IBB UAB

Author: Nati Infante

Programa Argó a l’IBB: Què podem fer per reduir la resistència als antibiòtics?

Programa Argó a l’IBB: Què podem fer per reduir la resistència als antibiòtics?

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L'Institut de Ciències de l'Educació de la UAB dóna suport a la transició entre la secundària i la universitat mitjançant el Programa Argó. Aquesta iniciativa permet ampliar el coneixement mutu entre la Universitat i la secundària, facilitar a l'alumnat de batxillerat i de cicles formatius la transició i l’acollida a la Universitat i per altra banda, oferir al professorat de secundària la possibilitat d’actualitzar coneixements i conèixer centres d’estudis, projectes i recerques que es fan a la UAB. Dins d’aquest programa, enguany s’ofereixen una trentena de cursos d’estiu impartits per diferents professors de la UAB experts en diferents disciplines i van dirigits a estudiants de 3r i de 4t d'ESO, Batxillerat i Cicles Formatius d’instituts de tot Catalunya. Del 5 al 9 de juliol,

An international collaboration uncovers several genetic markers associated with SARS-CoV-2 infection and COVID-19 severity.

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In March of 2020, thousands of scientists around the world united to answer a pressing and complex question: what genetic factors influence why some COVID-19 patients develop severe, life-threatening disease requiring hospitalization, while others escape with mild symptoms or none at all? This global effort, called the COVID-19 Host Genetics Initiative, was founded in March 2020 by Andrea Ganna, group leader at the Institute for Molecular Medicine Finland (FIMM), University of Helsinki and Mark Daly, director of FIMM and institute member at the Broad Institute of MIT and Harvard. The initiative has grown to be one of the most extensive collaborations in human genetics and currently includes more than 3,300 authors and 61 studies from 25 countries and The IBB researcher Mario Cácere
Comparative and Functional Genomics: “Mapping the human genetic architecture of COVID-19”

Comparative and Functional Genomics: “Mapping the human genetic architecture of COVID-19”

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COVID-19 Host Genetics Initiative. Mapping the human genetic architecture of COVID-19. Nature (2021). https://doi.org/10.1038/s41586-021-03767-x https://www.nature.com/articles/s41586-021-03767-x https://doi.org/10.1038/s41586-021-03767-x Abstract The genetic makeup of an individual contributes to susceptibility and response to viral infection. While environmental, clinical and social factors play a role in exposure to SARS-CoV-2 and COVID-19 disease severity1,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role...

The IBB wants to attract talent in the call for grants for the requalification of the Spanish university system for the 2021/2023 period

Highlights
From the Institute of Biotechnology and Biomedicine (IBB), the UAB's own institute, we are interested in being a receiving institution for young candidates to the grants Margarita Sales and also promote the incorporation of international talent through the grants María Zambrano (see grant typologies below)  The IBB’s mission is to discover and accelerate the development and implementation of relevant clinical knowledge and science-based products to make it easier for patients to live longer and in better conditions.  The IBB has an excellent scientific background in the field of biotechnology andbiomedicine and we stand out for collaborative and multidisciplinary research in order toadvance in the frontiers of knowledge and inno
Protein Folding and Conformational Diseases: “α-Helical peptidic scaffolds to target α-synuclein toxic species with nanomolar affinity”

Protein Folding and Conformational Diseases: “α-Helical peptidic scaffolds to target α-synuclein toxic species with nanomolar affinity”

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Nature Communications volume 12, Article number: 3752 (2021) Abstract α-Synuclein aggregation is a key driver of neurodegeneration in Parkinson’s disease and related syndromes. Accordingly, obtaining a molecule that targets α-synuclein toxic assemblies with high affinity is a long-pursued objective. Here, we exploit the biophysical properties of toxic oligomers and amyloid fibrils to identify a family of α-helical peptides that bind to these α-synuclein species with low nanomolar affinity, without interfering with the monomeric functional protein. This activity is translated into a high anti-aggregation potency and the ability to abrogate oligomer-induced cell damage. Using a structure-guided search we identify a human peptide expressed in the brain and the gastro

Human molecule able to block the toxic forms of the protein triggering Parkinson’s disease identified

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Researchers at the UAB and the UniZar have identified a human peptide found in the brain that blocks the α-synuclein aggregates involved in Parkinson's disease and prevents their neurotoxicity. The study, published in Nature Communications, suggests that this could be one of the organism's natural mechanisms with which to fight aggregation. The discovery may help to develop new therapeutic and diagnosis strategies for Parkinson's disease and other synuclein pathologies. The death of neurons specialised in the synthesis of dopamine, one of the brain's main neurotransmissors, deteriorates the motor and cognitive capacities of those with Parkinson's disease. The loss of these neurons is related to alpha-synuclein aggregation. Recent studies show that oligomers, the initial aggreg
Nanobiotechnology: “Human &-Galactosidase A Mutants: Priceless Tools to DevelopNovel Therapies for Fabry Disease”

Nanobiotechnology: “Human &-Galactosidase A Mutants: Priceless Tools to DevelopNovel Therapies for Fabry Disease”

News
Int. J. Mol. Sci. 2021, 22(12), 6518; https://www.mdpi.com/1422-0067/22/12/6518 Abstract Fabry disease (FD) is a lysosomal storage disease caused by mutations in the gene for the α-galactosidase A (GLA) enzyme. The absence of the enzyme or its activity results in the accumulation of glycosphingolipids, mainly globotriaosylceramide (Gb3), in different tissues, leading to a wide range of clinical manifestations. More than 1000 natural variants have been described in the GLA gene, most of them affecting proper protein folding and enzymatic activity. Currently, FD is treated by enzyme replacement therapy (ERT) or pharmacological chaperone therapy (PCT). However, as both approaches show specific drawbacks, new strategies (such as new forms of ERT, organ/cell transplant, substrate