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Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ
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Action of the tumor [22,36]. Indeed, abrogating galectin-1 expression renders tumor cells more susceptible to temozolamide treatment [22,41]. Finally, galectin-1 induces apoptosis of activated T-cells [42-46], prevents host animals from mounting tumor vaccine-induced immunity [47], and may cooperate with TGF-beta in GBM-induced immunosuppression [48,49]. In sum, galectin-1 expression may inversely
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S 1. Lefranc F, Facchini V, Kiss R: Proautophagic drugs: a novel means to combat apoptosis-resistant cancers, with a special emphasis on glioblastomas. Oncologist 2007, 12:1395?403. 2. Stupp R, Hegi ME, Mason WP, van den Bent MJ, Taphoorn MJ, Janzer RC, Ludwin SK, Allgeier A, Fisher B, Belanger K, Hau P, Brandes AA, Gijtenbeek J, Marosi C, Vecht CJ, Mokhtari K, Wesseling P, Villa S, Eisenhauer E,
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Assays of GBM cells stably transfected to over-express galectin-1, perfectly fit in with the previous studies mentioned above and highlight the importance of galectin-1 in the biologically aggressive behavior of experimental GBMs. While there was no enhancement of proliferation or change inattachment to fibronectin, galectin-1 upregulation induced more rapid two-dimensional migration and enhanced
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Y used model system for the analysis of vertebrate embryogenesis and organ development. While genetic methods are readily available in zebrafish, protocols for two dimensional (2D) gel electrophoresis and proteomics have yet to be developed. Results: As a prerequisite to carry out proteomic experiments with early zebrafish embryos, we developed a method to efficiently remove the yolk from large ba
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E study targeted larval stages 48 or 72 hpf (hours post fertilization), when the yolk to cell mass ratio is already decreased [5], however, without identifying the proteins. Therefore, it remains unclear whether at this stage analysis without deyolking provides satisfactory information about cellular proteins. Thus, the develop-ment of a reliable method to remove the interfering yolk from cells on
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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Bryos In the early embryo, the cells forming the embryo proper constitute only a minor volume of the embryo compared to the large yolk cell (Fig. 1B). The abundance of yolk proteins interferes with any proteomic application that intends to target the cells of the embryo proper. The major yolk protein Vitellogenin, a phospholipo-glycoprotein,Page 1 of(page number not for citation purposes)BMC Devel

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