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| 1 | E-cadherin transcriptional downer-gulation by promoter methylation but not mutation is related to epithelial-to-mesenehymal transition in breast cancer cells 显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 2 | E-cadherin tran scriptional downregulation by promoter methylation but not mutation is related to epithelial to mesenchymal transition in breast cancer cell lines 显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 3 | Beta2-microglobulin aberrations in diffuse large B-cell lymphoma of the testis and the central nervous system显示文摘 | Jordanova ES Riemersma SA Philippo K | 2003 | Int J Cancer2003，103，3： | 1 |
| 4 | E-cadherin transcrip-tional downregulation by promoter methylation but not mutation is re-lated to epithelial-to-mesenchymal transition in breast cancer cell lines显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 5 | Beta-2-microglobulin aberrations in diffuse large B-cell lymphoma of the testis and the central nervous system显示文摘 | Jordanova ES Riemersma SA Philippo K | 2003 | Int Cancer2003，103，3： | 1 |
| 6 | Build-ing Enterprise-wide Information Supply ChainsBased on the Fractal Concept显示文摘 | Patrick W Philippos K Apostolos V | 2003 | Integrated Manu-facturing Systems2003，14，5： | 1 |
| 7 | Beta-2-microglobulin aberrations in diffuse large B-cell lymphoma of the testis and the central nervous system 显示文摘 | Jordanova ES Riemersma SA Philippo K | 2003 | Int J Cancer2003，103，3： | 1 |
| 8 | E-cadherin transcriptional downregulation by promoter methylation but not mutation is related to epithelial-to-mesenchymal transition in breast cancer cell lines 显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 9 | E-eadherin transcrip- tional downregulation by promoter methylation but not mutation is relat- ed to epithelial-to-mesenehymal transition in breast cancer cell lines 显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 10 | E - cadherin transcriptional downregulation by promoter methylation but not mutation is related to epithelial - to - mesenchymal transition in breast cancer cell lines 显示文摘 | Lombaerts M van Wezel T Philippo K | 2006 | Br J Cancer2006，94，5： | 1 |
| 11 | Building enterprise-wide information supply chains based on the fractal concept显示文摘 | PATRICK W PHILIPPOS K APOSTOLOS V ADAMANTIOS K | 2003 | Integrated Manufacturing Systems2003，5，14： | 1 |
| 12 | Limitations of clonality anal- ysis of B cell proliferations using CDR3 polymerase chain reaction 显示文摘 | Hoeve MA Krol AD Philippo K | 2000 | Mol Pathol2000，53，4： | 1 |
| 13 | Beta2microglobulin aberrations in diffuse large B-cell lymphoma of the testis and the central nervous system显示文摘 | Jordanova ES Riemersma SA Philippo K et ai | 2003 | Int J Cancer2003，103，3： | 1 |
| 14 | Hemizygous deletions in the HLA region account for loss of heterozygosity in the majority of diffuse large B-cell lymphomas of the testis and the cen- tral nervous system 显示文摘 | Jordanova E S Riemersma S A Philippo K | 2002 | Genes Chromosomes Cancer2002，35，1： | 1 |
| 15 | Mutations in the HLA class II genes leading to loss of expression of HLA-DR and HLA-DQ in diffuse large B-cell lymphoma 显示文摘 | Jordanova E S Philippo K Giphart M J | 2003 | Immunogenetics2003，55，4： | 1 |
| 16 | E-cad- herin transcriptional downer-gulation by promoter methylation but not mutation is related to epithelial-to-mcsenchymal transition in breast cancer cells显示文摘 | LOMBAERTS M VAN WEZEL T PHILIPPO K | 2006 | Br J Cancer2006，94，5： | 1 |
| 17 | Limitation of clonality analysis of B cell proliferations using CDR3 polymerase chain reaction显示文摘 | Krol A D Philippo K | 2000 | J Clin Pathol: Mol Pathol2000，53，4： | 1 |
| 18 | Discrimination of membrane antigen affinity by B cells requires dominance of kinetic proofreading over serial engagement显示文摘B-cell receptor signaling in response to membrane-bound antigen increases with antigen affinity,a process known as affinity discrimination.We use computational modeling to show that B-cell affinity discrimination requires that kinetic proofreading predominate over serial engagement.We find that if B-cell receptors become signaling-capable immediately upon antigen binding,which results in decreasing serial engagement as affinity increases,then increasing affinity can lead to weaker signaling.Rather,antigen must stay bound to B-cell receptors for a threshold time of several seconds before becoming signaling-capable,a process similar to kinetic proofreading.This process overcomes the loss in serial engagement due to increasing antigen affinity,and replicates the monotonic increase in B-cell signaling with increasing affinity that has been observed in B-cell activation experiments.This finding matches well with the experimentally observed time(,20 s)required for the B-cell receptor signaling domains to undergo antigen and lipid raft-mediated conformational changes that lead to Src-family kinase recruitment.We hypothesize that the physical basis for a threshold time of antigen binding might lie in the formation timescale of B-cell receptor dimers.The time required for dimer formation decreases with increasing antigen affinity,thereby resulting in shorter threshold antigen binding times as affinity increases.Such an affinity-dependent kinetic proofreading requirement results in affinity discrimination very similar to that observed in biological experiments.B-cell affinity discrimination is critical to the process of affinity maturation and the production of high-affinity antibodies,and thus our results have important implications in applications such as vaccine design. | Philippos K Tsourkas Wanli Liu Somkanya C Das Susan K Pierce Subhadip Raychaudhuri | 2012 | Cellular & Molecular Immunology2012，9，1： | 0 |
| 19 | Monte Carlo study of B-cell receptor clustering mediated by antigen crosslinking and directed transport显示文摘It is known from experiments that in the presence of soluble antigen,B-cell receptors(BCRs)assemble into microclusters and then collect into a macrocluster known as a‘cap’.However,the mechanisms of BCR cluster formation during recognition of soluble antigens remain unclear.In previous work,we demonstrated that effective intrinsic attractions among BCRs can lead to the formation of small microclusters of BCR molecules.The effective intrinsic attractions could be caused by multivalent antigen binding,association with lipid rafts,or other biochemical factors.In the present study,we have developed and studied a Monte Carlo model of BCR clustering mediated by explicit binding and crosslinking of soluble bivalent antigens.Antigen crosslinking is shown to microcluster BCRs in an affinity-dependent manner and also in a biologically relevant timescale;however,antigen crosslinking alone does not appear to be sufficient for the formation of a single macrocluster of receptor molecules.We show that directed transport of BCRs is needed to drive the formation of large macroclusters.We constructed a simple model of directed transport,where BCR molecules diffuse towards the largest cluster or towards a random BCR microcluster,which results in a single macrocluster of receptor molecules.The mechanisms for both types of directed transport are compared using network-based metrics.We also develop and use appropriate network measures to analyze the effect of BCR and antigen concentration on BCR clustering,the stability of the formed clusters over time and the size of BCR–antigen crosslinked chains. | A Srinivas Reddy Philippos K Tsourkas Subhadip Raychaudhuri | 2011 | Cellular & Molecular Immunology2011，8，3： | 0 |
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