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Rtner and regulator of KSR1 and the MAPK pathway.One of the main functions of the scaffold protein CNKSR1 is the regulation of other cancer-related signaling pathways integrating output to different intracellular signaling cascades upon cellular stimulation by extracellular cues [11, 12, 17?0]. In breast and cervical cancer cell models, a pro-oncogenic potential has been demonstrated through ERK-i
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Nostics, INC, New Jersey) along with a human-specific mouse monoclonal anti-vimentin antibody (Dakocytomation,Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 4 ofTrappes, France). After incubation with the provided goat anti-mouse secondary antibody, staining developed with NovaRed Developing Reagent (Vector Laboratories, Burlingame, CA). Sections we
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Few of our U87 galectin1 clones. Parental U87MG cells, along with galectin-1 and acGFP-only clones were injected into the right caudate/putamen complex of nude mice. Tumors overexpressing galectin-1 shortened survival of their hosts compared to their parental counterparts (Figure 5). A few animals (7/20) bearing tumors expressing acGFP alone eventually exhibited neurological symptoms. The examinat
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Lioblastoma cell subpopulations with amplified EGFR. Genes Chromosomes Cancer 2004, 39:29?6. Simone NL, Bonner RF, Gillespie JW, Emmert-Buck MR, Liotta LA: Lasercapture microdissection: opening the microscopic frontier to molecular analysis. Trends Genet 1998, 14:272?76. Ruebel KH, Leontovich AA, Jin L, Stilling GA, Zhang H, Qian X, Nakamura N, Scheithauer BW, Kovacs K, Lloyd RV: Patterns of gene
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On problem with IRES vectors ?inability to transcribe the transcript following the IRES sequence if the first MCS is empty. The new pIRES2-acGFP1acGFP1 vector was used as a control for the pIRES2Gal1-acGFP1 construct. Both vectors were sequenced through their multiple cloning sites to ensure no PCRinduced mutations were present.Transfection and stable clone generationParental, control, and galecti
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Tin S, Mathieu V, Kiss R, Lefranc F: Galectins and gliomas. Brain Pathol 2010, 20:17?7. Mariani L, Beaudry C, McDonough WS, Hoelzinger DB, Kaczmarek E, Ponce F, Coons SW, Giese A, Seiler RW, Berens ME: Death-associated protein 3 (Dap3) is overexpressed in invasive glioblastoma cells in vivo and in glioma cell lines with induced motility phenotype in vitro. Clin Cancer Res 2001, 7:2480?489. Mariani
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Expression profile of glioblastoma multiforme invasive phenotype points to new therapeutic targets. Neoplasia 2005, 7:7?6. Zagzag D, Salnikow K, Chiriboga L, Yee H, Lan L, Ali MA, Garcia R, Demaria S, Newcomb EW: Downregulation of major histocompatibility complex antigens in invading glioma cells: stealth invasion of the brain. Lab Invest 2005, 85:328?41. Camby I, Belot N, Rorive S, Lefranc F, Mau
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Ly expressed at the tumor margin, promotes glioblastoma cell invasion. Molecular Cancer 2012 11:32.Submit your next manuscript to BioMed Central and take full advantage of:?Convenient online submission ?Thorough peer review ?No space constraints or color figure charges ?Immediate publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Research which is freely available for

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