Christian Widmann

Publications | Mémoires et thèses

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119 publications

2019 | 2018 | 2017 | 2016 | 2015 | 2014 | 2013 | 2012 | 2011 | 2010 | 2009 | 2008 | 2007 | 2006 | 2005 | 2004 | 2003 | 2002 | 2001 | 2000 | 1999 | 1998 | 1997 | 1996 | 1995 | 1994 | 1993 | 1992 | 1991 | 1989 |
 
The PI3K/Akt pathway is not a main driver in HDL-mediated cell protection.
Zheng A., Dubuis G., Ferreira CSM, Pétremand J., Vanli G., Widmann C., 2019/10. Cellular signalling, 62 p. 109347. Peer-reviewed.
 
Squalene: friend or foe for cancers.
Paolicelli R.C., Widmann C., 2019/08. Current opinion in lipidology, 30 (4) pp. 353-354. Peer-reviewed.
 
Identification of Clotrimazole Derivatives as Specific Inhibitors of Arenavirus Fusion.
Torriani G., Trofimenko E., Mayor J., Fedeli C., Moreno H., Michel S., Heulot M., Chevalier N., Zimmer G., Shrestha N. et al., 2019/03/15. Journal of virology, 93 (6). Peer-reviewed.
 
Burning fat to keep your stem cells? The role of fatty acid oxidation in various tissue stem cells.
Knobloch M., Widmann C., 2018/10. Current opinion in lipidology, 29 (5) pp. 426-427. Peer-reviewed.
 
Harnessing Oxidative Stress as an Innovative Target for Cancer Therapy.
Postovit L., Widmann C., Huang P., Gibson S.B., 2018. Oxidative medicine and cellular longevity, 2018 p. 6135739. Peer-reviewed.
 
Fatty acid metabolism regulates cell survival in specific niches.
Regazzi R., Widmann C., 2017/06. Current opinion in lipidology, 28 (3) pp. 284-285. Peer-reviewed.
 
The caspase-3/p120 RasGAP stress-sensing module reduces liver cancer incidence but does not affect overall survival in gamma-irradiated and carcinogen-treated mice.
Vanli G., Sempoux C., Widmann C., 2017/06. Molecular carcinogenesis, 56 (6) pp. 1680-1684. Peer-reviewed.
 
TAT-RasGAP317-326 Enhances Radiosensitivity of Human Carcinoma Cell Lines In Vitro and In Vivo through Promotion of Delayed Mitotic Cell Death.
Tsoutsou P., Annibaldi A., Viertl D., Ollivier J., Buchegger F., Vozenin M.C., Bourhis J., Widmann C., Matzinger O., 2017/05. Radiation research, 187 (5) pp. 562-569. Peer-reviewed.
Evaluation and validation of commercial antibodies for the detection of Shb.
Vanli G., Cuesta-Marban A., Widmann C., 2017. PLoS One, 12 (12) pp. e0188311. Peer-reviewed.
The Anticancer Peptide TAT-RasGAP317-326 Exerts Broad Antimicrobial Activity.
Heulot M., Jacquier N., Aeby S., Le Roy D., Roger T., Trofimenko E., Barras D., Greub G., Widmann C., 2017. Frontiers in microbiology, 8 p. 994. Peer-reviewed.
Acetate is the master of its fate, genetics, and molecular biology bimonthly update
Amati F., Widmann C., 2016/12. Current opinion in lipidology, 27 (6) pp. 636-637. Peer-reviewed.
The TAT-RasGAP317-326 anti-cancer peptide can kill in a caspase-, apoptosis-, and necroptosis-independent manner.
Heulot M., Chevalier N., Puyal J., Margue C., Michel S., Kreis S., Kulms D., Barras D., Nahimana A., Widmann C., 2016/09/27. Oncotarget, 7 (39) pp. 64342-64359. Peer-reviewed.
Aldehyde dehydrogenase activity plays a Key role in the aggressive phenotype of neuroblastoma.
Flahaut M., Jauquier N., Chevalier N., Nardou K., Balmas Bourloud K., Joseph J.M., Barras D., Widmann C., Gross N., Renella R. et al., 2016. Bmc Cancer, 16 (1) p. 781. Peer-reviewed.
Are HDL receptors really located where we think they are in the liver?
Rütti S., Widmann C., 2016. Current Opinion in Lipidology, 27 (4) pp. 424-425. Peer-reviewed.
Endoplasmic Reticulum Stress Links Oxidative Stress to Impaired Pancreatic Beta-Cell Function Caused by Human Oxidized LDL.
Plaisance V., Brajkovic S., Tenenbaum M., Favre D., Ezanno H., Bonnefond A., Bonner C., Gmyr V., Kerr-Conte J., Gauthier B.R. et al., 2016. PloS one, 11 (9) pp. e0163046. Peer-reviewed.
Assessment of the chemosensitizing activity of TAT-RasGAP317-326 in childhood cancers.
Chevalier N., Gross N., Widmann C., 2015. Plos One, 10 (3) pp. e0120487. Peer-reviewed.
 
