Fluofarma will be exhibitor at the EORTC-NCI-AACR Symposium that will be held
in Berlin, Germany, 16-19 November 2010.
The symposium, ‘Molecular Targets and Cancer Therapeutics’ will bring
together academics, scientists and representatives from the pharmaceutical
industry to discuss innovation in drug development, target selection and the
impact of new discoveries in molecular and cell biology. Feel free to meet us
at our booth n°F13.
Fluofarma will be attending the Bio-Connexion Congress in Paris, from October 6th to 7th. The BIO-connexion congres will highlight the new methods of toxicity testing in drug discovery.
Fluofarma will be attending the European Cancer Cluster Partnering 2010 in
Oslo, from September 15th to 17th.
Oslo Cancer Cluster (Norway) welcome key players from the international
oncology community on September 15th to 17th, 2010. This event will showcase
Europe’s most promising oncology companies to leading network of investors,
bigpharma and industry executives in an effort to build partnerships, attract
investment and foster further business collaborations.
Fluofarma is glad to announce a new scientific publication in the journal
"Analytical Chemistry":
Recombinant Differential Anchorage Probes that
Tower over the Spatial Dimension of Intracellular Signals for High Content
Screening and Analysis
Laura Schembria, Marion Zaneseb,
Gaelle Depierre-Plinetb, Muriel Petitb,
Assia Elkaoukabi-Chaibib, Loic Tauzinb,
Cristina Floreana,c, Lydia Lartiguea,
Chantal Medinaa, Christophe Reya,
Francis Bellocd, Josy Reiffersa,
François Ichasa,b and Francesca
De Giorgi*a,b
a INSERM U916, Institut Bergonié, 229 cours
de l'Argonne, 33076 Bordeaux, France
b Fluofarma, 2 rue Robert Escarpit, 33600
Pessac, France
c Università di Padova, 35121 Padova, Italia
d CHU de Bordeaux, Hôpital du Haut Lévèque,
33600 Pessac, France
* Corresponding author : francesca.degiorgi-ichas@inserm.fr
Abstract
Recombinant fluorescent probes allow the detection of molecular
events inside living cells. Many of them exploit the intracellular space to
provide positional signals and, thus, require detection by single cell
imaging. We describe here a novel strategy based on probes capable of encoding
the spatial dimension of intracellular signals into “all-or-none” fluorescence
intensity changes (differential anchorage probes, DAPs). The resulting signals
can be acquired in single cells at high throughput by automated flow
cytometry, (i) bypassing image acquisition and analysis, (ii) providing a
direct quantitative readout, and (iii) allowing the exploration of large
experimental series. We illustrate our purpose with DAPs for Bax and the
effector caspases 3 and 7, which are keys players in apoptotic cell death, and
show applications in basic research, high content multiplexed library
screening, compound characterization, and drug profiling.
Analytical Chemistry advance online publication October 29, 2009; doi: 10.1021/ac9015227
Roche adopts Fluofarma’s high-content screening
platform
Bordeaux (France), October 19, 2009 – Fluofarma, a leading
company in High Content Screening (HCS) technologies, which offers services
and counseling to the Pharmaceutical industry, announced today that it entered
into a multi-year agreement with Roche.
Read
More
Fluofarma cited in a Biocompare featured article “Flow Cytometry Gets a
Makeover”:
"If a cytometry system that adds imaging doesn’t suit your fancy,
Fluofarma has a high-content screening (HCS) platform that includes fully
automated flow cytometry, cell culture, and data analysis. They also offer a
proprietary line of recombinant fluorescent biosensors for use in HCS. 'The
combination of specifically engineered probes with analytical flow cytometry
dramatically broadens the application field of this detection technology,'
says Bruno Brisson, Fluofarma’s chief business officer, 'especially when image
segmentation is difficult, and when acquiring more than a few hundreds of
cells per condition is required. We have demonstrated that the use of these
instruments as the pivotal detection unit of versatile HCS detection platforms
is possible, and that it can supplant HCS by imaging in many key
applications'."
Read
more
Fluofarma is glad to announce a new scientific publication in the journal Cell
Research:
Outer membrane VDAC1 controls permeability
transition of the inner mitochondrial membrane in cellulo during
stress-induced apoptosis
Flora Tomaselloa,b, Angela Messinab,c, Lydia Lartiguea, Laura Schembria, Chantal Medinaa, Simona Reinab,c, Didier Thoravald, Marc Crouzetd, François Ichasa,e, Vito De Pintob,c and Francesca De Giorgia,e
a INSERM U916, Institut Bergonié, 229 cours de
l'Argonne, 33076 Bordeaux, France
b Dipartimento Scienze Chimiche, Università
di Catania, Catania, Italia
c Istituto Nazionale di Biomembrane e
Biosistemi, Sezione di Catania, Roma, Italia
d CNRS UMR 5095, Université Bordeaux 2, 146
rue Leo Saignat, 33076 Bordeaux, France
e Fluofarma, 2 rue Robert Escarpit, 33600
Pessac, France
Abstract:
Voltage-dependent anion channel (VDAC)1 is the main channel of
the mitochondrial outer membrane (MOM) and it has been proposed to be part of
the permeability transition pore (PTP), a putative multiprotein complex
candidate agent of the mitochondrial permeability transition (MPT). Working at
the single live cell level, we found that overexpression of VDAC1 triggers MPT
at the mitochondrial inner membrane (MIM). Conversely, silencing VDAC1
expression results in the inhibition of MPT caused by selenite-induced
oxidative stress. This MOM-MIM crosstalk was modulated by Cyclosporin A and
mitochondrial Cyclophilin D, but not by Bcl-2 and Bcl-xl, indicative of PTP
operation. VDAC1-dependent MPT engages a positive feedback loop involving
reactive oxygen species and p38-MAPK, and secondarily triggers a canonical
apoptotic response including Bax activation, cytochrome c release and
caspase 3 activation. Our data thus support a model of the PTP complex
involving VDAC1 at the MOM, and indicate that VDAC1-dependent MPT is an
upstream mechanism playing a causal role in oxidative stress-induced apoptosis.
Cell Research advance online publication 11 August 2009; doi:
10.1038/cr.2009.98