Search results for: Christian Widmann

Items from 1 to 20 out of 25 results

article

APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites

Daniel Constantin, Gilles Dubuis, María del Carmen Conde‐Rubio, Christian Widmann

The human genome contains 11 APOBEC (apolipoprotein B mRNA editing catalytic polypeptide‐like) cytidine deaminases classified into four families. These proteins function mainly in innate antiviral immunity and can also restrict endogenous retrotransposable element multiplication. The present study focuses on APOBEC3C (A3C), a member of the APOBEC3 subfamily. Some APOBEC3 proteins use their enzymatic...

article

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

Güliz Vanli, Christine Sempoux, Christian Widmann

Molecular Carcinogenesis > 56 > 6 > 1680 - 1684

Activation of oncogenes is the initial step in cellular transformation. Oncogenes favor aberrant proliferation, which, at least initially, induces cellular stress. This oncogenic stress can act as a safeguard mechanism against further transformation by inducing senescence or apoptosis. Yet, the few premalignant cells that tolerate and escape these senescent or apoptotic responses are those that will...

article

Aldehyde dehydrogenase activity plays a Key role in the aggressive phenotype of neuroblastoma

Marjorie Flahaut, Nicolas Jauquier, Nadja Chevalier, Katya Nardou, more

BMC Cancer > 2016 > 16 > 1 > 1-13

Background The successful targeting of neuroblastoma (NB) by associating tumor-initiating cells (TICs) is a major challenge in the development of new therapeutic strategies. The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers...

article

Combinative effects of β-Lapachone and APO866 on pancreatic cancer cell death through reactive oxygen species production and PARP-1 activation

Caroline S. Breton, Dominique Aubry, Vanessa Ginet, Julien Puyal, more

Biochimie > 2015 > 116 > Complete > 141-153

Pancreatic cancer (PC) is one of the most lethal human malignancies and a major health problem. Patients diagnosed with PC and treated with conventional approaches have an overall 5-year survival rate of less than 5%. Novel strategies are needed to treat this disease. Herein, we propose a combinatorial strategy that targets two unrelated metabolic enzymes overexpressed in PC cells: NAD(P)H:quinone...

article

The activity of the anti-apoptotic fragment generated by the caspase-3/p120 RasGAP stress-sensing module displays strict Akt isoform specificity

Güliz Vanli, Nieves Peltzer, Gilles Dubuis, Christian Widmann

Cellular Signalling > 2014 > 26 > 12 > 2992-2997

The caspase-3/p120 RasGAP module acts as a stress sensor that promotes pro-survival or pro-death signaling depending on the intensity and the duration of the stressful stimuli. Partial cleavage of p120 RasGAP generates a fragment, called fragment N, which protects stressed cells by activating Akt signaling. Akt family members regulate many cellular processes including proliferation, inhibition of...

article

Fragment N2, a caspase‐3‐generated RasGAP fragment, inhibits breast cancer metastatic progression

David Barras, Girieca Lorusso, Benoît Lhermitte, David Viertl, more

International Journal of Cancer > 135 > 1 > 242 - 247

The p120 RasGAP protein negatively regulates Ras via its GAP domain. RasGAP carries several other domains that modulate several signaling molecules such as Rho. RasGAP is also a caspase‐3 substrate. One of the caspase‐3‐generated RasGAP fragments, corresponding to amino acids 158–455 and called fragment N2, was previously reported to specifically sensitize cancer cells to death induced by various...

article

Caspase-3 and RasGAP: a stress-sensing survival/demise switch

Hadi Khalil, Mathieu J.M. Bertrand, Peter Vandenabeele, Christian Widmann

Trends in Cell Biology > 2014 > 24 > 2 > 83-89

The final decision on cell fate, survival versus cell death, relies on complex and tightly regulated checkpoint mechanisms. The caspase-3 protease is a predominant player in the execution of apoptosis. However, recent progress has shown that this protease paradoxically can also protect cells from death. Here, we discuss the underappreciated, protective, and prosurvival role of caspase-3 and detail...

article

GAP-independent functions of DLC1 in metastasis

David Barras, Christian Widmann

Cancer and Metastasis Reviews > 2014 > 33 > 1 > 87-100

Metastases are responsible for most cancer-related deaths. One of the hallmarks of metastatic cells is increased motility and migration through extracellular matrixes. These processes rely on specific small GTPases, in particular those of the Rho family. Deleted in liver cancer-1 (DLC1) is a tumor suppressor that bears a RhoGAP activity. This protein is lost in most cancers, allowing malignant cells...