Combinative effects of β-Lapachone and APO866 on pancreatic cancer cell death through reactive oxygen species production and PARP-1 activation.
Breton C.S., Aubry D., Ginet V., Puyal J., Heulot M., Widmann C., Duchosal M.A., Nahimana A., 2015. Biochimie, 116 pp. 141-153. Peer-reviewed.
Genetics and molecular biology: HDL plasticity and diversity of functions.
Rütti S., Widmann C., 2015. Current Opinion in Lipidology, 26 (6) pp. 596-597. Peer-reviewed.
HDLs, diabetes, and metabolic syndrome.
Vollenweider P., von Eckardstein A., Widmann C., 2015. pp. 405-421 dans Handbook of Experimental Pharmacology, SpringerOpen.
RasGAP Shields Akt from Deactivating Phosphatases in Fibroblast Growth Factor Signaling but Loses This Ability Once Cleaved by Caspase-3.
Cailliau K., Lescuyer A., Burnol A.F., Cuesta-Marbán Á., Widmann C., Browaeys-Poly E., 2015. Journal of Biological Chemistry, 290 (32) pp. 19653-19665. Peer-reviewed.
The caspase-3-p120-RasGAP module generates a NF-κB repressor in response to cellular stress.
Khalil H., Loukili N., Regamey A., Cuesta-Marban A., Santori E., Huber M., Widmann C., 2015. Journal of Cell Science, 128 (18) pp. 3502-3513. Peer-reviewed.
The δ-Opioid Receptor Affects Epidermal Homeostasis via ERK-Dependent Inhibition of Transcription Factor POU2F3.
Neumann C., Bigliardi-Qi M., Widmann C., Bigliardi P.L., 2015. Journal of Investigative Dermatology, 135 (2) pp. 471-480. Peer-reviewed.
A WXW Motif Is Required for the Anticancer Activity of the TAT-RasGAP317-326 Peptide.
Barras D., Chevalier N., Zoete V., Dempsey R., Lapouge K., Olayioye M.A., Michielin O., Widmann C., 2014. Journal of Biological Chemistry, 289 (34) pp. 23701-23711.
Caspase-3 and RasGAP: a stress-sensing survival/demise switch.
Khalil H., Bertrand M.J., Vandenabeele P., Widmann C., 2014. Trends In Cell Biology, 24 (2) pp. 83-89. Peer-reviewed.
Fragment N2, a caspase-3-generated RasGAP fragment, inhibits breast cancer metastatic progression
Barras D., Lorusso G., Lhermitte B., Viertl D., Rüegg C., Widmann C., 2014. International Journal of Cancer. Journal International Du Cancer, 135 (1) pp. 242-247. Peer-reviewed.
GAP-independent functions of DLC1 in metastasis.
Barras D., Widmann C., 2014. Cancer Metastasis Reviews, 33 (1) pp. 87-100. Peer-reviewed.
High-density lipoprotein, beta cells, and diabetes .
von Eckardstein A., Widmann C., 2014. Cardiovascular Research, 103 (3) pp. 384-394.
Inhibition of cell migration and invasion mediated by the TAT-RasGAP317-326 peptide requires the DLC1 tumor suppressor.
Barras D., Lorusso G., Rüegg C., Widmann C., 2014. Oncogene, 33 (44) pp. 5163-5172. Peer-reviewed.
TAT-RasGAP317-326-mediated tumor cell death sensitization can occur independently of Bax and Bak.
Annibaldi A., Heulot M., Martinou J.C., Widmann C., 2014. Apoptosis : An International Journal On Programmed Cell Death, 19 (4) pp. 719-733. Peer-reviewed.
 
