达TRPV1的神经元也能感知与高温和酸性等刺激相关的疼痛。TRPV1被称为磷脂酰肌醇4,5-二磷酸(PIP2)的膜磷脂水解激活。Prescott和Julius已经确定了PIP2在TRPV1上的直接结合位点，并表明这种相互作用的强度决定了通道的激活阈值。E. D. Prescott, D. Julius，一个模块化PIP2结合位点作为辣椒素受体敏感性的决定因素。科学学报，2003,33(5):387 - 387。【摘要】【全文】
{"title":"Hot Sites","authors":"Jonathan Rigelsford","doi":"10.1126/scisignal.1842003tw203","DOIUrl":"https://doi.org/10.1126/scisignal.1842003tw203","url":null,"abstract":"Capsaicin, a natural compound in chili peppers that produces a burning sensation in the mouth, acts through a pain receptor in the mammalian peripheral nervous system, the TRPV1 ion channel. Neurons expressing TRPV1 also perceive pain associated with stimuli such as high temperature and acidity. TRPV1 is activated by the hydrolysis of a membrane phospholipid called phosphatidylinositol 4,5-bisphosphate (PIP2). Prescott and Julius have identified a direct binding site on TRPV1 for PIP2 and show that the strength of this interaction determines the activation threshold of the channel. E. D. Prescott, D. Julius, A modular PIP2 binding site as a determinant of capsaicin receptor sensitivity. Science 300, 1284-1288 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"10 1","pages":"tw203 - tw203"},"PeriodicalIF":0.0,"publicationDate":"2003-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91364191","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}
Pub Date : 2003-05-27DOI: 10.1126/scisignal.1842003tw205
Dendritic cells (DCs) may play a role in host-pathogen interactions. For example, certain proteins expressed on DCs, such as DC-SIGN, can stimulate the efficiency of infection of target cells by the human immunodeficiency virus (HIV). McDonald et al. visualized individual particles of HIV in living cells and found that DC-associated HIV was recruited to the site of contact with target cells such as T cells. Simultaneously, the HIV receptor and coreceptor were recruited to the contact site. This recruitment effectively concentrates HIV, its receptor, and its coreceptor and presumably facilitates infection. D. McDonald, L. Wu, S. M. Bohks, V. N. KewalRamani, D. Unutmaz, T. J. Hope, Recruitment of HIV and its receptors to dendritic cell-T cell junctions. Science 300, 1295-1297 (2003). [Abstract] [Full Text]
{"title":"Infectious Synapse","authors":"","doi":"10.1126/scisignal.1842003tw205","DOIUrl":"https://doi.org/10.1126/scisignal.1842003tw205","url":null,"abstract":"Dendritic cells (DCs) may play a role in host-pathogen interactions. For example, certain proteins expressed on DCs, such as DC-SIGN, can stimulate the efficiency of infection of target cells by the human immunodeficiency virus (HIV). McDonald et al. visualized individual particles of HIV in living cells and found that DC-associated HIV was recruited to the site of contact with target cells such as T cells. Simultaneously, the HIV receptor and coreceptor were recruited to the contact site. This recruitment effectively concentrates HIV, its receptor, and its coreceptor and presumably facilitates infection. D. McDonald, L. Wu, S. M. Bohks, V. N. KewalRamani, D. Unutmaz, T. J. Hope, Recruitment of HIV and its receptors to dendritic cell-T cell junctions. Science 300, 1295-1297 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"64 1","pages":"tw205 - tw205"},"PeriodicalIF":0.0,"publicationDate":"2003-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91002367","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}
Pub Date : 2003-05-20DOI: 10.1126/scisignal.1832003tw198
