详细信息见 http://f1000biology.com/browse/CHEMBIOL/cell 国际生物学专家按F1000 Factor评出的细胞化学生物学国际优秀论文，你可以选择查阅近一周至近五年发表的优秀论文。 可按以下分类进行检索查阅： Chemical Biology Biocatalysis Bioinorganic Chemistry Biomimetic Chemistry Chemical Biology of the Cell Directed Molecular Evolution Macromolecular Chemistry Protein Chemistry Proteomics Small Molecule Chemistry
详细信息见 http://www.scimagojr.com/journalsearch.php?q=18434tip=sidclean=0 Cell Country : United States Subject Area : Biochemistry, Genetics and Molecular Biology Subject Category : Cell Biology , Molecular Biology Publisher : Cell Press . Publication type : Journals. ISSN : 00928674, 10974172 Coverage: 1974-2009 H Index : 431 Scope: For more than 30 years, top international researchers have relied on Cell to publish high impact papers that have come For more than 30 years, top international researchers have relied on Cell to publish high impact papers that have come to form the foundation of contemporary life science research. Founded by Benjamin Lewin (author of Genes), Cell remains at the forefront of exciting developments in biology, continually redefining the important areas of science with cutting edge papers. Published biweekly, Cell includes original research articles of exceptional significance in areas including molecular biology, biochemistry, cancer research, cell biology, developmental biology, genetics, immunology, microbiology, neurobiology, plant biology, structural biology and virology. ( source ) Show full scope Charts Data SJR indicator vs. Cites per Doc (2y) // The SJR indicator measures the scientific influence of the average article in a journal, it expresses how central to the global scientific discussion an average article of the journal is. Cites per Doc. (2y) measures the scientific impact of an average article published in the journal, it is computed using the same formula that journal impact factor (Thomson Reuters). Citation vs. Self-Citation // Evolution of the total number of citations and journal's self-citations received by a journal's published documents during the three previous years. Cites per Document vs. External Cites per Document // Evolution of the number of total cites per document and external cites per document (i.e. journal self-citations removed) received by a journal's published documents during the three previous years. Cites per Document in 2, 3 and 4 years windows // Evolution of Citations per Document to a journal's published documents during the two, three and four previous years. The two years line is equivalent to journal impact factor (Thomson Reuters) metric. International Collaboration // International Collaboration accounts for the articles that have been produced by researchers from several countries. The chart shows the ratio of a journal's documents signed by researchers from more than one country. Journal's Citable vs. Non Citable Documents // Not every article in a journal is considered primary research and therefore citable, this chart shows the ratio of a journal's articles including substantial research (research articles, conference papers, reviews and