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2. Supplementary Tables legend from Debio 0617B Inhibits Growth of STAT3-Driven Solid Tumors through Combined Inhibition of JAK, SRC, and Class III/V Receptor Tyrosine Kinases

Author

Murone, Maximilien, primary, Vaslin Chessex, Anne, primary, Attinger, Antoine, primary, Ramachandra, Raghuveer, primary, Shetty, Shankar J., primary, Daginakatte, Girish, primary, Sengupta, Saumitra, primary, Marappan, Sivapriya, primary, Dhodheri, Samiulla, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Brienza, Silvano, primary, Traxler, Peter, primary, Lang, Marc, primary, Aguet, Michel, primary, Zoete, Vincent, primary, Michielin, Olivier, primary, Nicholas, Courtney, primary, Johnson, Faye M., primary, Ramachandra, Murali, primary, and McAllister, Andres, primary

Published
2023
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3. Figure S8 from The Multi-kinase Inhibitor Debio 0617B Reduces Maintenance and Self-renewal of Primary Human AML CD34+ Stem/Progenitor Cells

Author

Murone, Maximilien, primary, Radpour, Ramin, primary, Attinger, Antoine, primary, Chessex, Anne Vaslin, primary, Huguenin, Anne-Laure, primary, Schürch, Christian M., primary, Banz, Yara, primary, Sengupta, Saumitra, primary, Aguet, Michel, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Massière, Frédéric, primary, Ramachandra, Murali, primary, McAllister, Andres, primary, and Riether, Carsten, primary

Published
2023
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4. Data from Debio 0617B Inhibits Growth of STAT3-Driven Solid Tumors through Combined Inhibition of JAK, SRC, and Class III/V Receptor Tyrosine Kinases

Author

Murone, Maximilien, primary, Vaslin Chessex, Anne, primary, Attinger, Antoine, primary, Ramachandra, Raghuveer, primary, Shetty, Shankar J., primary, Daginakatte, Girish, primary, Sengupta, Saumitra, primary, Marappan, Sivapriya, primary, Dhodheri, Samiulla, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Brienza, Silvano, primary, Traxler, Peter, primary, Lang, Marc, primary, Aguet, Michel, primary, Zoete, Vincent, primary, Michielin, Olivier, primary, Nicholas, Courtney, primary, Johnson, Faye M., primary, Ramachandra, Murali, primary, and McAllister, Andres, primary

Published
2023
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5. Data from The Multi-kinase Inhibitor Debio 0617B Reduces Maintenance and Self-renewal of Primary Human AML CD34+ Stem/Progenitor Cells

Author

Murone, Maximilien, primary, Radpour, Ramin, primary, Attinger, Antoine, primary, Chessex, Anne Vaslin, primary, Huguenin, Anne-Laure, primary, Schürch, Christian M., primary, Banz, Yara, primary, Sengupta, Saumitra, primary, Aguet, Michel, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Massière, Frédéric, primary, Ramachandra, Murali, primary, McAllister, Andres, primary, and Riether, Carsten, primary

Published
2023
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6. Supplementary Figures 1-3 from Debio 0617B Inhibits Growth of STAT3-Driven Solid Tumors through Combined Inhibition of JAK, SRC, and Class III/V Receptor Tyrosine Kinases

Author

Murone, Maximilien, primary, Vaslin Chessex, Anne, primary, Attinger, Antoine, primary, Ramachandra, Raghuveer, primary, Shetty, Shankar J., primary, Daginakatte, Girish, primary, Sengupta, Saumitra, primary, Marappan, Sivapriya, primary, Dhodheri, Samiulla, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Brienza, Silvano, primary, Traxler, Peter, primary, Lang, Marc, primary, Aguet, Michel, primary, Zoete, Vincent, primary, Michielin, Olivier, primary, Nicholas, Courtney, primary, Johnson, Faye M., primary, Ramachandra, Murali, primary, and McAllister, Andres, primary

Published
2023
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7. Supplementary Figures legend from Debio 0617B Inhibits Growth of STAT3-Driven Solid Tumors through Combined Inhibition of JAK, SRC, and Class III/V Receptor Tyrosine Kinases

