Hot Papers

L.A. Lasky, M.S. Singer, T.A. Yednock, D. Dowbenko, et al., "Cloning of a lymphocyte homing receptor reveals a lectin domain," Cell, 56, 1045-55, 24 March 1989. Lawrence A. Lasky (Genentech Inc., South San Francisco): "The trafficking of leukocytic cells to various regions of the vascular system during normal and inflammatory immune responses involves a number of cell surface adhesion molecules. One of the more interesting of these molecules is the homing receptor, so named because it allows white cells to home in on peripheral lymph nodes, and perhaps, sites of inflammation. Previous work demonstrated that this receptor may contain a sugar recognition site involved with adhesion. The molecular cloning of the murine homing receptor, reported in this paper, demonstrated that this adhesion receptor also contains a carbohydrate recognition, or lectin, motif. This exciting result showed that this receptor appears to direct leukocytes to peripheral lymph nodes by recognition of and adhesion to unknown carbohydrates expressed in certain endothelial cells. The homing receptor, thus, may belong to a new class of cellular adhesion molecules, which appear to utilize carbohydrate-lectin adhesion for specific cell-cell interactions." H.-J.S. Huang, J.-K. Yee, J.-Y. Shew, P.-L. Chen, R. Bookstein, T. Friedmann, E.Y.-H.P. Lee, W.-H. Lee, "Suppression of the neoplastic phenotype by replacement of the RB gene in human cancer cells," Science, 242, 1563-6, 16 December 1988. Wen-Hwa Lee (University of California at San Diego, La Jolla): "The existence of genes that suppress tumor formation was proposed more than a decade ago on the basis of cell fusion experiments between normal and neoplastic cells. Characteristic genetic changes in tumor cells also suggested that a loss of certain cellular genes could contribute to the neoplastic phenotype, but this had not been shown directly. The first candidate for such a tumor suppressor gene, RB, which controls susceptibility to the childhood ocular tumor retinoblastoma, was cloned a few years ago. To demonstrate its biologic activity, and to test the idea of tumor suppression by a single gene, we reintroduced the normal RB gene into human retinoblastoma cells using a recombinant retroviral vector. A dramatic biologic effect was observed, wherein tumorigenic retinoblastoma cells became completely nontumorigenic in nude mice after RB reconstitution. These results represent a landmark study in the genetic suppression of cancer and its potential clinical applications." W.C. Sha, C.A. Nelson, R.D. Newberry, D.M. Kranz, et al., "Positive and negative selection of an antigen receptor on T cells in transgenic mice," Nature, 336, 73-6, 3 November 1988. Bill Sha (Washington University School of Medicine, St. Louis): "T-cell maturation in the thymus is an unusual developmental system. The somatic rearrangement of antigen receptor genes is coupled to a biphasic selection process that involves selection both for and against maturation of individual thymocytes. The tremendous diversity of antigen receptors that is generated during T-cell differentiation has made it difficult to study the precise role played by receptor affinity for self-MHC (major histocompatibility complex) antigens. We, along with several other groups, were able to bypass this complexity by introducing the antigen receptor genes from a single, well-characterized T-cell clone into transgenic mice. This allowed us to clearly demonstrate that autoreactive T cells are deleted in the thymus and that maturation of T cells is significantly enhanced by successful interactions with self-MHC antigens." G. Draetta, F. Luca, J. Westendorf, L. Brizuela, et al., "cdc2 protein kinase is complexed with both cyclin A and B: evidence for proteolytic inactivation of MPF," Cell, 56, 829-38, 10 March 1989. Giulio Draetta (European Molecular Biology Laboratory, Heidelberg, W.Ger.): "In March 1988, at a meeting in Cold Spring Harbor, David Beach and I presented data on the activation of the cdc2 kinase during the cell cycle in human cells. A 62 kd protein (p62) progressively accumulated and associated with cdc2, forming a complex that was maximally active during mitosis. Joan Ruderman (Duke University, Durham, N.C.) suggested that p62 might be a cyclin [The Scientist, Hot Team, March 5, 1990, page 22]. Joan had shown that cyclin mRNA induces maturation of Xenopus oocytes. Using the clam system, we showed that cdc2 and cyclin form complexes that display active kinase activity at mitosis. We proposed that cyclin proteolysis provides the mechanism of mitosis-promoting factor (MPF) inactivation and, thus, exit from mitosis. Further studies have demonstrated that cdc2 and cyclin form a stoichiometric complex in a number of different species and that this complex constitutes the MPF."

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