short reviews) in three years windows. Journal's Cited vs. Uncited Documents // Ratio of a journal's items, grouped in three years windows, that have been cited at least once vs. those not cited during the following year. Indicators 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 SJR 31,610 29,031 23,518 21,230 19,641 17,043 16,015 14,170 14,117 12,802 Total Documents 354 350 372 363 368 407 463 552 555 535 Total Docs. (3years) 1.359 1.246 1.132 1.076 1.085 1.103 1.138 1.238 1.422 1.570 Total References 15.869 16.586 15.337 16.154 14.525 15.867 16.621 19.365 19.486 18.726 Total Cites (3years) 47.364 41.329 32.730 29.356 28.885 27.413 26.671 26.632 29.440 32.388 Self Cites (3years) 908 894 664 543 502 455 482 601 699 633 Citable Docs. (3years) 1.136 1.023 909 837 837 820 821 855 955 1.023 Cites / Doc. (4years) 41,69 40,14 37,18 34,61 34,08 34,13 32,05 31,38 30,91 31,75 Cites / Doc. (3years) 41,69 40,40 36,01 35,07 34,51 33,43 32,49 31,15 30,83 31,66 Cites / Doc. (2years) 40,43 38,21 35,73 34,35 33,05 33,28 31,62 30,68 29,86 31,86 References / Doc. 44,83 47,39 41,23 44,50 39,47 38,99 35,90 35,08 35,11 35,00 Cited Docs. 1.335 1.221 1.112 1.048 1.054 1.044 1.045 1.083 1.240 1.358 Uncited Docs. 24 25 20 28 31 59 93 155 182 212 % International Collaboration 29,66 20,00 20,43 22,87 24,18 25,55 27,43 22,46 24,68 21,12
看到这里谈论熵的兴致颇高，也来凑个热闹： 2007 年，以提出细胞复制衰老而享誉世界的美国加州大学教授 Leonard Hayflick 向世界宣告衰老已经不再是个谜：熵增决定衰老，基因决定寿命 然而， Hayflick 教授关于生物体的熵增生化概念却出现了许多粗浅的甚至谬误的表述。这到底是怎么回事呢？ 例如， Hayflick 教授在文章中大谈，根据热力学定律则有： 1 ）防止化学键断裂以及其它结构变化是生命的至要 (The prevention of chemical bond breakage, among other structural changes, is absolutely essential for life) ； 2 ）能量散失会导致生物失活及分子变性 (The dispersal of energy may result in a biologically inactive or malfunctioning molecule) ； 3 ）甚至把生物的寿命与生命体细胞个数达到阿伏加德罗常数（ 6x10 23 ）相捆绑（ the molecules present at the beginning of a biological lineage are unlikely to be present in that lineage when it reaches Avogadro s Number of about 6x10 23 cells ）； 我们知道生命体与非生命体有一个重要的区别：生命体不仅不惧怕能量丧失，甚至对种种损伤造成的化学键的断裂也无所畏惧 生物体具有高效地甚至是完美地防御修复和更新的能力。上述种种对于生物体衰老生化的外行言辞，简单幼稚地把热力学定律往衰老上套，说明了 Hayflick 教授在衰老生化领域的知识断层，尽管 Hayflick 作为一个老年学的领军科学家在鸟瞰衰老科学大世界时越来越清醒地知道了熵增生化一定包含着衰老过程的真谛（薛定谔假说），但是对于具体的熵增生化地解释却显得捉襟见肘。 那么熵增到底如何导致了生物体的衰老呢？ 2003 年，《中国老年学杂志》在第 9 期刊首发表了一篇笔者的文章，题为衰老，生命与熵增之战，在老年学研究领域首次一语道破天机地指出了熵增衰老的具体生化内涵，简言之，即所谓生物体内的熵增就是与龄俱增的老年色素类不可逆生化产物的累积。例如 , 生物体与衰老相关的不可修复性生化垃圾的主要成分是高级糖基化终产物（ AGEs ）和高级脂质过氧化终产物（ ALEs ）。因为 AGEs 和 ALEs 的自由能较正常生物大分子低，体内对于这些老年色素类聚合物又没有相应的媒解体系，因而在体内逐渐发生稳定地蓄积，从而造成皮肤起皱，血管硬化，组织纤维化等生理性老化性状。 2005 年，美国《实验老年学（ Experimental Gerontology ）》杂志进一步刊出了中国科学家关于衰老本质的论文，全面系统地解读了生物体在能量代谢过程中由于生化副反应而造成熵增性生物垃圾蓄积的具体过程。中国科学家的画龙点睛之作，一语道破天机地揭示了衰老过程的生化本质，终而导致了 2006 和 2007 年国际老年学界泰斗们的衰老不再是未解之谜的突然认知大转变。（尽管该领域的国际学术大师至今仍三缄其口，不愿坦率地承认中国科学家在解密衰老之谜上道破天机的贡献，导致了今年诺贝尔奖评审委员会也在衰老问题上继续拎不清）。 这个关于衰老本质认知的脑筋急转弯，如同著名的斯芬克思之谜，一经点破，似乎真有些简单得令人不知所措。 大道至简，衰老也不例外！