Author

Murone, Maximilien, primary, Vaslin Chessex, Anne, primary, Attinger, Antoine, primary, Ramachandra, Raghuveer, primary, Shetty, Shankar J., primary, Daginakatte, Girish, primary, Sengupta, Saumitra, primary, Marappan, Sivapriya, primary, Dhodheri, Samiulla, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Brienza, Silvano, primary, Traxler, Peter, primary, Lang, Marc, primary, Aguet, Michel, primary, Zoete, Vincent, primary, Michielin, Olivier, primary, Nicholas, Courtney, primary, Johnson, Faye M., primary, Ramachandra, Murali, primary, and McAllister, Andres, primary

Published
2023
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8. Tables S1-S5 from The Multi-kinase Inhibitor Debio 0617B Reduces Maintenance and Self-renewal of Primary Human AML CD34+ Stem/Progenitor Cells

Author

Murone, Maximilien, primary, Radpour, Ramin, primary, Attinger, Antoine, primary, Chessex, Anne Vaslin, primary, Huguenin, Anne-Laure, primary, Schürch, Christian M., primary, Banz, Yara, primary, Sengupta, Saumitra, primary, Aguet, Michel, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Massière, Frédéric, primary, Ramachandra, Murali, primary, McAllister, Andres, primary, and Riether, Carsten, primary

Published
2023
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9. Supplementary Tables 1-4 from Debio 0617B Inhibits Growth of STAT3-Driven Solid Tumors through Combined Inhibition of JAK, SRC, and Class III/V Receptor Tyrosine Kinases

Author

Murone, Maximilien, primary, Vaslin Chessex, Anne, primary, Attinger, Antoine, primary, Ramachandra, Raghuveer, primary, Shetty, Shankar J., primary, Daginakatte, Girish, primary, Sengupta, Saumitra, primary, Marappan, Sivapriya, primary, Dhodheri, Samiulla, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Brienza, Silvano, primary, Traxler, Peter, primary, Lang, Marc, primary, Aguet, Michel, primary, Zoete, Vincent, primary, Michielin, Olivier, primary, Nicholas, Courtney, primary, Johnson, Faye M., primary, Ramachandra, Murali, primary, and McAllister, Andres, primary

Published
2023
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10. Supplementary Methods and Materials from The Multi-kinase Inhibitor Debio 0617B Reduces Maintenance and Self-renewal of Primary Human AML CD34+ Stem/Progenitor Cells

Author

Murone, Maximilien, primary, Radpour, Ramin, primary, Attinger, Antoine, primary, Chessex, Anne Vaslin, primary, Huguenin, Anne-Laure, primary, Schürch, Christian M., primary, Banz, Yara, primary, Sengupta, Saumitra, primary, Aguet, Michel, primary, Rigotti, Stefania, primary, Bachhav, Yogeshwar, primary, Massière, Frédéric, primary, Ramachandra, Murali, primary, McAllister, Andres, primary, and Riether, Carsten, primary

Published
2023
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14. Supplementary Figure 1 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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15. Supplementary Figure 3 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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16. Supplementary Figure 2 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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17. Data from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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18. Supplementary Figure 4 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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19. Supplementary Table 1 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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20. Supplementary Table 2 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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21. Supplementary Figure Legend 1 from Bcl9/Bcl9l Are Critical for Wnt-Mediated Regulation of Stem Cell Traits in Colon Epithelium and Adenocarcinomas

Author

Deka, Jürgen, primary, Wiedemann, Norbert, primary, Anderle, Pascale, primary, Murphy-Seiler, Fabienne, primary, Bultinck, Jennyfer, primary, Eyckerman, Sven, primary, Stehle, Jean-Christophe, primary, André, Sylvie, primary, Vilain, Nathalie, primary, Zilian, Olav, primary, Robine, Sylvie, primary, Delorenzi, Mauro, primary, Basler, Konrad, primary, and Aguet, Michel, primary

