FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2978259956> ?p ?o ?g. }

• W2978259956 abstract "Splicing in cancer Proteins are functional molecules responsible for every biochemical process that sustain living organisms. However, how genetic information is expanded to generate amazing diversity of proteins during development and in cancer remains still mostly unresolved. The mechanism we have to account for this diversity is known as splicing. Information-containing RNA molecules, copies of the DNA in our genes, are processed during splicing to give the templates for protein production, also called translation. Splicing can then generate different templates which give rise to different proteins with diverse functions from a single gene. Therefore, splicing is under constant control in the cell to guarantee its correct functioning. Not surprisingly, alterations in splicing are common in disease. Cancer, for example, presents incorrect splicing of genes important for the defence against tumours or genes causing cancer generating non-functional or hyper-functional proteins respectively. Looking to understand the reason behind this variation, we focused on the spliceosome, the cellular apparatus that carries out splicing. The spliceosome is formed by more than 200 proteins, also termed splicing factors. Given its diverse protein composition and the fact that protein production is increased in cancer, we proposed that changes in the quantity of some of those proteins could change the composition of the complex and maybe cause the splicing errors observed in cancer. Key proteins for splicing are actively regulated in cancer To study this, we imitated the early stages of cancer by expressing cancer-provoking genes in normal human cells. In these cells, we measured the production of the proteins constituting the spliceosome noticing that, as we proposed, some of them were being synthesized more than in normal cells. A group of proteins highly affected was identified as the U2 complex. The role of this complex in the spliceosome is to ensure that splicing occurs appropriately and its incorrect functioning is linked to splicing alterations. After observing the U2 complex regulation in cancer cells, we focused on understanding how it happened. Our analysis of RNA regulatory regions reveal novel selective mechanisms for aberrant function of specific U2 components in cancer cells. U2 spliceosome as a potential clinical target All in all, our study helped understand how the spliceosome, the molecular machine in charge of splicing, is altered in the early stages of cancer. We revealed how the U2 complex, integral for correct splicing, is strongly regulated in tumour conditions. Proving the association between changes in the levels of these splicing factors and splicing alterations in cancer, together with our discoveries on how these changes take place, could open new treatment opportunities in the field. Master’s Degree Project in Molecular Genetics, Biotechnology, Molecular Biology, 60 credits, 2019. Supervisor: Cristian Bellodi, RNA and Stem Cell Biology, Division of Molecular Hematology, BMC. (Less)" @default.
• W2978259956 created "2019-10-10" @default.
• W2978259956 creator A5002216791 @default.
• W2978259956 date "2019-01-01" @default.
• W2978259956 modified "2023-09-26" @default.
• W2978259956 title "Translational control of the spliceosome under oncogenic stress" @default.
• W2978259956 hasPublicationYear "2019" @default.
• W2978259956 type Work @default.
• W2978259956 sameAs 2978259956 @default.
• W2978259956 citedByCount "0" @default.
• W2978259956 crossrefType "journal-article" @default.
• W2978259956 hasAuthorship W2978259956A5002216791 @default.
• W2978259956 hasConcept C104317684 @default.
• W2978259956 hasConcept C105580179 @default.
• W2978259956 hasConcept C194583182 @default.
• W2978259956 hasConcept C40000846 @default.
• W2978259956 hasConcept C54355233 @default.
• W2978259956 hasConcept C54458228 @default.
• W2978259956 hasConcept C67705224 @default.
• W2978259956 hasConcept C70721500 @default.
• W2978259956 hasConcept C73758832 @default.
• W2978259956 hasConcept C86803240 @default.
• W2978259956 hasConcept C95444343 @default.
• W2978259956 hasConceptScore W2978259956C104317684 @default.
• W2978259956 hasConceptScore W2978259956C105580179 @default.
• W2978259956 hasConceptScore W2978259956C194583182 @default.
• W2978259956 hasConceptScore W2978259956C40000846 @default.
• W2978259956 hasConceptScore W2978259956C54355233 @default.
• W2978259956 hasConceptScore W2978259956C54458228 @default.
• W2978259956 hasConceptScore W2978259956C67705224 @default.
• W2978259956 hasConceptScore W2978259956C70721500 @default.
• W2978259956 hasConceptScore W2978259956C73758832 @default.
• W2978259956 hasConceptScore W2978259956C86803240 @default.
• W2978259956 hasConceptScore W2978259956C95444343 @default.
• W2978259956 hasLocation W29782599561 @default.
• W2978259956 hasOpenAccess W2978259956 @default.
• W2978259956 hasPrimaryLocation W29782599561 @default.
• W2978259956 hasRelatedWork W1518186650 @default.
• W2978259956 hasRelatedWork W1561049053 @default.
• W2978259956 hasRelatedWork W1972083681 @default.
• W2978259956 hasRelatedWork W1990590160 @default.
• W2978259956 hasRelatedWork W2002369761 @default.
• W2978259956 hasRelatedWork W2005844899 @default.
• W2978259956 hasRelatedWork W2043750605 @default.
• W2978259956 hasRelatedWork W2056524757 @default.
• W2978259956 hasRelatedWork W2077723816 @default.
• W2978259956 hasRelatedWork W2316483819 @default.
• W2978259956 hasRelatedWork W2567246900 @default.
• W2978259956 hasRelatedWork W2632151615 @default.
• W2978259956 hasRelatedWork W2765541253 @default.
• W2978259956 hasRelatedWork W2804809782 @default.
• W2978259956 hasRelatedWork W2979731173 @default.
• W2978259956 hasRelatedWork W7261346 @default.
• W2978259956 hasRelatedWork W76362285 @default.
• W2978259956 hasRelatedWork W9306685 @default.
• W2978259956 hasRelatedWork W2240725506 @default.
• W2978259956 hasRelatedWork W2739775482 @default.
• W2978259956 isParatext "false" @default.
• W2978259956 isRetracted "false" @default.
• W2978259956 magId "2978259956" @default.
• W2978259956 workType "article" @default.