article

TAT-RasGAP_317–326-mediated tumor cell death sensitization can occur independently of Bax and Bak

Alessandro Annibaldi, Mathieu Heulot, Jean-Claude Martinou, Christian Widmann

Apoptosis > 2014 > 19 > 4 > 719-733

The increase of cancer specificity and efficacy of anti-tumoral agents are prime strategies to overcome the deleterious side effects associated with anti-cancer treatments. We described earlier a cell-permeable protease-resistant peptide derived from the p120 RasGAP protein, called TAT-RasGAP_317–326, as being an efficient tumor-specific sensitizer to apoptosis induced by genotoxins in vitro and in...

article

HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality

Julien Puyal, Jannick Pétremand, Gilles Dubuis, Coralie Rummel, more

Molecular and Cellular Endocrinology > 2013 > 381 > 1-2 > 291-301

HDLs protect pancreatic beta cells against apoptosis induced by several endoplasmic reticulum (ER) stressors, including thapsigargin, cyclopiazonic acid, palmitate and insulin over-expression. This protection is mediated by the capacity of HDLs to maintain proper ER morphology and ER functions such as protein folding and trafficking. Here, we identified a distinct mode of protection exerted by HDLs...

article

UV-B induces cytoplasmic survivin expression in mouse epidermis

Nieves Peltzer, Paul Bigliardi, Christian Widmann

Journal of Dermatological Science > 2012 > 67 > 3 > 196-199

article

The role of endogenous and exogenous RasGAP-derived fragment N in protecting cardiomyocytes from peroxynitrite-induced apoptosis

Hadi Khalil, Nathalie Rosenblatt, Lucas Liaudet, Christian Widmann

Free Radical Biology and Medicine > 2012 > 53 > 4 > 926-935

Peroxynitrite (PN) is a potent nitrating and oxidizing agent generated during various pathological situations affecting the heart. The negative effects of PN result, at least in part, from its ability to activate caspases and apoptosis. RasGAP is a ubiquitously expressed protein that is cleaved sequentially by caspase-3. At low caspase-3 activity, RasGAP is cleaved into an N-terminal fragment, called...

article

Corrigendum to “Caspase substrates and neurodegenerative diseases”

Natasa Bulat, Christian Widmann

Brain Research Bulletin > 2010 > 81 > 1 > 196

article

Caspase substrates and neurodegenerative diseases

Natasa Bulat, Christian Widmann

Brain Research Bulletin > 2009 > 80 > 4-5 > 251-267

Apoptosis is induced by the cleavage of a subset of cellular proteins by proteases of the caspase family. Numerous (hundreds) caspase substrates have been described but only for a few of them is the function of their cleavage by caspases well understood. In this review, apoptosis and caspases will first be introduced. The main focus will then be directed to the caspase substrates, the actual “workers”...

article

Role of the sub-cellular localization of RasGAP fragment N2 for its ability to sensitize cancer cells to genotoxin-induced apoptosis

Alessandro Annibaldi, David Michod, Linda Vanetta, Steeve Cruchet, more

Experimental Cell Research > 2009 > 315 > 12 > 2081-2091

The specific sensitization of tumor cells to the apoptotic response induced by genotoxins is a promising way of increasing the efficacy of chemotherapies. The RasGAP-derived fragment N2, while not regulating apoptosis in normal cells, potently sensitizes tumor cells to cisplatin- and other genotoxin-induced cell death. Here we show that fragment N2 in living cells is mainly located in the cytoplasm...

article

Role of the transcriptional factor C/EBPβ in free fatty acid-elicited β-cell failure

Valérie Plaisance, Véronique Perret, Dimitri Favre, Amar Abderrahmani, more

Molecular and Cellular Endocrinology > 2009 > 305 > 1-2 > 47-55

Fatty acids can favour the development of Type 2 diabetes by reducing insulin secretion and inducing apoptosis of pancreatic β-cells. Here, we show that sustained exposure of the β-cell line MIN6 or of isolated pancreatic islets to the most abundant circulating fatty acid palmitate increases the level of C/EBPβ, an insulin transcriptional repressor. In contrast, two unsaturated fatty acids, oleate...