Published
2023
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33. A stroma-related gene signature predicts resistance to neoadjuvant chemotherapy in breast cancer

Author

Farmer, Pierre, Bonnefoi, Herve, Anderle, Pascale, Cameron, David, Wirapati, Pratyakasha, Becette, Veronique, Andre, Sylvie, Piccart, Martine, Campone, Mario, Brain, Etienne, MacGrogan, Gaetan, Petit, Thierry, Jassem, Jacek, Bibeau, Frederic, Blot, Emmanuel, Bogaerts, Jan, Aguet, Michel, Bergh, Jonas, Iggo, Richard, and Delorenzi, Mauro

Subjects
Breast cancer -- Drug therapy, Breast cancer -- Research, Neoadjuvant therapy -- Health aspects, Drug resistance -- Genetic aspects, Drug resistance -- Research, Genes -- Physiological aspects, Genes -- Research
Abstract

To better understand the relationship between tumor-host interactions and the efficacy of chemotherapy, we have developed an analytical approach to quantify several biological processes observed in gene expression data sets. We tested the approach on tumor biopsies from individuals with estrogen receptor-negative breast cancer treated with chemotherapy. We report that increased stromal gene expression predicts resistance to preoperative chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC) in subjects in the EORTC 10994/131G 00-01 trial. The predictive value of the stromal signature was successfully validated in two independent cohorts of subjects who received chemotherapy but not in an untreated control group, indicating that the signature is predictive rather than prognostic. The genes in the signature are expressed in reactive stroma, according to reanalysis of data from microdissected breast tumor samples. These findings identify a previously undescribed resistance mechanism to FEC treatment and suggest that antistromal agents may offer new ways to overcome resistance to chemotherapy., &&&& Preoperative chemotherapy leads to the disappearance of the primary tumor (pathological complete response; pCR) in less than 10% of estrogen receptor-positive breast tumors and in 20-30% of estrogen receptor-negative [...]

Published
2009

34. Notch signaling is required for normal prostatic epithelial cell proliferation and differentiation

Author

Wang, Xi-De, Leow, Ching Ching, Zha, Jiping, Tang, Zhijun, Modrusan, Zora, Radtke, Freddy, Aguet, Michel, and Sauvage, Frederic J. de

Subjects
Cell differentiation -- Research, Cell proliferation -- Research, Cellular signal transduction -- Research, DNA microarrays -- Usage, Prostate -- Research, Biological sciences
Abstract

The role of Notch1 gene in prostate cell proliferation and differentiation, using microarray analysis, is presented.

Published
2006

35. TBX3 acts as tissue-specific component of the Wnt/β-catenin transcriptional complex

Author

Zimmerli, Dario, primary, Borrelli, Costanza, additional, Jauregi-Miguel, Amaia, additional, Söderholm, Simon, additional, Brütsch, Salome, additional, Doumpas, Nikolaos, additional, Reichmuth, Jan, additional, Murphy-Seiler, Fabienne, additional, Aguet, MIchel, additional, Basler, Konrad, additional, Moor, Andreas E, additional, and Cantù, Claudio, additional

Published
2020
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36. Author response: TBX3 acts as tissue-specific component of the Wnt/β-catenin transcriptional complex

Author

Zimmerli, Dario, primary, Borrelli, Costanza, additional, Jauregi-Miguel, Amaia, additional, Söderholm, Simon, additional, Brütsch, Salome, additional, Doumpas, Nikolaos, additional, Reichmuth, Jan, additional, Murphy-Seiler, Fabienne, additional, Aguet, MIchel, additional, Basler, Konrad, additional, Moor, Andreas E, additional, and Cantù, Claudio, additional

Published
2020
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37. TBX3 acts as tissue-specific component of the Wnt/β-catenin enhanceosome

Author

Zimmerli, Dario, primary, Borrelli, Costanza, additional, Jauregi-Miguel, Amaia, additional, Söderholm, Simon, additional, Brütsch, Salome, additional, Doumpas, Nikolaos, additional, Reichmuth, Jan, additional, Murphy-Seiler, Fabienne, additional, Aguet, Michel, additional, Basler, Konrad, additional, Moor, Andreas E., additional, and Cantù, Claudio, additional

Published
2020
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38. Demonstration of an interferon (gamma)-dependent tumor surveillance system in immunocompetent mice

Author

Kaplan, Daniel H., Shankaran, Vijay, Dighe, Anand S., Stockert, Elisabeth, Aguet, Michel, Old, Lloyd J., and Schreiber, Robert D.