The activity of the anti-apoptotic fragment generated by the caspase-3/p120 RasGAP stress-sensing module displays strict Akt isoform specificity.
Vanli G., Peltzer N., Dubuis G., Widmann C., 2014. Cellular Signalling, 26 (12) pp. 2992-2997. Peer-reviewed.
Triglyceride and HDL: the entangled pair.
Amati F., Widmann C., 2014. Current Opinion in Lipidology, 25 (5) pp. 404-405. Peer-reviewed.
Genetics and molecular biology: HDL-endoplasmic reticulum connection and cholesterol sensor.
Widmann C., 2013. Current Opinion In Lipidology, 24 (1) pp. 103-104.
HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality.
Puyal J., Pétremand J., Dubuis G., Rummel C., Widmann C., 2013. Molecular and Cellular Endocrinology, 381 (1-2) pp. 291-301. Peer-reviewed.
Role of mTOR, Bad, and Survivin in RasGAP Fragment N-Mediated Cell Protection.
Peltzer N., Vanli G., Yang J.Y., Widmann C., 2013. Plos One, 8 (6) pp. e68123.
The control of lipid-induced inflammation by macrophages.
Jaccard E., Widmann C., 2013. Current Opinion in Lipidology, 24 (6) pp. 528-529.
Caspase-3 Protects Stressed Organs against Cell Death.
Khalil H., Peltzer N., Walicki J., Yang J.Y., Dubuis G., Gardiol N., Held W., Bigliardi P., Marsland B., Liaudet L. et al., 2012. Molecular and Cellular Biology, 32 (22) pp. 4523-4533. Peer-reviewed.
Genetics and molecular biology: miRNAs take the HDL ride.
Regazzi R., Widmann C., 2012. Current Opinion in Lipidology, 23 (2) pp. 165-166.
 
HDLs protect pancreatic β-cells against ER stress by restoring protein folding and trafficking.
Pétremand J., Puyal J., Chatton J.Y., Duprez J., Allagnat F., Frias M., James R.W., Waeber G., Jonas J.C., Widmann C., 2012. Diabetes, 61 (5) pp. 1100-1111.
The role of endogenous and exogenous RasGAP-derived fragment N in protecting cardiomyocytes from peroxynitrite-induced apoptosis.
Khalil H., Rosenblatt N., Liaudet L., Widmann C., 2012. Free Radical Biology and Medicine, 53 (4) pp. 926-935.
UV-B induces cytoplasmic survivin expression in mouse epidermis.
Peltzer N., Bigliardi P., Widmann C., 2012. Journal of Dermatological Science, 67 (3) pp. 196-199.
 
A Cell Permeable Rasgap-derived Peptide Sensitizes Cancer Cells To Radiotherapy
Viertl D., Annibaldi A., Oezsahin M., Mirimanoff R., Widmann C., Matzinger O., 2011. pp. S738 dans ASTRO 2011, 53rd Annual Meeting of the American Society for Radiation Oncology, International Journal of Radiation Oncology Biology Physics. Peer-reviewed.
 
Genetics and molecular biology: fatty acids and endoplasmic reticulum stress.
Pétremand J., Widmann C., 2011. Current Opinion in Lipidology, 22 (4) pp. 315-316.
Promises of apoptosis-inducing peptides in cancer therapeutics.
Barras D., Widmann C., 2011. Current Pharmaceutical Biotechnology, 12 (8) pp. 1153-65.
RasGAP-derived fragment N increases the resistance of beta cells towards apoptosis in NOD mice and delays the progression from mild to overt diabetes.
Bulat N., Jaccard E., Peltzer N., Khalil H., Yang J.Y., Dubuis G., Widmann C., 2011. PLoS One, 6 (7) pp. e22609.
Revisiting G3BP1 as a RasGAP binding protein: sensitization of tumor cells to chemotherapy by the RasGAP 317-326 sequence does not involve G3BP1.
Annibaldi A., Dousse A., Martin S., Tazi J., Widmann C., 2011. PLoS One, 6 (12) pp. e29024. Peer-reviewed.
 
Glucose metabolism in cancer cells.
Annibaldi A., Widmann C., 2010. Current Opinion in Clinical Nutrition and Metabolic Care, 13 (4) pp. 466-470. Peer-reviewed.
 
