Pub Date : 2002-02-12DOI: 10.1126/scisignal.1192002tw67
In cancer cells, abnormal methylation patterns of DNA sequences are often present. By examining the role of the PML-RAR fusion gene, a well-studied translocation in leukemia, Di Croce et al. demonstrate that transcriptional silencing in cancer cells can occur through the recruitment of a DNA methyltransferase (Dnmt) by the PML-RAR fusion protein. Recruitment of Dnmts results in the hypermethylation of a PML-RAR target gene, RARβ2. In the presence of PML-RAR and Dnmt, cell differentiation was blocked, but this block could be overcome by administration of retinoic acid. Hence, transcription factors associated with neoplasia can function in methylation-linked silencing of genes important for growth and differentiation. Furthermore, the work shows that a genetic change in cancer can induce epigenetic gene silencing. L. Di Croce, V. A. Raker, M. Corsaro, F. Fazi, M. Fanelli, M. Faretta, F. Fuks, F. Lo Coco, T. Kouzarides, C. Nervi, S. Minucci, P. G. Pelicci, Methyltransferase recruitment and DNA hypermethylation of target promoters by an oncogenic transcription factor. Science 295, 1079-1082 (2002). [Abstract] [Full Text]
在癌细胞中，DNA序列的异常甲基化模式经常存在。Di Croce等人通过研究PML-RAR融合基因(一种在白血病中得到充分研究的易位基因)的作用，证明PML-RAR融合蛋白可以通过募集DNA甲基转移酶(Dnmt)在癌细胞中发生转录沉默。Dnmts的募集导致PML-RAR靶基因RARβ2的高甲基化。在PML-RAR和Dnmt存在的情况下，细胞分化被阻断，但这种阻断可以通过给予维甲酸来克服。因此，与肿瘤相关的转录因子可以在甲基化相关的对生长和分化重要的基因沉默中发挥作用。此外，这项工作表明，癌症的基因变化可以诱导表观遗传基因沉默。L. Di Croce, V. A. Raker, M. Corsaro, F. Fazi, M. Fanelli, M. Faretta, F. Fuks, F. Lo Coco, T. Kouzarides, C. Nervi, S. Minucci, P. G. Pelicci，甲基转移酶募集和靶启动子的DNA超甲基化。科学295,1079-1082(2002)。【摘要】【全文】
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Pub Date : 2002-01-29DOI: 10.1126/scisignal.1172002tw42
The duration of signals emanating from the T cell receptor (TCR) is finely regulated through several processes that control protein half-life, posttranslational modification of proteins, and the recruitment of inhibitory proteins. Egen and Allison have found that the inhibitory protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is recruited to the immunological synapse, in direct proportion to the strength of the TCR signal, where it acts to extinguish TCR-dependent signals. CTLA-4 in T cells that were cultured with antigen-presenting cells (APCs) bearing agonistic or weakly agonistic peptides translocated to microtubule-organizing centers (MTOCs) close to the site of T cell-APC apposition. However, only T cells stimulated with the stronger agonist peptides led to the movement of CTLA-4 to the immune synapse at the plasma membrane. These data suggest that the location of CTLA-4 is dependent on the strength of the signal sent by the TCR. More important, the data suggest a reason why T cells would need a mechanism to inhibit TCR-dependent signaling after a strong signal is elicited. It is in an organism's best interest to have a widely varied immune response to a pathogen. Strong signals by a few T cells (that have high affinity for an antigen) could quickly lead to the proliferation of a very small subset of T cells at the expense of a diverse group of proliferating T cells with varying degrees of affinity for the antigen. Thus, a large number of T cells would recognize a very narrow repertoire of antigen--clearly a situation to the pathogen's advantage. However, by recruiting CTLA-4 to the immune synapse, the prolonged signaling that would be mediated by strongly agonistic antigens is attenuated, such that weakly stimulated T cells have an opportunity to proliferate and increase the diversity of T cell-mediated responses. J. G. Egen, J. P. Allison, Cytotoxic T lymphocyte antigen-4 accumulation in the immunological synapse is regulated by TCR signal strength. Immunity 16, 23-35 (2002). [Online Journal]
