The publication-citation matrix and its derived quantities

We give an overview of the main data of a publication-citation matrix. We show how impact factors are defined, and, in particular, point out the difference between the synchronous and the diachronous impact factor. The advantages and disadvantages of using both as tools in research evaluation are discussed.     

原核表达载体pHsaE1αβ的构建和人丙酮酸脱氢酶的表达与纯化

以质粒pQE9为原型载体, 将编码hPDH的α和β亚基的cDNA串联克隆到该载体上, 成功地构建了hPDH基因的表达载体pHsaE1αβ. 并在大肠杆菌中表达了hPDH, 通过 亲和层析法进行纯化, 对一些生物化学性质进行表征.     

Additions to the vascular flora of Wyoming

Eight species previously unreported for Wyoming are listed. A range extension is noted for Erigeron humilis, and Cymopterus bipinnatus is verified as occurring in Wyoming.     

外显生长指数

基于一篇文章所引用的参考文献和该文的被引频次两个维度,提出了衡量该文外显成长度的相对指标.该研究涉及的引用数据及每条参考文献的被引数据均来自网络版科学引文索引(Web of Science),检索日期为2010年4月最后一周.     

SCF(FBW7) regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

The effective use of targeted therapy is highly dependent on the identification of responder patient populations. Loss of FBW7, which encodes a tumour-suppressor protein, is frequently found in various types of human cancer, including breast cancer, colon cancer and T-cell acute lymphoblastic leukaemia (T-ALL). In line with these genomic data, engineered deletion of Fbw7 in mouse T cells results in T-ALL, validating FBW7 as a T-ALL tumour suppressor. Determining the precise molecular mechanisms by which FBW7 exerts antitumour activity is an area of intensive investigation. These mechanisms are thought to relate in part to FBW7-mediated destruction of key proteins relevant to cancer, including Jun, Myc, cyclin E and notch 1 (ref. 9), all of which have oncoprotein activity and are overexpressed in various human cancers, including leukaemia. In addition to accelerating cell growth, overexpression of Jun, Myc or notch 1 can also induce programmed cell death. Thus, considerable uncertainty surrounds how FBW7-deficient cells evade cell death in the setting of upregulated Jun, Myc and/or notch 1. Here we show that the E3 ubiquitin ligase SCF(FBW7) (a SKP1-cullin-1-F-box complex that contains FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family member, for ubiquitylation and destruction in a manner that depends on phosphorylation by glycogen synthase kinase 3. Human T-ALL cell lines showed a close relationship between FBW7 loss and MCL1 overexpression. Correspondingly, T-ALL cell lines with defective FBW7 are particularly sensitive to the multi-kinase inhibitor sorafenib but resistant to the BCL2 antagonist ABT-737. On the genetic level, FBW7 reconstitution or MCL1 depletion restores sensitivity to ABT-737, establishing MCL1 as a therapeutically relevant bypass survival mechanism that enables FBW7-deficient cells to evade apoptosis. Therefore, our work provides insight into the molecular mechanism of direct tumour suppression by FBW7 and has implications for the targeted treatment of patients with FBW7-deficient T-ALL.