MAP/ERK kinase kinase 1 (MEKK1) mediates transcriptional repression by interacting with polycystic kidney disease-1 (PKD1) promoter-bound p53 tumor suppressor protein.
Islam M.R., Jimenez T., Pelham C., Rodova M., Puri S., Magenheimer B.S., Maser R.L., Widmann C., Calvet J.P., 2010. Journal of Biological Chemistry, 285 (50) pp. 38818-38831. Peer-reviewed.
 
Mécanisme moléculaire de protection des HDLs contre le stress du réticulum endoplasmique dans la cellule beta pancréatique. [Molecular mechanisms of HDLs to protect against the endoplasmic reticulum stress in pancreatic beta cell.]
Petremand J., Chatton J. Y., Waeber G., Widmann C., 2010. p. 4 dans Congrès Francophone Annuel de Diabétologie SFD 201, Diabete and Metabolism. Peer-reviewed.
 
The HDL: adipocyte connection.
Pétremand J., Widmann C., 2010. Current Opinion In Lipidology, 21 (4) pp. 388-389.
Effect of RasGAP N2 fragment-derived peptide on tumor growth in mice.
Michod D., Annibaldi A., Schaefer S., Dapples C., Rochat B., Widmann C., 2009/06. Journal of the National Cancer Institute, 101 (11) pp. 828-832. Peer-reviewed.
 
Role of the transcriptional factor C/EBPbeta in free fatty acid-elicited beta-cell failure.
Plaisance V., Perret V., Favre D., Abderrahmani A., Yang J.Y., Widmann C., Regazzi R., 2009/06. Molecular and Cellular Endocrinology, 305 (1-2) pp. 47-55. Peer-reviewed.
 
ABC transporters: HDL-regulated gatekeepers at the endothelial border.
Jaccard E., Widmann C., 2009. Current Opinion in Lipidology, 20 (6) pp. 526-527.
 
Caspase substrates and neurodegenerative diseases.
Bulat N., Widmann C., 2009. Brain Research Bulletin, 80 (4-5) pp. 251-267.
Expression of the NH(2)-terminal fragment of RasGAP in pancreatic beta-cells increases their resistance to stresses and protects mice from diabetes.
Yang J.Y., Walicki J., Jaccard E., Dubuis G., Bulat N., Hornung J.P., Thorens B., Widmann C., 2009. Diabetes, 58 (11) pp. 2596-2606. Peer-reviewed.
 
Genetics and molecular biology: so, so complex HDLs!
Jaccard E., Widmann C., 2009. Current Opinion in Lipidology, 20 (3) pp. 254-255. Peer-reviewed.
Glucagon-like peptide-1 protects beta-cells against apoptosis by increasing the activity of an IGF-2/IGF-1 receptor autocrine loop.
Cornu M., Yang J.Y., Jaccard E., Poussin C., Widmann C., Thorens B., 2009. Diabetes, 58 (8) pp. 1816-1825. Peer-reviewed.
 
Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta cells.
Pétremand J., Bulat N., Butty A.C., Poussin C., Rütti S., Au K., Ghosh S., Mooser V., Thorens B., Yang J.Y. et al., 2009. Molecular Endocrinology, 23 (10) pp. 1572-1586. Peer-reviewed.
 
LDLs stimulate p38 MAPKs and wound healing through SR-BI independently of Ras and PI3 kinase.
Bulat N., Waeber G., Widmann C., 2009. Journal of Lipid Research, 50 (1) pp. 81-89. Peer-reviewed.
 
Role of the sub-cellular localization of RasGAP fragment N2 for its ability to sensitize cancer cells to genotoxin-induced apoptosis.
Annibaldi A., Michod D., Vanetta L., Cruchet S., Nicod P., Dubuis G., Bonvin C., Widmann C., 2009. Experimental Cell Research, 315 (12) pp. 2081-2091. Peer-reviewed.
Alterations in microRNA expression contribute to fatty acid-induced pancreatic beta-cell dysfunction.
Lovis P., Roggli E., Laybutt D.R., Gattesco S., Yang J.Y., Widmann C., Abderrahmani A., Regazzi R., 2008. Diabetes, 57 (10) pp. 2728-2736.
 
Exendin-4 protects beta-cells from interleukin-1 beta-induced apoptosis by interfering with the c-Jun NH2-terminal kinase pathway.
Ferdaoussi M., Abdelli S., Yang J.Y., Cornu M., Niederhauser G., Favre D., Widmann C., Regazzi R., Thorens B., Waeber G. et al., 2008. Diabetes, 57 (5) pp. 1205-1215. Peer-reviewed.
 
