4 research departments
750 employees
45 nationalities
55 research teams
16 ERC laureates
260 publications per year
24000 m² lab area

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Fondation universite de Strasbourg
Wed, September 25th - Sat, September 28th 2019

33rd Internationnal Mammalian Genome Conference

Wednesday, June 19th 2019 - 11 a.m.
Pr Andrea Ballabio

How the lysosome tells the nucleus what to do.

Tuesday, June 25th 2019 - 11 a.m.
Pr Dmitri Ermolenko

Regulation of Protein Synthesis by mRNA Structure

Tuesday, June 25th 2019 - 11 a.m.
Dr Anthony Beucher

Regulation of pancreatic beta cell transcription factors by lncRNAs

Friday, June 28th 2019 - 11 a.m.
Dr Giulia Rancati

Experimental evolution of eukaryotic cells

Palmarès prix de thèse SBS : Prix de la Fondation Unistra 2017 Société de Biologie de Strasbourg : Patrick LAURETTE


A new therapeutic strategy for myotubular myopathy

Cross sections of muscles. Left the normal muscle fibers, in the middle those of a diseased mouse and on the right those of a diseased mouse overexpressing Bin1

March 20, 2019

After identifying amphiphysin 2 as a potential therapeutic target in some congenital myopathies, researchers in Jocelyn Laporte's team at the IGBMC (CNRS/Inserm/Université de Strasbourg) were able to specifically modulate the level of this molecule and to reduce all signs of a severe form of myopathy. These results, published on March 20, 2019, in the journal Science translational medicine, offer new therapeutic perspectives for these myopathies.

 

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Identification of a new partnership in gene expression regulation

On the left, compact chromatin. On the right, decondensed chromatin following the interaction of mutated TFIIH with the GCN5 enzyme.

March 20, 2019

Patients with a combined form of xeroderma pigmentosum and Cockayne syndrome have a wide range of clinical characteristics, including photosensitivity of the skin, predisposition to cancer and developmental disorders. At the origin of this rare genetic disease, a mutation of a subunit of the gene encoding TFIIH that plays a key role both in gene transcription and in gene repair. By studying patients' cells, researchers from Frédéric Coin's team at the IGBMC (CNRS/Inserm/Unistra) showed that the interaction of the TFIIH complex with the GCN5 enzyme leads to an increase in the enzymatic activity of GCN5, resulting in an uncontrolled remodelling of the chromatin and an overexpression of a large number of genes that may cause certain symptoms in patients.These results are published on March 20, 2019 in the journal Nature Communication.

 

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Université de Strasbourg
INSERM
CNRS

IGBMC - CNRS UMR 7104 - Inserm U 1258
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