{"title":"Celebrating T Cell Diversity","authors":"","doi":"10.1126/scisignal.1172002tw42","DOIUrl":"https://doi.org/10.1126/scisignal.1172002tw42","url":null,"abstract":"The duration of signals emanating from the T cell receptor (TCR) is finely regulated through several processes that control protein half-life, posttranslational modification of proteins, and the recruitment of inhibitory proteins. Egen and Allison have found that the inhibitory protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is recruited to the immunological synapse, in direct proportion to the strength of the TCR signal, where it acts to extinguish TCR-dependent signals. CTLA-4 in T cells that were cultured with antigen-presenting cells (APCs) bearing agonistic or weakly agonistic peptides translocated to microtubule-organizing centers (MTOCs) close to the site of T cell-APC apposition. However, only T cells stimulated with the stronger agonist peptides led to the movement of CTLA-4 to the immune synapse at the plasma membrane. These data suggest that the location of CTLA-4 is dependent on the strength of the signal sent by the TCR. More important, the data suggest a reason why T cells would need a mechanism to inhibit TCR-dependent signaling after a strong signal is elicited. It is in an organism's best interest to have a widely varied immune response to a pathogen. Strong signals by a few T cells (that have high affinity for an antigen) could quickly lead to the proliferation of a very small subset of T cells at the expense of a diverse group of proliferating T cells with varying degrees of affinity for the antigen. Thus, a large number of T cells would recognize a very narrow repertoire of antigen--clearly a situation to the pathogen's advantage. However, by recruiting CTLA-4 to the immune synapse, the prolonged signaling that would be mediated by strongly agonistic antigens is attenuated, such that weakly stimulated T cells have an opportunity to proliferate and increase the diversity of T cell-mediated responses. J. G. Egen, J. P. Allison, Cytotoxic T lymphocyte antigen-4 accumulation in the immunological synapse is regulated by TCR signal strength. Immunity 16, 23-35 (2002). [Online Journal]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"24 1","pages":"tw42 - tw42"},"PeriodicalIF":0.0,"publicationDate":"2002-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87333892","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 : 2002-01-29DOI: 10.1126/scisignal.1172002tw47
Helicobacter pylori is a prevalent human parasite (infecting half the world's population) and is linked to a variety of gut disorders, including severe gastritis and gastric carcinoma. Higashi et al. have elucidated the steps taken by the bacterial CagA protein that transform host cells. After CagA protein is injected by H. pylori into host cells, it is phosphorylated on tyrosine residues by host kinases. Phosphorylated CagA then binds to the Src homology 2 (SH2) domain-containing tyrosine phosphatase (SHP-2), which stimulates SHP-2 translocation to the cell surface where it displays its phosphatase activity. Active membrane-associated SHP-2 then stimulates morphological changes in the host cell that are the prelude to cellular transformation. H. Higashi, R. Tsutsumi, S. Muto, T. Sugiyama, T. Azuma, M. Asaka, M. Hatakeyama, SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pylori CagA protein. Science 295, 683-686 (2002). [Abstract] [Full Text]