Generation of a tightly regulated all-cis beta cell-specific tetracycline-inducible vector.
Bulat N., Widmann C., 2008. Biotechniques, 45 (4) pp. 411, 414, 416 passim.
 
Genetics and molecular biology: HDLs and their multiple ways to protect cells.
Pétremand J., Abderrahmani A., Widmann C., 2008. Current Opinion in Lipidology, 19 (1) pp. 95-97. Peer-reviewed.
 
High density lipoproteins protect pancreatic beta cells by targeting 4E-BP1 : 512
Petremand J., Butty A.C., Yang J.Y., Natasa B., Poussin C., Thorens B., Waeber G., Widmann C., 2008. pp. S210 dans Minutes of the 43rd General Assembly of the European Association for the Study of Diabetes, Diabetologia. Peer-reviewed.
 
Lipid metabolism: sphingolipids- from membrane constituents to signaling molecules that control cell-to-cell communications.
Pétremand J., Widmann C., 2008. Current Opinion in Lipidology, 19 (6) pp. 620-621.
 
Mécanismes moléculaires de la fonction anti-apoptotique des HDLs sur la cellule béta pancréatique : 4E-BP1 comme potentielle cible thérapeutique. [Molecular mechanisms of anti-apoptotic function of HDLs on pancreatic beta cells : 4E-BP1 as a potential therapeutic target]
Petremand J., Butty A.C., Yang J.Y., Bulat N., Poussin C., Thorens B., Widmann C., Waeber G., 2008. pp. A23 dans Alfediam 2008, Congrès Annuel de l'Association de Langue Française pour l'Etude du Diabète et des Maladies Métaboiques, Diabetes and Metabolism. Peer-reviewed.
 
DNA-damage sensitizers: potential new therapeutical tools to improve chemotherapy
Michod D., Widmann C., 2007/08. Critical Reviews in Oncology/Hematology, 63 (2) pp. 160-71.
 
TAT-RasGAP317-326 requires p53 and PUMA to sensitize tumor cells to genotoxins
Michod D., Widmann C., 2007/05. Molecular Cancer Research, 5 (5) pp. 497-507.
 
High resolution crystal structures of the p120 RasGAP SH3 domain
Ross B., Kristensen O., Favre D., Walicki J., Kastrup J. S., Widmann C., Gajhede M., 2007/02. Biochemical and Biophysical Research Communications, 353 (2) pp. 463-8.
 
Effect of the TAT-RasGAP(317-326) peptide on apoptosis of human malignant mesothelioma cells and fibroblasts exposed to meso-tetra-hydroxyphenyl-chlorin and light.
Pittet O., Petermann D., Michod D., Krueger T., Cheng C., Ris H.B., Widmann C., 2007. Journal of photochemistry and photobiology. B, Biology, 88 (1) pp. 29-35. Peer-reviewed.
Human high-density lipoprotein particles prevent activation of the JNK pathway induced by human oxidised low-density lipoprotein particles in pancreatic beta cells.
Abderrahmani A., Niederhauser G., Favre D., Abdelli S., Ferdaoussi M., Yang J.Y., Regazzi R., Widmann C., Waeber G., 2007. Diabetologia, 50 (6) pp. 1304-1314. Peer-reviewed.
 
Splice variant-specific stabilization of JNKs by IB1/JIP1.
Yang J.Y., Moulin N., van Bemmelen M.X., Dubuis G., Tawadros T., Haefliger J.A., Waeber G., Widmann C., 2007. Cellular signalling, 19 (10) pp. 2201-7. Peer-reviewed.
 
Interleukin-8 secretion by fibroblasts induced by low density lipoproteins is p38 MAPK-dependent and leads to cell spreading and wound closure.
Dobreva I., Waeber G., James R.W., Widmann C., 2006. Journal of Biological Chemistry, 281 (1) pp. 199-205. Peer-reviewed.
 
Lipoproteins and mitogen-activated protein kinase signaling: a role in atherogenesis?
Dobreva I., Waeber G., Widmann C., 2006. Current opinion in lipidology, 17 (2) pp. 110-21. Peer-reviewed.
 
