A5058370548- RNA Interference and Gene Delivery
- Advanced biosensing and bioanalysis techniques
- Click Chemistry and Applications
- Cell death mechanisms and regulation
- Nanoparticle-Based Drug Delivery
- Hair Growth and Disorders
- DNA Repair Mechanisms
- Nuclear Structure and Function
- Nerve injury and regeneration
- Chemical Synthesis and Analysis
- Neurogenesis and neuroplasticity mechanisms
- Monoclonal and Polyclonal Antibodies Research
Délégation Paris 7
2015-2016
Inserm
2015-2016
Hôpital Saint-Louis
2015-2016
Université Paris Cité
2015-2016
Sorbonne Paris Cité
2016
Rutgers, The State University of New Jersey
2016
Abstract AAC-11 is an antiapoptotic protein that upregulated in most cancer cells. Increased expression of confers a survival advantage when cells are challenged with various stresses and contributes to tumor invasion metastases, whereas its deregulation reduces resistance chemotherapeutic drugs. The effect may be clinically relevant as correlates poor prognosis several human cancers. Thus, inactivation might constitute attractive approach for developing therapeutics. We have developed...
Beside its central role in the mitochondria-dependent cell death pathway, apoptotic protease activating factor 1 (Apaf-1) is involved DNA damage response through cell-cycle arrest induced by genotoxic stress. This non-apoptotic function requires a nuclear translocation of Apaf-1 during G1-to-S transition. However, mechanisms that trigger accumulation upon remain to be investigated. Here we show main 4 isoforms can undergo and restore deficient MEFs cycle S phase following stress activation...
Axo-glial interactions are critical for myelination and the domain organization of myelinated fibers. Cell adhesion molecules belonging to Cadm family, in particular Cadm3 (axonal) its heterophilic binding partner Cadm4 (Schwann cell), mediate these along internode. Using targeted shRNA-mediated knockdown, we show that removal axonal promotes Schwann cell vitro DRG neuron/Schwann myelinating system. Conversely, over-expressing on surface neuron axons results an almost complete inability by...
<div>Abstract<p>AAC-11 is an antiapoptotic protein that upregulated in most cancer cells. Increased expression of AAC-11 confers a survival advantage when cells are challenged with various stresses and contributes to tumor invasion metastases, whereas its deregulation reduces resistance chemotherapeutic drugs. The effect may be clinically relevant as correlates poor prognosis several human cancers. Thus, inactivation might constitute attractive approach for developing...
<p>This file contains Supplementary Figures S1 and S2 legends</p>
<p>This file contains the supplementary Table S1, which amino-acid sequences of peptides used in study, Figure S1 shows that RT53 increases drug-induced cell death and disrupts endogenous AAC-11-Acinus interaction S2 does not induce detectable cytochrome c, AIF Smac release from isolated mitochondria accumulate mitochondria</p>
<p>This file contains Supplementary Figures S1 and S2 legends</p>
<p>This file contains the supplementary Table S1, which amino-acid sequences of peptides used in study, Figure S1 shows that RT53 increases drug-induced cell death and disrupts endogenous AAC-11-Acinus interaction S2 does not induce detectable cytochrome c, AIF Smac release from isolated mitochondria accumulate mitochondria</p>
<div>Abstract<p>AAC-11 is an antiapoptotic protein that upregulated in most cancer cells. Increased expression of AAC-11 confers a survival advantage when cells are challenged with various stresses and contributes to tumor invasion metastases, whereas its deregulation reduces resistance chemotherapeutic drugs. The effect may be clinically relevant as correlates poor prognosis several human cancers. Thus, inactivation might constitute attractive approach for developing...