幽门螺杆菌是一种普遍存在的人类寄生虫(感染了世界上一半的人口)，与多种肠道疾病有关，包括严重的胃炎和胃癌。Higashi等人已经阐明了细菌CagA蛋白转化宿主细胞的步骤。当幽门螺杆菌将CagA蛋白注入宿主细胞后，它在酪氨酸残基上被宿主激酶磷酸化。磷酸化的CagA随后结合Src同源性2 (SH2)结构域酪氨酸磷酸酶(SHP-2)，刺激SHP-2转运到细胞表面，在那里它显示其磷酸酶活性。活性膜相关SHP-2随后刺激宿主细胞的形态变化，这是细胞转化的前奏。H. Higashi, R. Tsutsumi, S. Muto, T. Sugiyama, T. Azuma, M. Asaka, M. Hatakeyama, SHP-2酪氨酸磷酸酶作为幽门螺杆菌CagA蛋白的细胞内靶点。科学295,683-686(2002)。【摘要】【全文】
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Pub Date : 2002-01-22DOI: 10.1126/scisignal.1162002tw32
Two different mechanisms guide the development of the central nervous system. Molecular signals initially guide developing neurons to the correct position and, once neuronal activity begins, repeated stimulation helps synapses form and mature. Takasu et al. (see the Perspective by Ghosh) describe a signaling mechanism that may integrate these two processes. Ephrins and their receptors are cell-surface proteins that participate in interactions of developing axons and dendrites that are largely independent of neuronal activity. However, the activation of the EphB subtype of ephrin receptors in rat neurons potentiated signaling by N-methyl-D-aspartate (NMDA)-type glutamate receptors, which mediate activity-dependent effects on developing neurons. Activated EphB proteins were associated physically with NMDA receptors and caused the activation of the Src tyrosine kinase, which apparently phosphorylates the NMDA receptor and thus modulates activity-dependent control of neuronal gene expression. M. A. Takasu, M. B. Dalva, R. E. Zigmond, M. E. Greenberg, Modulation of NMDA receptor-dependent calcium influx and gene expression through EphB receptors. Science 295, 491-495 (2002). [Abstract] [Full Text] A. Ghosh, Learning more about NMDA receptor regulation. Science 295, 449-450 (2002). [Full Text]
两种不同的机制指导中枢神经系统的发育。分子信号最初引导发育中的神经元到正确的位置，一旦神经元活动开始，反复的刺激有助于突触的形成和成熟。Takasu等人(参见Ghosh的观点)描述了一种可能整合这两个过程的信号机制。ephrin及其受体是参与轴突和树突相互作用的细胞表面蛋白，在很大程度上独立于神经元活动。然而，大鼠神经元中ephrin受体EphB亚型的激活增强了n -甲基-d -天冬氨酸(NMDA)型谷氨酸受体的信号传导，该受体介导发育神经元的活性依赖性作用。活化的EphB蛋白与NMDA受体物理相关，并引起Src酪氨酸激酶的激活，该激酶明显磷酸化NMDA受体，从而调节神经元基因表达的活性依赖性控制。高松，李晓明，李晓明，李晓明。NMDA受体依赖性钙内流的基因表达调控。科学通报，2004(2)。【摘要】【全文】A. Ghosh, learn more about NMDA受体调控。科学295,449-450(2002)。(全文)
{"title":"Coordinating Synaptic Development","authors":"","doi":"10.1126/scisignal.1162002tw32","DOIUrl":"https://doi.org/10.1126/scisignal.1162002tw32","url":null,"abstract":"Two different mechanisms guide the development of the central nervous system. Molecular signals initially guide developing neurons to the correct position and, once neuronal activity begins, repeated stimulation helps synapses form and mature. Takasu et al. (see the Perspective by Ghosh) describe a signaling mechanism that may integrate these two processes. Ephrins and their receptors are cell-surface proteins that participate in interactions of developing axons and dendrites that are largely independent of neuronal activity. However, the activation of the EphB subtype of ephrin receptors in rat neurons potentiated signaling by N-methyl-D-aspartate (NMDA)-type glutamate receptors, which mediate activity-dependent effects on developing neurons. Activated EphB proteins were associated physically with NMDA receptors and caused the activation of the Src tyrosine kinase, which apparently phosphorylates the NMDA receptor and thus modulates