Impaired Akt activity down-modulation, caspase-3 activation, and apoptosis in cells expressing a caspase-resistant mutant of RasGAP at position 157
Yang J. Y., Walicki J., Michod D., Dubuis G., Widmann C., 2005/08. Molecular Biology of the Cell, 16 (8) pp. 3511-20.
 
Mecanismes de survie au stress cellulaire. [Survival mechanisms to cellular stress]
Widmann C., 2005/04. Revue Médicale Suisse, 1 (17) pp. 1141-6.
Cholesterol is the major component of native lipoproteins activating the p38 mitogen-activated protein kinases.
Dobreva I., Zschörnig O., Waeber G., James R.W., Widmann C., 2005. Biological chemistry, 386 (9) pp. 909-18. Peer-reviewed.
 
Expression of an uncleavable N-terminal RasGAP fragment in insulin-secreting cells increases their resistance toward apoptotic stimuli without affecting their glucose-induced insulin secretion.
Yang J.Y., Walicki J., Abderrahmani A., Cornu M., Waeber G., Thorens B., Widmann C., 2005. Journal of Biological Chemistry, 280 (38) pp. 32835-32842. Peer-reviewed.
 
Partial cleavage of RasGAP by caspases is required for cell survival in mild stress conditions
Yang J. Y., Michod D., Walicki J., Murphy B. M., Kasibhatla S., Martin S. J., Widmann C., 2004/12. Molecular and Cellular Biology, 24 (23) pp. 10425-36.
 
A RasGAP-derived cell permeable peptide potently enhances genotoxin-induced cytotoxicity in tumor cells
Michod D., Yang J. Y., Chen J., Bonny C., Widmann C., 2004/11. Oncogene, 23 (55) pp. 8971-8.
 
Surviving the kiss of death
Yang J. Y., Michod D., Walicki J., Widmann C., 2004/09. Biochemical Pharmacology, 68 (6) pp. 1027-31.
RasGTPase-activating protein is a target of caspases in spontaneous apoptosis of lung carcinoma cells and in response to etoposide
Bartling B., Yang J. Y., Michod D., Widmann C., Lewensohn R., Zhivotovsky B., 2004/06. Carcinogenesis, 25 (6) pp. 909-21.
 
Islet-brain (IB)/JNK-interacting proteins (JIPs): future targets for the treatment of neurodegenerative diseases?
Moulin N., Widmann C., 2004/04. Current Neurovascular Research, 1 (2) pp. 111-27.
 
LDLs induce fibroblast spreading independently of the LDL receptor via activation of the p38 MAPK pathway.
Dobreva I., Waeber G., Mooser V., James R.W., Widmann C., 2003. Journal of lipid research, 44 (12) pp. 2382-90. Peer-reviewed.
 
A subset of caspase substrates functions as the Jekyll and Hyde of apoptosis
Yang J. Y., Widmann C., 2002/12. European Cytokine Network, 13 (4) pp. 404-6.
 
The RasGAP N-terminal fragment generated by caspase cleavage protects cells in a Ras/PI3K/Akt-dependent manner that does not rely on NFkappa B activation.
Yang J.Y., Widmann C., 2002/04. Journal of Biological Chemistry, 277 (17) pp. 14641-14646. Peer-reviewed.
 
Apoptosis stimulated by the 91-kDa caspase cleavage MEKK1 fragment requires translocation to soluble cellular compartments.
Schlesinger T.K., Bonvin C., Jarpe M.B., Fanger G.R., Cardinaux J.R., Johnson G.L., Widmann C., 2002/03. Journal of Biological Chemistry, 277 (12) pp. 10283-10291. Peer-reviewed.
 
Role of the amino-terminal domains of MEKKs in the activation of NF kappa B and MAPK pathways and in the regulation of cell proliferation and apoptosis
Bonvin C., Guillon A., van Bemmelen M. X., Gerwins P., Johnson G. L., Widmann C., 2002/02. Cellular Signalling, 14 (2) pp. 123-31.
 
Antiapoptotic signaling generated by caspase-induced cleavage of RasGAP
Yang J. Y., Widmann C., 2001/08. Molecular and Cellular Biology, 21 (16) pp. 5346-58.
 
In vitro activity of MEKK2 and MEKK3 in detergents is a function of a valine to serine difference in the catalytic domain
Widmann C., Sather S., Oyer R., Johnson G. L., Dreskin S. C., 2001/05. Biochimica et Biophysica Acta-Protein Structure and Molecular Enzymology, 1547 (1) pp. 167-73. Peer-reviewed.
 