Subjects
Mice -- Physiological aspects, Tumor suppressor genes -- Research, Autoimmunity -- Research, Science and technology
Abstract

This study demonstrates that endogenously produced interferon [Gamma] (IFN-[Gamma]) forms the basis of a tumor surveillance system that controls development of both chemically induced and spontaneously arising tumors in mice. Compared with wild-type mice, mice lacking sensitivity to either IFN-[Gamma] (i.e., IFN-[Gamma] receptor-deficient mice) or all IFN family members (i.e., Stat1-deficient mice) developed tumors more rapidly and with greater frequency when challenged with different doses of the chemical carcinogen methylcholanthrene. In addition, IFN-[Gamma]insensitive mice developed tumors more rapidly than wild-type mice when bred onto a background deficient in the p53 tumor suppressor gene. IFN-[Gamma]-insensitive [p53.sup.-/-] mice also developed a broader spectrum of tumors compared with mice lacking p53 alone. Using tumor cells derived from methylcholanthrene-treated IFN-[Gamma]-insensitive mice, we found IFN-[Gamma]'s actions to be mediated at least partly through its direct effects on the tumor cell leading to enhanced tumor cell immunogenicity. The importance and generality of this system is evidenced by the finding that certain types of human tumors become selectively unresponsive to IFN-[Gamma]. Thus, IFN-[Gamma] forms the basis of an extrinsic tumor-suppressor mechanism in immunocompetent hosts.

Published
1998

39. Mutations in and genes cause congenital heart defects by tissue-specific perturbation of Wnt/β-catenin signaling

Author

Cantù, Claudio, Felker, Anastasia, Zimmerli, Dario, Prummel, Karin D, Cabello, Elena M, Chiavacci, Elena, Méndez-Acevedo, Kevin M, Kirchgeorg, Lucia, Burger, Sibylle, Ripoll, Jorge, Valenta, Tomas, Hausmann, George, Vilain, Nathalie, Aguet, Michel, Burger, Alexa, Panáková, Daniela, Basler, Konrad, Mosimann, Christian, University of Zurich, and Mosimann, Christian

Subjects
1309 Developmental Biology, 1311 Genetics, 570 Life sciences, biology, 10124 Institute of Molecular Life Sciences
Published
2018

40. Interferon-gamma impacts at multiple points during the progression of autoimmune diabetes

Author

Wang, Bo, Andre, Isabelle, Gonzalez, Antonio, Katz, Jonathan D., Aguet, Michel, Benoist, Christophe, and Mathis, Diane

Subjects
Autoimmune diseases -- Analysis, Cytokines -- Analysis, Diabetes -- Physiological aspects, Interferon -- Research, Science and technology
Abstract

The role of interferon-[Gamma] in autoimmune diabetes was assessed by breeding a null mutation of the interferon-[Gamma] receptor [Alpha] chain into the nonobese diabetic mouse strain, as well as into a simplified T cell receptor transgenic model of diabetes. In contrast to a previous report on abrogation of the interferon-[Gamma] gene, mutation of the gene encoding its receptor led to drastic effects on disease in both mouse lines. Nonobese diabetic mice showed a marked inhibition of insulitis - both the kinetics and penetrance - and no signs of diabetes; the transgenic model exhibited near-normal insulitis, but this never evolved into diabetes, either spontaneously or after experimental provocation. This failure could not be explained by perturbations in the ratio of T helper cell phenotypes; rather, it reflected a defect in antigen-presenting cells or in the islet [Beta] cell targets.