activity-dependent control of neuronal gene expression. M. A. Takasu, M. B. Dalva, R. E. Zigmond, M. E. Greenberg, Modulation of NMDA receptor-dependent calcium influx and gene expression through EphB receptors. Science 295, 491-495 (2002). [Abstract] [Full Text] A. Ghosh, Learning more about NMDA receptor regulation. Science 295, 449-450 (2002). [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"52 1","pages":"tw32 - tw32"},"PeriodicalIF":0.0,"publicationDate":"2002-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87023607","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 : 2002-01-15DOI: 10.1126/scisignal.1152002tw20
Src-homology 3 domains (SH3 domains) are so named for their similarity to a region in the proto-oncogene protein kinase Src. SH3 domain family members bind to protein domains characterized by paired proline residues, and so mediate protein-protein interactions in cell signaling and cytoskeleton reorganization. Tong et al. (see the Perspective by Gerstein et al.) used phage display to search peptide libraries of random sequences to identify preferred binding motifs for the various SH3 domains. They then searched the predicted proteome of Saccharomyces cerevisiae for potential binding partners, and also used a two-hybrid assay to identify proteins that interacted with the various SH3 domains when expressed in yeast. The common interactions from the networks predicted by each of these procedures were then assessed for likely biological significance. A. H. Y. Tong, B. Drees, G. Nardelli, G. D. Bader, B. Brannetti, L. Castagnoli, M. Evangelista, S. Ferracuti, B. Nelson, S. Paoluzi, M. Quondam, A. Zucconi, C. W. V. Hogue, S. Fields, C. Boone, G. Cesareni, A combined experimental and computational strategy to define protein interaction networks for peptide recognition modules. Science 295, 321-324 (2002). [Abstract] [Full Text] M. Gerstein, N. Lan, R. Jansen, Integrating interactomes. Science 295, 284-287 (2002). [Abstract] [Full Text]
Src同源3结构域(SH3结构域)因其与原癌基因蛋白激酶Src中的一个区域相似而得名。SH3结构域家族成员结合以配对脯氨酸残基为特征的蛋白质结构域，从而介导细胞信号传导和细胞骨架重组中的蛋白质相互作用。Tong等人(参见Gerstein等人的观点)使用噬菌体展示来搜索随机序列的肽库，以确定各种SH3结构域的首选结合基序。然后，他们搜索了酿酒酵母的预测蛋白质组，寻找潜在的结合伙伴，并使用双杂交试验鉴定了在酵母中表达时与各种SH3结构域相互作用的蛋白质。这些程序预测的网络的共同相互作用，然后评估可能的生物学意义。A. H. Y. Tong, B. Drees, G. Nardelli, G. D. Bader, B. Brannetti, L. Castagnoli, M. Evangelista, S. Ferracuti, B. Nelson, S. Paoluzi, M. Quondam, A. Zucconi, C. W. V. Hogue, S. Fields, C. Boone, G. Cesareni，一种结合实验和计算策略来定义蛋白质相互作用网络的肽识别模块。科学295,321-324(2002)。[摘要]M. Gerstein, N. Lan, R. Jansen。科学295,284-287(2002)。【摘要】【全文】
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Pub Date : 2002-01-15DOI: 10.1126/scisignal.1152002tw21
The serine-threonine kinase protein kinase D (PKD) binds to the trans-Golgi network (TGN) in mammalian cells and is involved in the release of transport vesicles destined for the plasma membrane. Baron and Malhotra (see the Perspective by Bankaitis) now show that in order for PKD to bind to the TGN, it must specifically bind to the lipid diacylglycerol. When concentrations of this lipid were reduced in cells, both PKD recruitment to the TGN and transport out of the TGN were inhibited. C. L. Baron, V. Malhotra, Role of diacylglycerol in PKD recruitment to the TGN and protein transport to the plasma membrane. Science 295, 325-328 (2002). [Abstract] [Full Text] V. A. Bankaitis, Slick recruitment to the Golgi. Science 295, 290-291 (2002). [Full Text]