Reovirus infection activates JNK and the JNK-dependent transcription factor c-Jun.
Clarke P., Meintzer S.M., Widmann C., Johnson G.L., Tyler K.L., 2001. Journal of Virology, 75 (23) pp. 11275-11283.
MEK kinase 1 gene disruption alters cell migration and c-Jun NH2-terminal kinase regulation but does not cause a measurable defect in NF-kappa B activation.
Yujiri T., Ware M., Widmann C., Oyer R., Russell D., Chan E., Zaitsu Y., Clarke P., Tyler K., Oka Y. et al., 2000. Proceedings of the National Academy of Sciences of the United States of America, 97 (13) pp. 7272-7277. Peer-reviewed.
 
Reovirus-induced apoptosis is mediated by TRAIL.
Clarke P., Meintzer S.M., Gibson S., Widmann C., Garrington T.P., Johnson G.L., Tyler K.L., 2000. Journal of Virology, 74 (17) pp. 8135-8139.
 
Spatial, temporal and subcellular localization of islet-brain 1 (IB1), a homologue of JIP-1, in mouse brain.
Pellet J.B., Haefliger J.A., Staple J.K., Widmann C., Welker E., Hirling H., Bonny C., Nicod P., Catsicas S., Waeber G. et al., 2000. European Journal of Neuroscience, 12 (2) pp. 621-632. Peer-reviewed.
 
The gene MAPK8IP1, encoding islet-brain-1, is a candidate for type 2 diabetes.
Waeber G., Delplanque J., Bonny C., Mooser V., Steinmann M., Widmann C., Maillard A., Miklossy J., Dina C., Hani E.H. et al., 2000. Nature genetics, 24 (3) pp. 291-5. Peer-reviewed.
 
Differential involvement of MEK kinase 1 (MEKK1) in the induction of apoptosis in response to microtubule-targeted drugs versus DNA damaging agents.
Gibson S., Widmann C., Johnson G.L., 1999. The Journal of biological chemistry, 274 (16) pp. 10916-22. Peer-reviewed.
 
Mitogen-activated protein kinase: conservation of a three-kinase module from yeast to human.
Widmann C., Gibson S., Jarpe M.B., Johnson G.L., 1999. Physiological Reviews, 79 (1) pp. 143-180.
 
Anti-apoptotic versus pro-apoptotic signal transduction: checkpoints and stop signs along the road to death
Jarpe M. B., Widmann C., Knall C., Schlesinger T. K., Gibson S., Yujiri T., Fanger G. R., Gelfand E. W., Johnson G. L., 1998/09. Oncogene, 17 (11 Reviews) pp. 1475-82.
 
MEK kinase 1, a substrate for DEVD-directed caspases, is involved in genotoxin-induced apoptosis
Widmann C., Gerwins P., Johnson N. L., Jarpe M. B., Johnson G. L., 1998/04. Molecular and Cellular Biology, 18 (4) pp. 2416-29.
 
Caspase-dependent cleavage of signaling proteins during apoptosis. A turn-off mechanism for anti-apoptotic signals
Widmann C., Gibson S., Johnson G. L., 1998/03. Journal of Biological Chemistry, 273 (12) pp. 7141-7.
 
14-3-3 proteins interact with specific MEK kinases
Fanger G. R., Widmann C., Porter A. C., Sather S., Johnson G. L., Vaillancourt R. R., 1998/02. Journal of Biological Chemistry, 273 (6) pp. 3476-83.
 
Potentiation of apoptosis by low dose stress stimuli in cells expressing activated MEK kinase 1
Widmann C., Johnson N. L., Gardner A. M., Smith R. J., Johnson G. L., 1997/11. Oncogene, 15 (20) pp. 2439-47.
 
Internalization and homologous desensitization of the GLP-1 receptor depend on phosphorylation of the receptor carboxyl tail at the same three sites.
Widmann C., Dolci W., Thorens B., 1997/07. Molecular Endocrinology, 11 (8) pp. 1094-1102.
 
The regulation of anoikis: MEKK-1 activation requires cleavage by caspases
Cardone M. H., Salvesen G. S., Widmann C., Johnson G., Frisch S. M., 1997/07. Cell, 90 (2) pp. 315-23.
 