Published
1997

41. Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway

Author

Meraz, Marco A., White, J. Michael, Sheehan, Kathleen C.F., Bach, Erika A., Rodig, Scott J., Dighe, Anand S., Kaplan, Daniel H., Riley, Joan K., Greenlund, Andrew C., Campbell, Dayle, Carver-Moore, Karen, DuBois, Raymond N., Clark, Ross, Aguet, Michel, and Schreiber, Robert D.

Subjects
Cellular signal transduction -- Genetic aspects, Cytokines -- Genetic aspects, Biological sciences
Abstract

The janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway has been shown to be involved in many biological processes. JAK proteins are bound to cytokine receptors and signaling is triggered when cytokine binding induces receptor dimerization whereas STAT proteins are activated by tyrosine phosphorylation to form homodimers and heterodimers that activate cytokine-inducible genes. However, there is no information regarding the mechanism by which pathway specificity is manifested. An experiment on mice deficient in STAT1 is discussed to elucidate this mechanism.

Published
1996

43. Ligand-induced autoregulation of IFN-gamma receptor beta chain expression in T helper cell subsets

Author

Bach, Erika A., Szabo, Susanne J., Dighe, Anand S., Ashkenazi, Avi, Aguet, Michel, Murphy, Kenneth M., and Schreiber, Robert D.

Subjects
Immune response -- Physiological aspects, Interferon gamma -- Physiological aspects, CD4 lymphocytes -- Physiological aspects, Science and technology, Physiological aspects
Abstract

Interferon γ (IFN-γ) responsiveness in certain cells depends on the state of cellular differentiation or activation. Here an in vitro developmental system was used to show that IFN-γ produced during generation of the [CD4.sup.+] T helper cell type 1 ([T.sub.H]l) subset extinguishes expression of the IFN-γ receptor β subunit, resulting in [T.sub.H]1 cells that are unresponsive to IFN-γ. This β chain loss also occurred in IFN-γ-treated [T.sub.H]2 cells and thus represents a specific response of [CD4.sup.+] T cells to IFN-γ rather than a [T.sub.H]1-specific differentiation event. These results define a mechanism of cellular desensitization where a cytokine down-regulates expression of a receptor subunit required primarily for signaling and not ligand binding., Recently it was reported that [T.sub.H]1 and [T.sub.H]2 cells develop opposing patterns of responsiveness to the cytokines interleukin-12 (IL- 12) and IFN-γ, with [T.sub.H]1 retaining only IL-12 responsiveness and [T.sub.H]2 [...]

Published
1995

44. Dissection of the extracellular human interferon gamma receptor alpha-chain into two immunoglobulin-like domains. Production in an Escherichia coli thioredoxin gene fusion expression system and recognition by neutralizing antibodies

Author

Williams, Geoffrey, Ruegg, Nicole, Birch, Ashley, Weber, Christoph, Hofstadter, Klaus, Robinson, John A., Aguet, Michel, Garotta, Gianni, Schlatter, Daniel, and Huber, Walter

Subjects
Interferon gamma -- Structure, Chemical bonds -- Analysis, Biological sciences, Chemistry
Abstract

Experimental methods enable the production of the N-terminal domain of the extracellular interferon gamma receptor (IFN gamma R) as a thioredoxin-IFN gamma R fragment fusion protein with a native-like fold in Escherichia coli cytoplasm. The native-like structure is generated by spontaneous disulfide bond formation between Cys60 and Cys68 residues. The beta-sheet and reverse turn are present in the folded state of this receptor fragment. By similar techniques, the second domain of IFN gamma R can also be produced, but with less spontaneity.

Published
1995

45. A novel member of the interferon receptor family complements functionality of the murine interferon gamma receptor in human cells

Author

Hemmi, Silvio, Bohni, Ruth, Stark, Gerlinde, Marco, Francesco Di, and Aguet, Michel

Subjects
Cellular signal transduction -- Research, Interferon gamma -- Research, Mice -- Genetic aspects, Membrane proteins -- Analysis, Biological sciences
Abstract

An additional species-specific element required for signal transduction because of the inadequate expression of the human interferon gamma receptor (IFN-gamma R) in mouse cells in rendering biological sensitivity to human IFN-gamma and vice versa, is established. Human HEp-2 cells expressing the murine IFN-gamma R completely sensitive to murine IFN-gamma results from the resultant cDNA upon stable transfection. It encodes a novel acid type 1 transmembrane protein that is part of the IFN receptor family.