丝氨酸-苏氨酸激酶蛋白激酶D (PKD)在哺乳动物细胞中与反式高尔基网络(TGN)结合，并参与向质膜释放运输囊泡。Baron和Malhotra(见Bankaitis的观点)现在表明，为了使PKD与TGN结合，它必须特异性地与脂质二酰基甘油结合。当细胞中这种脂质浓度降低时，PKD向TGN的募集和TGN外的转运都受到抑制。C. L. Baron, V. Malhotra，二酰基甘油在PKD募集到TGN和蛋白质转运到质膜中的作用。科学295,325-328(2002)。【摘要】【全文】V. A. Bankaitis, Slick招募到高尔基人。科学295,290-291(2002)。(全文)
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Pub Date : 2001-12-18DOI: 10.1126/scisignal.1132001tw464
Hepatitis B virus (HBV) infects 300 million people worldwide and causes liver disease and cancer. The X-protein of HBV is essential for viral infection and has been implicated in carcinogenesis, but its exact role has been enigmatic. It is known to infiltrate cell signaling pathways and to activate modest transcription from various promoters, as well as strongly activate viral replication in certain cell lines. The X-protein activates Src without interacting directly with Src. Bouchard et al. (see the Perspective by Ganem) have now discovered that this activation is mediated the activation of another kinase called Pyk. The activation of Pyk is caused by a release of calcium from intracellular stores (most likely the mitochondrion) triggered by X-protein. M. J. Bouchard, L.-H. Wang, R. J. Schneider, Calcium signaling by HBx protein in hepatitis B virus DNA replication. Science 294, 2376-2378 (2001). [Abstract] [Full Text] D. Ganem, The X files--one step closer to closure. Science 294, 2299-2300 (2001). [Full Text]
乙型肝炎病毒(HBV)感染了全世界3亿人，并导致肝脏疾病和癌症。HBV的x蛋白是病毒感染所必需的，并与癌变有关，但其确切作用仍是谜。众所周知，它可以渗透细胞信号通路，激活各种启动子的适度转录，并在某些细胞系中强烈激活病毒复制。x蛋白激活Src而不直接与Src相互作用。Bouchard等人(参见Ganem的观点)现在发现，这种激活是由另一种名为Pyk的激酶的激活介导的。Pyk的激活是由x蛋白触发的细胞内储存(最有可能是线粒体)钙的释放引起的。M. J.布沙尔，l . h .;乙肝病毒DNA复制中HBx蛋白钙信号转导的研究。科学294,2376-2378(2001)。【摘要】【全文】D. Ganem, The X files——离结案又近了一步。科学29,2299-2300(2001)。(全文)
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Pub Date : 2001-12-18DOI: 10.1126/scisignal.1132001tw461
Genome sequencing projects have revealed thousands of genes of unknown functions. For the budding yeast Saccharomyces cerevisiae, large-scale gene deletion analysis has shown that >80% of the ~6200 predicted or known yeast genes are not required for viability. Thus, many genes and pathways of eukaryotic cells may be functionally redundant, or may not show easily recognizable phenotypes if perturbed. To address this problem, Tong et al. developed an automated method for systematic construction of double mutants called synthetic genetic array (SGA) analysis. A yeast strain that carries a mutation in the "query" gene is linked to a selectable marker and crossed to members of a collection of haploid deletion strains in which almost every nonessential gene in the yeast genome is represented. If a double mutant cannot be produced or grows much more slowly than normal, it is an indication that there may be a functional interaction between the two genes. Putative interactions that are identified through this technology can then be readily confirmed by tetrad analysis. Eight query genes involved in cytoskeletal organization, DNA repair, or unknown functions were analyzed, resulting in the construction of a network identifying 291 putative genetic interactions involving 204 genes. A. H. Y. Tong, M. Evangelista, A. B. Parsons, H. Xu, G. D. Bader, N. Pagé, M. Robinson, S. Raghibizadeh, C. W. V. Hogue, H. Bussey, B. Andrews, M. Tyers, C. Boone, Systematic genetic analysis with ordered arrays of yeast deletion mutants. Science 294, 2364-2368 (2001). [Abstract] [Full Text]