MEKKs, GCKs, MLKs, PAKs, TAKs, and tpls: upstream regulators of the c-Jun amino-terminal kinases?
Fanger G. R., Gerwins P., Widmann C., Jarpe M. B., Johnson G. L., 1997/02. Current Opinion in Genetics and Development, 7 (1) pp. 67-74.
 
The functional half-life of H-2Kd-restricted T cell epitopes on living cells
Eberl G., Widmann C., Corradin G., 1996/09. European Journal of Immunology, 26 (9) pp. 1993-9.
 
Signal transduction and desensitization of the glucagon-like peptide-1 receptor.
Thorens B., Widmann C., 1996/07. Acta Physiologica Scandinavica, 157 (3) pp. 317-319.
 
Desensitization and phosphorylation of the glucagon-like peptide-1 (GLP-1) receptor by GLP-1 and 4-phorbol 12-myristate 13-acetate.
Widmann C., Dolci W., Thorens B., 1996/01. Molecular Endocrinology, 10 (1) pp. 62-75.
 
Heterologous desensitization of the glucagon-like peptide-1 receptor by phorbol esters requires phosphorylation of the cytoplasmic tail at four different sites.
Widmann C., Dolci W., Thorens B., 1996. Journal of Biological Chemistry, 271 (33) pp. 19957-19963.
 
Prix Apollinaire Bouchardat 1996. Aspects moléculaires du contrôle de la sécrétion d'insuline [1996 Apollinaire Bouchardat Prize. Molecular aspects of control of insulin secretion].
Thorens B., Gremlich S., Roduit R., Widmann C., 1996. Journées Annuelles de Diabétologie De L'hôtel-dieu pp. 55-68.
 
Agonist-induced internalization and recycling of the glucagon-like peptide-1 receptor in transfected fibroblasts and in insulinomas.
Widmann C., Dolci W., Thorens B., 1995/08. Biochemical Journal, 310 (1) pp. 203-214.
 
Signal transduction by the cloned glucagon-like peptide-1 receptor: comparison with signaling by the endogenous receptors of beta cell lines.
Widmann C., Bürki E., Dolci W., Thorens B., 1994/05. Molecular Pharmacology, 45 (5) pp. 1029-1035.
 
Cloning and functional expression of the human islet GLP-1 receptor. Demonstration that exendin-4 is an agonist and exendin-(9-39) an antagonist of the receptor.
Thorens B., Porret A., Bühler L., Deng S.P., Morel P., Widmann C., 1993/11. Diabetes, 42 (11) pp. 1678-1682.
 
T helper epitopes enhance the cytotoxic response of mice immunized with MHC class I-restricted malaria peptides
Widmann C., Romero P., Maryanski J. L., Corradin G., Valmori D., 1992/10. Journal of Immunological Methods, 155 (1) pp. 95-9.
 
H-2-restricted cytolytic T lymphocytes specific for HLA display T cell receptors of limited diversity
Casanova J. L., Cerottini J. C., Matthes M., Necker A., Gournier H., Barra C., Widmann C., MacDonald H. R., Lemonnier F., Malissen B. et al., 1992/08. Journal of Experimental Medicine, 176 (2) pp. 439-47.
 
Immunization with synthetic peptides containing a defined malaria epitope induces a highly diverse cytotoxic T lymphocyte response. Evidence that two peptide residues are buried in the MHC molecule.
Romero P., Eberl G., Casanova J.L., Cordey A.S., Widmann C., Luescher I.F., Corradin G., Maryanski J.L., 1992. Journal of immunology, 148 (6) pp. 1871-1878. Peer-reviewed.
 
Differential stability of antigenic MHC class I-restricted synthetic peptides
Widmann C., Maryanski J. L., Romero P., Corradin G., 1991/12. Journal of Immunology, 147 (11) pp. 3745-51.
 
T cell receptor genes in a series of class I major histocompatibility complex-restricted cytotoxic T lymphocyte clones specific for a Plasmodium berghei nonapeptide: implications for T cell allelic exclusion and antigen-specific repertoire
Casanova J. L., Romero P., Widmann C., Kourilsky P., Maryanski J. L., 1991/12. Journal of Experimental Medicine, 174 (6) pp. 1371-83.
 
Delineation of several DR-restricted tetanus toxin T cell epitopes
Demotz S., Lanzavecchia A., Eisel U., Niemann H., Widmann C., Corradin G., 1989/01. Journal of Immunology, 142 (2) pp. 394-402.
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