[OFER-TRABEC] NAC: Contrato Postdoctoral en C. elegans

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---Procedencia:
Institución:Instituto de Investigaciones Biomédicas de Bellvitge-IDIBELL
Contacto correo-e:jceron@idibell.cat
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We offer a postdoctoral position (starting on September 2011, work contract for 2 years) to work in C. elegans to study the implication of four splicing-related genes in the human rare disease Retinitis pigmentosa. The position is now available for immediate incorporation.
This project is funded by La Marató de TV3 Foundation.

Candidates should have a Ph.D. or equivalent. Experience with C. elegans, Bioinformatic (RNA-seq analysis), neurobiology or splicing mechanisms is a strong plus. English is the common language used in our lab.

Our lab is part of Bellvitge Institute for Biomedical Research (IDIBELL) (Barcelona, Spain) that provides an excellent scientific environment for translational biomedical research.
We are equipped with state-of-the-art tools for C. elegans research as RNAi and Y2H libraries, microinjector, confocal microscope, gene-gun for ballistic transformation ….

Applicants should send a cover letter, CV and names/email addresses for 2 references to jceron@idibell.cat . Deadline for applications: July 15th

Julián Cerón Ph.D
Genetics and Functional Genomics in C. elegans Group. Molecular Genetics Lab.
Bellvitge Institute for Biomedical Research (IDIBELL). Gran via 199, l'Hospitalet 08907, Barcelona, Spain.
tel: +34 93 260 7416. email: jceron@idibell.cat websites: www.gusano.info , www.idibell.cat

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Información complementaria de la oferta:
Main Project: Functional roles of splicing factors in autosomal dominant Retinitis pigmentosa (ad-RP): uncovering molecular mechanisms in Caenorhabditis elegans to explore novel therapies.
Summary of the Project: Retinitis pigmentosa is a rare disease affecting 1 in 4000 people worldwide (more than 1.5 million people) and producing a progressive loss of vision through the life. There are 13 loci associated with Familial autosomal dominant Retinitis pigmentosa (ad-RP) and four of those are pre-mRNA splicing factors. Despite about 7000 PUBMED entries for RP, molecular mechanisms by which mutations in these ubiquitously expressed splicing factors cause this photoreceptor-specific disease remain unknown. The main goal of this project is to shed light on the molecular mechanisms inherent in this process by using genetic and genomic tools with the corresponding C. elegans homologs, which are very well conserved.

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