基因组测序项目已经揭示了数千个功能未知的基因。对于出芽酵母Saccharomyces cerevisiae，大规模基因缺失分析表明，在约6200个预测或已知的酵母基因中，>80%是不需要生存的。因此，真核细胞的许多基因和途径可能在功能上是冗余的，或者如果受到干扰，可能不会显示容易识别的表型。为了解决这个问题，Tong等人开发了一种自动化的双突变体系统构建方法，称为合成基因阵列(SGA)分析。携带“查询”基因突变的酵母菌株与一个可选择的标记相连接，并与一组单倍体缺失菌株的成员杂交，其中几乎代表了酵母菌基因组中的每一个非必需基因。如果不能产生双突变体或比正常突变体生长得慢得多，则表明两个基因之间可能存在功能相互作用。通过这种技术确定的假定相互作用可以很容易地通过四分体分析加以证实。研究人员分析了涉及细胞骨架组织、DNA修复或未知功能的8个查询基因，从而构建了一个网络，确定了涉及204个基因的291个假定的遗传相互作用。A. H. Y. Tong, M. Evangelista, A. B. Parsons, H. Xu, G. D. Bader, N. pageer, M. Robinson, S. Raghibizadeh, C. W. V. Hogue, H. Bussey, B. Andrews, M. Tyers, C. Boone，酵母缺失突变体有序阵列的系统遗传分析。科学29,2364-2368(2001)。【摘要】【全文】
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Pub Date : 2001-12-11DOI: 10.1126/scisignal.1122001tw460
In vertebrate olfactory neurons, odor molecules stimulate the opening of cyclic nucleotide-gated channels (CNGs). The resulting influx of Ca2+ ions also triggers a negative-feedback mechanism in which channel activity is inhibited when bound to a Ca2+-calmodulin (CaM) complex. This mechanism promotes olfactory adaptation and allows animals to evaluate the odor environment continually. Two groups have determined that two of the channel's three subunits are required for odor adaptation. Munger et al. show that channels from mice lacking the CNGA4 subunit exhibited slower Ca2+-CaM-mediated inhibition. Bradley et al. have used a heterologous expression system to show that both the CNGA4 and CNGB1b subunits facilitate Ca2+-CaM binding to the open state of channel. S. D. Munger, A. P. Lane, H. Zhong, T. Leinders-Zufall, K.-W. Yau, F. Zufall, R. R. Reed, Central role of the CNGA4 channel subunit in Ca2+-calmodulin-dependent odor adaptation. Science 294, 2172-2175 (2001). [Online Journal] J. Bradley, D. Reuter, S. Frings, Facilitation of calmodulin-mediated odor adaptation by cAMP-gated channel subunits. Science 294, 2176-2178 (2001). [Online Journal]
在脊椎动物嗅觉神经元中，气味分子刺激环核苷酸门控通道(CNGs)的打开。由此产生的Ca2+离子内流也触发了负反馈机制，当与Ca2+-钙调蛋白(CaM)复合物结合时，通道活性被抑制。这一机制促进了嗅觉适应，使动物能够不断地评估气味环境。两个研究小组已经确定，该通道的三个亚基中有两个是气味适应所必需的。Munger等人表明，缺乏CNGA4亚基的小鼠通道表现出较慢的Ca2+- cam介导的抑制。Bradley等人使用异源表达系统表明，CNGA4和CNGB1b亚基都能促进Ca2+-CaM结合到通道的开放状态。S. D. Munger, A. P. Lane，钟洪，T. Leinders-Zufall, k.w。邱，朱福尔，里德，CNGA4通道亚基在Ca2+钙调素依赖性气味适应中的核心作用。科学29(2001)，2172-2175。[网络杂志]张建军，张建军，张建军，等。钙调素介导的气味调节的研究进展。科学29,2176-2178(2001)。(在线期刊)
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Pub Date : 2001-12-04DOI: 10.1126/scisignal.1112001tw447
Attenuating a cellular signal is just as critical as inducing it. For example, regulator of G protein signaling (RGS) proteins modulate the signaling output from receptor-coupled heterotrimeric G proteins. Zheng et al. (see the Perspective by von Zastrow and Mostov) have identified what has been an elusive RGS for the Gαs class of G proteins. Named RGS-PX1, it also contains a membrane-interacting PhoX domain whose presence suggests a link between G protein signaling and vesicle trafficking in cells. B. Zheng, Y.-C. Ma, R. S. Ostrom, C. Lavoie, G. N. Gill, P. A. Insel, X.-Y. Huang, M. G. Farquhar, RGS-PX1, a GAP for Gαs and sorting nexin in vesicular trafficking. Science 294, 1939-1942 (2001). [Abstract] [Full Text] M. von Zastrow, K. Mostov, A new thread in an intricate web. Science 294, 1845-1847 (2001). [Full Text]
衰减手机信号与诱导手机信号同样重要。例如，G蛋白信号调节蛋白(RGS)调节受体偶联异三聚体G蛋白的信号输出。Zheng等人(见von Zastrow和Mostov的观点)已经确定了Gαs类G蛋白的难以捉摸的RGS。它被命名为RGS-PX1，还包含一个与膜相互作用的PhoX结构域，其存在表明G蛋白信号传导与细胞中囊泡运输之间存在联系。郑B.， yyc .。马，R. S. Ostrom, C. Lavoie, G. N. Gill, P. A. Insel, x.y。黄明辉，黄明辉，黄明辉，RGS-PX1, g - α - s与分选连接蛋白在囊泡转运中的GAP。科学294,1939-1942(2001)。[摘要]M. von Zastrow, K. Mostov，复杂网络中的新线索。科学294,1845-1847(2001)。(全文)
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