article

Splice variant-specific stabilization of JNKs by IB1/JIP1

Jiang-Yan Yang, Nathalie Moulin, Miguel X. van Bemmelen, Gilles Dubuis, more

Cellular Signalling > 2007 > 19 > 10 > 2201-2207

Islet-Brain 1 (IB1) (also called JNK-interacting protein 1; JIP1) is a scaffold protein that tethers components of the JNK mitogen-activated protein kinase pathway inducing a modulation of the activity and the target specificity of the JNK kinases. Dysfunctions in IB1 have been associated with diseases such as early type II diabetes. To gain more insight in the functions of IB1, its ability to modulate...

article

DNA-damage sensitizers: Potential new therapeutical tools to improve chemotherapy

David Michod, Christian Widmann

Critical Reviews in Oncology / Hematology > 2007 > 63 > 2 > 160-171

Agents that induce DNA damage in cells – the so-called genotoxins – have successfully been used for decades to treat patients with tumors. Genotoxins alter the DNA of cells, which is detected by DNA damage sensors and which leads to the activation of p53. Activation of p53 can lead to the death of cancer cells. The efficacy of genotoxins in humans is however limited by their toxicity to normal tissues...

article

Effect of the TAT-RasGAP317–326 peptide on apoptosis of human malignant mesothelioma cells and fibroblasts exposed to meso-tetra-hydroxyphenyl-chlorin and light

Olivier Pittet, David Petermann, David Michod, Thorsten Krueger, more

Journal of Photochemistry & Photobiology, B: Biology > 2007 > 88 > 1 > 29-35

5,10,15,20-Tetrakis(m-hydroxyphenyl)chlorin (mTHPC)-mediated photodynamic therapy (PDT) has shown insufficient tumor selectivity for the treatment of pleural mesothelioma. Tumor selectivity of mTHPC-PDT may be enhanced in the presence of the TAT-RasGAP _317–326 peptide which has the potential to specifically sensitize tumor cells to cytostatic agents.H-meso-1 and human fibroblast cell cultures,...

article

High resolution crystal structures of the p120 RasGAP SH3 domain

Birthe Ross, Ole Kristensen, Dimitri Favre, Joël Walicki, more

Biochemical and Biophysical Research Communications > 2007 > 353 > 2 > 463-468

X-ray structures of two crystal forms of the Src homology 3 domain (SH3) of the Ras GTPase activating protein (RasGAP) were determined at 1.5 and 1.8Å resolution. The overall structure comprises a single domain with two tightly packed β-sheets linked by a short helical segment. An important motif for peptide binding in other SH3 domains is not conserved in RasGAP. The RasGAP SH3 domain forms dimers...

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INFONA - science communication portal

Search results for: Christian Widmann

APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites

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

Aldehyde dehydrogenase activity plays a Key role in the aggressive phenotype of neuroblastoma

Combinative effects of β-Lapachone and APO866 on pancreatic cancer cell death through reactive oxygen species production and PARP-1 activation

The activity of the anti-apoptotic fragment generated by the caspase-3/p120 RasGAP stress-sensing module displays strict Akt isoform specificity

Fragment N2, a caspase‐3‐generated RasGAP fragment, inhibits breast cancer metastatic progression

Caspase-3 and RasGAP: a stress-sensing survival/demise switch

GAP-independent functions of DLC1 in metastasis

TAT-RasGAP_317–326-mediated tumor cell death sensitization can occur independently of Bax and Bak

HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality

UV-B induces cytoplasmic survivin expression in mouse epidermis

The role of endogenous and exogenous RasGAP-derived fragment N in protecting cardiomyocytes from peroxynitrite-induced apoptosis

Corrigendum to “Caspase substrates and neurodegenerative diseases”

Caspase substrates and neurodegenerative diseases

Role of the sub-cellular localization of RasGAP fragment N2 for its ability to sensitize cancer cells to genotoxin-induced apoptosis

Role of the transcriptional factor C/EBPβ in free fatty acid-elicited β-cell failure

Splice variant-specific stabilization of JNKs by IB1/JIP1

DNA-damage sensitizers: Potential new therapeutical tools to improve chemotherapy

Effect of the TAT-RasGAP317–326 peptide on apoptosis of human malignant mesothelioma cells and fibroblasts exposed to meso-tetra-hydroxyphenyl-chlorin and light

High resolution crystal structures of the p120 RasGAP SH3 domain

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