Published
1994

46. Generation of nitric oxide and induction of major histocompatibility complex class II antigen in macrophages from mice lacking the interferon gamma receptor

Author

Ryutaro Kamijo, Shapiro, Deborah, Junming Le, Sui Huang, Aguet, Michel, and Vilcek, Jan

Subjects
Histocompatibility -- Influence, Cytokines -- Usage, Science and technology
Abstract

Investigations of the indication of macrophage stimulation in the absence of an operational interferon gamma (IFN-gamma) receptor and the degree to which cytokines could substitute IFN-gamma in the induction of nitric oxide or major histocompatibility complex class II antigen (Ia) expression in peritoneal macrophages revealed that in thioglycollate-elicited macrophages from wild-type mice, tumor necrosis factor (TNF) by itself was almost useless in stimulating release of NO2-, but TNF stimulated NO2- release in the presence of IFN-gamma.

Published
1993

47. Immune response in mice that lack the interferon-gamma receptor

Author

Hendriks, Wiljan, Althage, Alana, Hemmi, Silvio, Bluethmann, Horst, Kamijo, Ryutaro, Vilcek, Jan, Zinkernagel, Rolf M., and Aguet, Michel

Subjects
Interferon -- Research, T cells -- Research, Immune response -- Research, Cell receptors -- Research, Science and technology, Research
Abstract

Interferon-γ (IFN-γ) exerts pleiotropic effects, including antiviral activity, stimulation of macrophages and natural killer cells, and increased expression of major histocompatibility complex antigens. Mice without the IFN-γ receptor had no overt anomalies, and their immune system appeared to develop normally. However, mutant mice had a defective natural resistance; they had increased susceptibility to infection by Listeria monocytogenes and vaccinia virus despite normal cytotoxic and T helper cell responses. Immunoglobulin isotype analysis revealed that IFN-γ is necessary for a normal antigenspecific immunoglobulin G2a response. These mutant mice offer the possibility for the further elucidation of IFN-γ-mediated functions by transgenic cell- or tissue-specific reconstitution of a functional receptor., The IFN-γ receptor (IFN-γR) is a unique cell surface receptor that appears to be expressed almost ubiquitously (1, 2). To inactivate the murine IFN-γR gene, we transfected embryonic stem (ES) [...]

Published
1993

48. Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein

Author

Bueler, Hansruedi, Fischer, Marek, Lang, Yolande, Bluethmann, Horst, Lipp, Hans-Peter, DeArmond, Stephen J., Prusiner, Stanley B., Aguet, Michel, and Weissmann, Charles

Subjects
Membrane proteins -- Research, Prions -- Research, Scrapie -- Development and progression, Spongiform encephalopathy -- Development and progression, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1992

49. Functional characterization of a hybrid human-mouse interferon gamma receptor: evidence for species-specific interaction of the extracellular receptor domain with a putative signal transducer

Author

Hemmi, Silvio, Merlin, Gilles, and Aguet, Michel

Subjects
Cellular signal transduction -- Research, Interferon gamma -- Research, Science and technology
Abstract

Human interferon gamma receptors (huIFN-gammaR) expressed in mouse cells exhibit identical binding properties as those expressed in human cells yet remain insensitive to human gamma interferon. Studies show that the huIFN-gammaR must first interact with cofactors expressed by human chromosome 21 to become sensitive. A hydrid interferon receptor consisting of human extracellular and murine transmembrane and cytoplasmic domains was created to determine the receptor region at which this interaction occurs. Receptors expressed in murinecells containing human chromosome 21, were sensitive to gamma interferon, suggesting that cofactors, which mediate gamma interferon sensitivity, interactwith the extracellular domain of huIFN-gammaR.

Published
1992

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