http://news.sciencenet.cn/htmlpaper/2009102795303297611.shtm 细胞免疫学研究取得新进展 25年前王小宁教授观察到NK细胞钻入瘤细胞的光镜照片和在瘤细胞内死亡的电镜照片 本次发现NK细胞在瘤细胞内的凋亡形态和ezrin敲除瘤细胞阻碍NK细胞进入的照片 华南理工大学生物科学与工程学院博士研究生一年级学生王珊在导师王小宁的指导下在细胞免疫学方面研究获得突破，相关成果文章Internalization of NK cells into tumor cells requires ezrin and leads to programmed cell-in-cell death发表在《细胞研究》（ Cell Research ）在线版上。 王珊是文章的第一作者，通讯作者是其导师王小宁教授。 王小宁教授25年前在研究免疫细胞NK细胞与肿瘤细胞相互作用时曾发现，NK细胞可以钻入瘤细胞内，不但可以从内部杀伤瘤细胞，更重要的是大多进入肿瘤的NK细胞反被瘤细胞杀伤。2007年，美国科学家在Cell发表论文也证实一些瘤细胞可以互相钻入同质瘤细胞，进入的细胞的主要命运也主要表现为胞内死亡，并且是一种新的细胞死亡方式，称为Entosis，与王小宁教授20多年前的发现十分相像。Entosis的作者随后阅读了王小宁20多年前的研究论文，认为与其发现十分相似并在其随后发表在Nature Review杂志的综述论文中对此做了正面引用。 王小宁小组克服重重实验条件上的困难，组合了温州医学院、南方医科大学学术资源，通过与中国科技大学姚雪彪教授的通力合作，历经两年时间，利用现代细胞与分子生物学技术再次证实其25五年前的发现是正确的，即NK细胞可以进入瘤细胞，并且主要命运表现为胞内死亡。 而且，这种死亡是一种不同于前述entosis的新的胞内死亡方式，为进一步探讨免疫细胞与肿瘤相互作用的机理和新的生物学意义提供了新的视角，也为细胞生物学提供了新的细胞研究模式。（来源：生物通 小茜） 更多阅读 《细胞研究》发表论文摘要（英文） http://www.gopubmed.org/web/gopubmed/WEB1mOWEB10O00d000j10020001000f01000j100300.y statistics Top Years Publications 2008 3 2007 3 2009 2 Top Countries Publications China 1 France 1 Top Cities Publications Guangzhou 1 Wenzhou 1 Villejuif 1 Top Journals Publications Cell Res 1 Cell Death Differ 1 Medicina-buenos Aire 1 1 2 3 Top Terms Publications Cell Death 7 Neoplasms 4 Apoptosis 3 apoptosis 2 cell death 2 programmed cell death 2 Caspases 2 Humans 2 Animals 2 Extracellular Matrix 2 Epithelial Cells 2 recognition of apoptotic cell 1 retinal cell programmed cell death 1 glial cell apoptosis 1 positive regulation of caspase activity 1 Killer Cells, Natural 1 Killer Cells 1 DNA Fragmentation 1 Caspase 3 1 immune response 1 1 2 3 1 2 Top Authors Publications Brugge J 2 Nomenclature Committee on Cell Death 2009 1 Kroemer G 1 Galluzzi L 1 Vandenabeele P 1 Abrams J 1 Alnemri E 1 Baehrecke E 1 Blagosklonny M 1 El-Deiry W 1 Golstein P 1 Green D 1 Hengartner M 1 Knight R 1 Kumar S 1 Lipton S 1 Malorni W 1 Nuez G 1 Peter M 1 Tschopp J 1 1 2 Internalization of NK cells into tumor cells requires ezrin and leads to programmed cell-in-cell death. PMID: 19786985 Related Articles Authors: Wang, S , Guo, Z , Xia, P , Liu, T , Wang, J , Li, S , Sun, L , Lu, J , Wen, Q , Zhou, M , Ma, L , Ding, X , Wang, X , Yao, X Journal: Cell Res , 2009 Abstract: Cytotoxic lymphocytes are key players in the orchestration of immune response and elimination of defective cells. We have previously reported that natural killer ( NK ) cells enter target tumor cells, leading to either target cell death or self-destruction within tumor cells. However, it has remained elusive as to the fate of NK cells after internalization and whether the heterotypic cell-in-cell process is different from that of the homotypic cell-in-cell event recently named entosis . Here, we show that NK cells undergo a cell-in-cell process with the ultimate fate of apoptosis within tumor cells and reveal that the internalization process requires the actin cytoskeletal regulator, ezrin. To visualize how NK cells enter into tumor cells, we carried out real-time dual color imaging analyses of NK cell internalization into tumor cells. Surprisingly, most NK cells commit to programmed cell death after their entry into tumor cells, which is distinctively different from entosis observed in the homotypic cell-in-cell process. The apoptotic cell death of the internalized NK cells was evident by activation