Expression of Interest

Contact Person/Scientist in Charge

  • Name and surname: Pablo Gastaminza Landart
  • Email: pgastaminzaSPAMFILTER@cnb.csic.es

CNB CSIC

Department / Institute / Centre

  • Name: Department Molecular and Cellular Biology (CNB-CSIC)
  • Address:
  • Province: Madrid

Research Area

  • Life Sciences (LIF)

Brief description of the institution:

The National Centre for Biotechnolgy (CNB) is a research centre that forms part of the Spanish National Research Council (Consejo Superior de Investigaciones Científicas, CSIC), Spain’s most important public scientific institution. The CNB opened in 1992 to lead in developing modern biotechnology in Spain. Our principal objectives are to:

- Acquire knowledge and develop new technologies in the areas of human and animal health, agriculture and the environment.

- Promote knowledge and technology transfer for the benefit of society.

- Train future generations of researchers and technologists.

- Engage and inform society about advances and the benefits of biotechnology.

The CNB is distinguished by its versatile interdisciplinary research that combines molecular biology methods with the latest technology in the fields of functional and structural biology. We are a team of more than 600 professionals committed to research excellence. The CNB has been recognised by an international jury as one of the eight Severo Ochoa Centres of Excellence in medicine and the life sciences.

We hope these pages will awaken the reader’s interest in our work and our results. Here you will find up-to-date information on our centre’s organisation and mission, our research lines, our recent contributions to science and innovation, forthcoming scientific events and outreach activities, as well as training opportunities, job offers, and other useful data.

Brief description of the Centre/Research Group (including URL if applicable):

Centro Nacional de Biotecnología.

http://www.cnb.csic.es/index.php/en/the-cnb/welcome-to-the-cnb

Hepatitis C virus infection laboratory

HCV establishes chronic infections in humans, which are for the most part subclinical, but that lead to the development of life-threatening pathologies such as cirrhosis and hepatocellular carcinoma (HCC). Although immune system-mediated events are major players in HCV pathogenesis, the interference of HCV with cell homeostasis, in particular with lipid metabolism, is emerging as a key determinant of the disease progression.

HCV infection constitutes a great model of subversion of the cellular metabolism by viruses that promote the survival of anomalous, rogue cells as a strategy for persistence. Thus, we think that the capacity of HCV of enabling cell survival, while inflicting a severe damage to the cell may be used as a biological probe to unravel molecular mechanisms that are common to other pathologies. Despite the enormous success of the new, specific therapies against HCV and the perspective of a cure for the virus in a medium term, we believe that the study of the molecular mechanisms underlying HCV pathogenesis are still pertinent as they may teach us how to revert HCV-induced pathologies but also it may open new avenues in the treatment of pathologies with common molecular mechanisms, including other viral infections. In this sense, our studies are not exclusively limited to understanding HCV infection only but they are also meant to understand basic principles of the cellular response to different stress situations.

Project description:

Sigma-1 receptor (SIGMAR1) is an ER membrane protein specifically enriched in mitochondria-associated membranes (MAMs), a cellular hub for cellular signaling in basal metabolism and in response to stress, including virus infection. Loss of function of SIGMAR1 gene has been linked to neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), Parkinson´s or Alzheimer´s disease, whereas the severity of some types of cancer positively correlates with SIGMAR1 expression. The involvement of SIGMAR1 in these human pathologies is likely related with a putative role in cellular proteostasis, response to cellular stress and cell survival, mechanisms for which molecular details are scarce. Our group recently identified SIGMAR1 as a host gene that regulates the rate of hepatitis C virus infection initiation, at a step downstream of primary viral protein translation leading to progeny viral RNA accumulation. Intriguingly, SIGMAR1 dependence was less evident in cells expressing a mutant, inactive form of the cytoplasmic dsRNA sensor retinoic acid-inducible protein 1 (RIG-I), suggesting that SIGMAR1 silencing may lead to enhanced innate responses against RNA viruses, thus limiting early aspects of HCV infection.

Using RNAi against SIGMAR1, we have shown that innate response to RNA virus infection by SIGMAR1-deficient cells is faster and stronger than that in control cells, as verified IFN-beta promoter activation profile in response to Sendai (SenV) virus infection. We want to follow up on these studies to fit  SIGMAR1 into the known chart of functional interactions leading to interferon beta production upon viral infection but also to increase our knowledge on the molecular interactions regulated by SIGMAR1 during innate immune responses.

Applications

Documents: CV and Support Letters

Deadline: August 31, 2017

I want to contact the Institution

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