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- W3196328089 abstract "The Mediterranean mussel is one of the most economically relevant bivalve mollusk species in Europe and China. The absence of massive mortalities and their resistance to pathogens affecting other cultured bivalves has been under study in recent years. The transcriptome response of this species to different immune stimuli has been extensively studied, and even the complexity of its genome, which has recently been sequenced, has been suggested as one of the factors contributing to this resistance. However, studies concerning the non-coding RNA profiles remain practically unexplored-especially those corresponding to the lncRNAs. To the best of our knowledge, this is the second characterization and study of lncRNAs in this bivalve species. In this work, we identified the potential repertoire of lncRNAs expressed in mussel hemocytes, and using RNA-Seq we analyzed the lncRNA profile of mussel hemocytes stimulated in vitro with three different immune stimuli: LPS, poly I:C, and β-glucans. Compared to unstimulated hemocytes, LPS induced the highest modulation of lncRNAs, whereas poly I:C and β-glucans induced a similar discrete response. Based on the potential cis-regulatory activity of the lncRNAs, we identified the neighboring protein-coding genes of the regulated lncRNAs to estimate-at least partially-the processes in which they are implicated. After applying correlation analyses, it seems that-especially for LPS-the lncRNAs could participate in the regulation of gene expression, and substantially contribute to the immune response." @default.
- W3196328089 created "2021-09-13" @default.
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- W3196328089 date "2021-09-09" @default.
- W3196328089 modified "2023-10-07" @default.
- W3196328089 title "Differential Expression of Long Non-Coding RNA (lncRNA) in Mediterranean Mussel (Mytilus galloprovincialis) Hemocytes under Immune Stimuli" @default.
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- W3196328089 doi "https://doi.org/10.3390/genes12091393" @default.
- W3196328089 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8468332" @default.
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