of caspase 3 and DNA fragmentation. Furthermore, NK cell death after internalization is attenuated by the caspase inhibitor, Z- VAD -FMK, confirming apoptosis as the mode of NK cell death within tumor cells. To determine protein factors essential for the entry of NK cells into tumor cells, we carried out siRNA-based knockdown analysis and discovered a critical role of ezrin in NK cell internalization. Importantly, PKA -mediated phosphorylation of ezrin promotes the NK cell internalization process. Our findings suggest a novel regulatory mechanism by which ezrin governs NK cell internalization into tumor cells. Affiliation: School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510641, China Wenzhou Medical College, Wenzhou 325035, China . Wikipedia: Actin , Alpha-actin , Apoptosis , B-DNA , Benign neoplasm , Beta-actin , CASP3 , Cancer , Caspase-3 , Caspase 3 , Caspases , Cell death , DNA , DNA fragmentation , Deoxyribonucleic Acid , Double-stranded DNA , Enteritis , F-actin , F actin , G-actin , G actin , Government , Immunity , Immunization , K Cell , K cells , Killer cell , Killer cells, natural , Lymphocyte , NK Cell , NK cells , Natural Killer Cells , Natural Killer cell , Nature , Neoplasm , Phosphorylation , Proteins , Tumor , Variolation Title: Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009. PMID: 18846107 Related Articles Authors: Kroemer, G , Galluzzi, L , Vandenabeele, P , Abrams, J , Alnemri, E S , Baehrecke, E H , Blagosklonny, M V , El-Deiry, W S , Golstein, P , Green, D R , Hengartner, M , Knight, R A , Kumar, S , Lipton, S A , Malorni, W , Nuez, G , Peter, M E , Tschopp, J , Yuan, J , Piacentini, M , Zhivotovsky, B , Melino, G , Nomenclature Committee on Cell Death 2009 Journal: Cell Death Differ , Vol. 16 (1): 3-11 , 2009 Abstract: Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ' entosis ', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'. Affiliation: INSERM, U848, Villejuif F-94805, France . kroemer@igr.fr Pubmed MeSH: Animals , Humans Wikipedia: Apoptosis , Autophagocytosis , Autophagy , Caspases , Cell death , Cellular autophagy , Necrosis , Recommendation , Vacuole Title: PMID: 18786892 Related Articles Authors: Barcat, J A Journal: Medicina (B Aires) , Vol. 68 (4): 315-7 , 2008 No abstract given. Pubmed MeSH: Animals , Apoptosis , Cell Death , Cell Transformation, Neoplastic , Endocytosis , Humans , Neoplasm Invasiveness Wikipedia: Cannibalism Title: Emperipolesis, entosis and beyond: dance with fate. PMID: 18521104 Related Articles Authors: Xia, P , Wang, S , Guo, Z , Yao, X Journal: Cell Res , Vol. 18 (7): 705-7 , 2008 No abstract given. Affiliation: Division of Cellular Dynamics, Hefei National Laboratory for Physical Sciences at Nano-scale, and University of Science Technology of China, Hefei 230027, China . Pubmed MeSH: Animals , Cell Adhesion , Cell Communication , Humans , Killer Cells, Natural , Lymphocytes , Neoplasms Title: PMID: 18334170 Related Articles Authors: Mailleux, A A , Overholtzer, M , Brugge, J S Journal: Med Sci (Paris) , Vol. 24 (3): 246-8 , 2008 No abstract given. Pubmed MeSH: Adenocarcinoma , Animals , Breast Neoplasms , Cell Adhesion , Cell Line, Tumor , Humans , Microscopy, Confocal , Microscopy, Electron , Neoplasm Proteins , Vacuoles , rho GTP-Binding Proteins , rho-Associated Kinases Wikipedia: Benign neoplasm , Cancer , Cell death , Neoplasm , Tumor Title: Entosis : cell death by invasion. PMID: 18059358 Related Articles Authors: LeBot, N Journal: Nat Cell Biol , Vol. 9 (12): 1346 , 2007 No abstract given. Pubmed MeSH: Breast Neoplasms , Cell Adhesion , Cell Culture Techniques , Epithelial Cells , Extracellular Matrix , Humans , Neoplasm Metastasis , Pleural Effusion, Malignant , Tumor Cells, Cultured Wikipedia: Cell death Title: A nonapoptotic cell death process, entosis , that occurs by cell-in-cell invasion. PMID: 18045538 Related Articles Authors: Overholtzer, M , Mailleux, A A , Mouneimne, G , Normand, G , Schnitt, S J , King, R W , Cibas, E S , Brugge, J S Journal: Cell , Vol. 131 (5): 966-79 , 2007 Abstract: Epithelial cells require attachment to extracellular matrix (ECM) to suppress an apoptotic cell death program termed anoikis. Here we describe a nonapoptotic cell death program in matrix-detached cells that is initiated by a previously unrecognized and unusual process involving the invasion of one cell into another, leading to a transient state in which a live cell is contained within a neighboring host cell. Live internalized cells are either degraded by lysosomal enzymes or released. We term this cell internalization process entosis and present evidence for entosis as a mechanism underlying the commonly observed cell-in-cell cytological feature in human cancers. Further we propose that entosis is driven by compaction force associated with adherens junction formation in the absence of integrin engagement and may represent an intrinsic tumor suppression mechanism for cells that are detached from ECM. Affiliation: Department of Cell Biology, Harvard Medical School, Boston , MA 02115, USA . Pubmed MeSH: Actins , Apoptosis , Autophagy , Breast Neoplasms , Cadherins , Carcinoma , Cell Adhesion , Cell Communication , Humans , Models, Biological , Myosin Type II , Tumor Cells, Cultured , rho GTP-Binding Proteins , rho-Associated Kinases Wikipedia: Adherens junction , Anoikis , Benign neoplasm , Cancer , Cell death , Enzymes , Epithelial cell , Extracellular matrices , Extracellular matrix , Integrins , Lysosome , Neoplasm , Tumor , Zonula Adherens Title: Entosis : it's a cell-eat-cell world. PMID: 18045529 Related Articles Authors: White, E Journal: Cell , Vol. 131 (5): 840-2 , 2007 Abstract: In this issue, Overholtzer et al. (2007) describe a new nonapoptotic cell death pathway termed entosis in mammary epithelial cells that have detached from the extracellular matrix (ECM). Given that surviving detachment from the ECM is an event associated with the progression of epithelial cancers, entosis --along with apoptosis--may contribute to tumor suppression by promoting the elimination of cancer cells. Affiliation: Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Rutgers University, 679 Hoes Lane, Piscataway, NJ 08854, USA . ewhite@cabm.rutgers.edu Pubmed MeSH: Animals , Apoptosis , Autophagy , Cell Communication , Epithelium , Mammary Glands, Animal , Mice , Models, Biological Wikipedia: Benign neoplasm , Cancer , Cell death , Epithelial cell , Extracellular matrices , Extracellular matrix , Neoplasm , Tumor 王珊论文全文见附件： entosis