Viral infection activates type I interferon genes. This process requires the cooperative activation of several transcription factors, including interferon regulatory factor (IRF)-3 and IFR-7. Signals such as double-stranded RNA lead to the phosphorylation of IRF-3 and IRF-7 by a yet-uncharacterized virus-activated kinase (VAK). Sharma et al. now show that the component of VAK responsible for IRF-3 and IRF-7 phosphorylation is IKKε-TBK-1, an IKK-related kinase complex. Foy et al. observed that the hepatitis C virus (HCV) serine protease (NS3/4A) blocks IFR-3 phosphorylation. Thus, HCV has evolved a mechanism of obstructing the cellular interferon response, potentially through the proteolytic cleavage of this IKKε-TBK-1 complex. S. Sharma, B. R. tenOever, N. Grandvaux, G.-P. Zhou, R. Lin, J. Hiscott, Triggering the interferon antiviral response through an IKK-related pathway. Science 300 1148-1151 (2003). [Abstract] [Full Text] E. Foy, K. Li, C. Wang, R. Sumpter Jr., M. Ikeda, S. M. Lemon, M. Gale Jr., Regulation of interferon regulatory factor-3 by the hepatitis C virus serine protease. Science 300, 1145-1148 (2003). [Abstract] [Full Text]
病毒感染激活I型干扰素基因。这一过程需要多种转录因子的协同激活，包括干扰素调节因子(IRF)-3和IFR-7。双链RNA等信号导致IRF-3和IRF-7被一种尚未表征的病毒活化激酶(VAK)磷酸化。Sharma等人现在表明，VAK中负责IRF-3和IRF-7磷酸化的成分是IKKε-TBK-1，一种ikk相关的激酶复合物。Foy等人观察到丙型肝炎病毒(HCV)丝氨酸蛋白酶(NS3/4A)阻断IFR-3磷酸化。因此，HCV已经进化出一种阻碍细胞干扰素反应的机制，可能是通过IKKε-TBK-1复合物的蛋白水解裂解。S. Sharma, B. R. tenOever, N. Grandvaux, g . p。周瑞麟，林瑞麟，周俊杰。干扰素抗病毒反应在ikk相关通路中的作用。科学通报(2003)。[摘要]E. Foy, K. Li, C. Wang, R. Sumpter Jr.， M. Ikeda, S. M. Lemon, M. Gale Jr.，干扰素调节因子-3在丙型肝炎病毒丝氨酸蛋白酶中的调控作用。科学通报，2003,11(5)。【摘要】【全文】
{"title":"Making and Breaking an Antiviral Response","authors":"","doi":"10.1126/scisignal.1832003tw198","DOIUrl":"https://doi.org/10.1126/scisignal.1832003tw198","url":null,"abstract":"Viral infection activates type I interferon genes. This process requires the cooperative activation of several transcription factors, including interferon regulatory factor (IRF)-3 and IFR-7. Signals such as double-stranded RNA lead to the phosphorylation of IRF-3 and IRF-7 by a yet-uncharacterized virus-activated kinase (VAK). Sharma et al. now show that the component of VAK responsible for IRF-3 and IRF-7 phosphorylation is IKKε-TBK-1, an IKK-related kinase complex. Foy et al. observed that the hepatitis C virus (HCV) serine protease (NS3/4A) blocks IFR-3 phosphorylation. Thus, HCV has evolved a mechanism of obstructing the cellular interferon response, potentially through the proteolytic cleavage of this IKKε-TBK-1 complex. S. Sharma, B. R. tenOever, N. Grandvaux, G.-P. Zhou, R. Lin, J. Hiscott, Triggering the interferon antiviral response through an IKK-related pathway. Science 300 1148-1151 (2003). [Abstract] [Full Text] E. Foy, K. Li, C. Wang, R. Sumpter Jr., M. Ikeda, S. M. Lemon, M. Gale Jr., Regulation of interferon regulatory factor-3 by the hepatitis C virus serine protease. Science 300, 1145-1148 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"43 1","pages":"TW198 - tw198"},"PeriodicalIF":0.0,"publicationDate":"2003-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78548731","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}
Pub Date : 2003-05-06DOI: 10.1126/scisignal.1812003tw182
The decline of cortical functions with age occurs not only in humans but also in monkeys. Degradation of intracortical inhibition may underlie these declines. Leventhal et al. tested this hypothesis by applying either γ-amino-butyric acid (GABA) or GABA receptor agonists directly on neurons in the primary visual cortex of old macaque monkeys. This treatment improved orientation and direction selectivity to visual stimuli in neurons of aged monkeys, but not in young ones. A. G. Leventhal, Y. Wang, M. Pu, Y. Zhou, Y. Ma, GABA and its agonists improved visual cortical function in senescent monkeys. Science 300, 812-815 (2003). [Abstract] [Full Text]
随着年龄的增长，皮质功能的衰退不仅发生在人类身上，也发生在猴子身上。皮质内抑制的退化可能是这些衰退的基础。Leventhal等人通过将γ-氨基丁酸(GABA)或GABA受体激动剂直接应用于老年猕猴初级视觉皮层的神经元来验证这一假设。这种处理改善了老年猴子神经元对视觉刺激的定向和方向选择性，但在年轻猴子中没有。A. G. Leventhal，王艳，濮明，周艳，马艳，GABA及其激动剂对衰老猴子视觉皮质功能的改善。科学通报，2003,32(2)。【摘要】【全文】
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