http://www.sciencenet.cn/htmlnews/2009/9/223207.shtm 《科学信号传导》：科学家揭示细胞如何感受信息产生信号 将帮助科学家更好地理解信号传入细胞内部后发生的情况 科学家早已知道，细胞之间会通过一种称作信号传导的复杂过程进行交谈。当这些信号出现差错，就可能导致糖尿病、关节炎以及癌症等多种疾病。科学家目前对于发生于细胞膜上的信号传收情况已经进行了大量的研究，但是对于进入膜后的情况却知之甚少。结果，对于市场上的许多药物，科学家并不是十分清楚它们对于细胞功能所具有的影响。 英国曼彻斯特大学的科学家近日开发出一种新技术，将能帮助科学家理解这些信号如何通过细胞膜进入细胞内部，并触发一系列复杂的生物学过程。相关论文发表在《科学信号传导》（ Science Signaling ）上。 论文通讯作者、曼彻斯特大学生命科学系系主任Martin Humphries教授说：信号让细胞以一种类似于我们品尝食物和水的方式来品尝环境。就像红葡萄酒有多种不同的微妙的味道一样，细胞也能尝到构成其环境的数千种分子。我们的发现解释了细胞如何在分子水平上阐释这些不同的味道，从而产生一个总体的信号。我们开发的技术将帮助科学家检测细胞表面受体如何将信息传给细胞内数百种蛋白。特别是，它将能帮助科学家同时关注所有这些组分。 这项研究将会在科学界激起强烈的兴趣，有望导致更好的药物设计和更快的药物递送时间。此外，它还将帮助科学家更全面地认识我们的身体机能。 http://stke.sciencemag.org/cgi/content/abstract/sigtrans;2/87/ra51 Sci. Signal. , 8 September 2009 Vol. 2, Issue 87, p. ra51 RESEARCH Proteomic Analysis of Integrin-Associated Complexes Identifies RCC2 as a Dual Regulator of Rac1 and Arf6 Jonathan D. Humphries 1 ,2 * , Adam Byron 1 ,2 * , Mark D. Bass 1 ,2 , Sue E. Craig 1 ,2 , John W. Pinney 2 , David Knight 2 , and Martin J. Humphries 1 ,2 1 Wellcome Trust Centre for Cell-Matrix Research, University of Manchester, Manchester M13 9PT, UK. 2 Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK. * These authors contributed equally to this work. Present address: Centre for Bioinformatics, Division of Molecular Biosciences, Imperial College London, London SW7 2AZ, UK. Abstract: The binding of integrin adhesion receptors to their extracellular matrix ligands controls cell morphology, movement, survival, and differentiation in various developmental, homeostatic, and disease processes. Here, we report a methodology to isolate complexes associated with integrin adhesion receptors, which, like other receptor-associated signaling complexes, have been refractory to proteomic analysis. Quantitative, comparative analyses of the proteomes of two receptor-ligand pairs, 4 1 vascular cell adhesion molecule1 and 5 1 fibronectin, defined both core and receptor-specific components. Regulator of chromosome condensation2 (RCC2) was detected in the 5 1 fibronectin signaling network at an intersection between the Rac1 and adenosine 5'-diphosphate ribosylation factor 6 (Arf6) subnetworks. RCC2 knockdown enhanced fibronectin-induced activation of both Rac1 and Arf6 and accelerated cell spreading, suggesting that RCC2 limits the signaling required for membrane protrusion and delivery. Dysregulation of Rac1 and Arf6 function by RCC2 knockdown also abolished persistent migration along fibronectin fibers, indicating a functional role for RCC2 in directional cell movement. This proteomics workflow now opens the way to further dissection and systems-level analyses of adhesion signaling. To whom correspondence should be addressed. E-mail: martin.humphries@manchester.ac.uk
标签: 细胞
