bibliography.bib

@article{gibson2022a,
  title = {Therapeutic {{Metabolic Reprograming Using microRNAs}}: {{From Cancer}} to {{HIV Infection}}},
  shorttitle = {Therapeutic {{Metabolic Reprograming Using microRNAs}}},
  author = {Gibson, Mark S. and {Noronha-Estima}, Cl{\'a}udia and {Gama-Carvalho}, Margarida},
  year = {2022},
  month = feb,
  journal = {Genes},
  volume = {13},
  number = {2},
  pages = {273},
  publisher = {{Multidisciplinary Digital Publishing Institute}},
  issn = {2073-4425},
  doi = {10.3390/genes13020273},
  abstract = {MicroRNAs (miRNAs) are crucial regulators of cellular processes, including metabolism. Attempts to use miRNAs as therapeutic agents are being explored in several areas, including the control of cancer progression. Recent evidence suggests fine tuning miRNA activity to reprogram tumor cell metabolism has enormous potential as an alternative treatment option. Indeed, cancer growth is known to be linked to profound metabolic changes. Likewise, the emerging field of immunometabolism is leading to a refined understanding of how immune cell proliferation and function is governed by glucose homeostasis. Different immune cell types are now known to have unique metabolic signatures that switch in response to a changing environment. T-cell subsets exhibit distinct metabolic profiles which underlie their alternative differentiation and phenotypic functions. Recent evidence shows that the susceptibility of CD4+ T-cells to HIV infection is intimately linked to their metabolic activity, with many of the metabolic features of HIV-1-infected cells resembling those found in tumor cells. In this review, we discuss the use of miRNA modulation to achieve metabolic reprogramming for cancer therapy and explore the idea that the same approach may serve as an effective mechanism to restrict HIV replication and eliminate infected cells.},
  copyright = {http://creativecommons.org/licenses/by/3.0/},
  langid = {english},
  keywords = {cancer,HIV,immunometabolism,metabolism,microRNAs,therapy},
  file = {/home/gil/Zotero/storage/B6J4E8LX/Gibson et al. - 2022 - Therapeutic Metabolic Reprograming Using microRNAs.pdf}
}

@article{kumar2021,
  title = {Developmental Bifurcation of Human {{T}} Follicular Regulatory Cells},
  author = {Kumar, Saumya and Fonseca, V{\'a}lter R. and Ribeiro, Filipa and Basto, Afonso P. and {\'A}gua-Doce, Ana and Monteiro, Marta and Elessa, Dik{\'e}l{\'e}l{\'e} and Miragaia, Ricardo J. and Gomes, Tom{\'a}s and Piaggio, Eliane and Segura, Elodie and {Gama-Carvalho}, Margarida and Teichmann, Sarah A. and Graca, Luis},
  year = {2021},
  month = may,
  journal = {Science Immunology},
  volume = {6},
  number = {59},
  pages = {eabd8411},
  publisher = {{American Association for the Advancement of Science}},
  doi = {10.1126/sciimmunol.abd8411},
  abstract = {Germinal centers (GCs) are anatomic structures where B cells undergo affinity maturation, leading to production of high-affinity antibodies. The balance between T follicular helper (TFH) and regulatory (TFR) cells is critical for adequate control of GC responses. The study of human TFH and TFR cell development has been hampered because of the lack of in vitro assays reproducing in vivo biology, along with difficult access to healthy human lymphoid tissues. We used a single-cell transcriptomics approach to study the maturation of TFH and TFR cells isolated from human blood, iliac lymph nodes (LNs), and tonsils. As independent tissues have distinct proportions of follicular T cells in different maturation states, we leveraged the heterogeneity to reconstruct the maturation trajectory for human TFH and TFR cells. We found that the dominant maturation of TFR cells follows a bifurcated trajectory from precursor Treg cells, with one arm of the bifurcation leading to blood TFR cells and the other leading to the most mature GC TFR cells. Overall, our data provide a comprehensive resource for the transcriptomics of different follicular T cell populations and their dynamic relationship across different tissues.}
}

@article{lopes2021,
  title = {Genomic {{Tackling}} of {{Human Satellite DNA}}: {{Breaking Barriers}} through {{Time}}},
  shorttitle = {Genomic {{Tackling}} of {{Human Satellite DNA}}},
  author = {Lopes, Mariana and Louzada, Sandra and {Gama-Carvalho}, Margarida and Chaves, Raquel},
  year = {2021},
  month = jan,
  journal = {International Journal of Molecular Sciences},
  volume = {22},
  number = {9},
  pages = {4707},
  publisher = {{Multidisciplinary Digital Publishing Institute}},
  issn = {1422-0067},
  doi = {10.3390/ijms22094707},
  abstract = {(Peri)centromeric repetitive sequences and, more specifically, satellite DNA (satDNA) sequences, constitute a major human genomic component. SatDNA sequences can vary on a large number of features, including nucleotide composition, complexity, and abundance. Several satDNA families have been identified and characterized in the human genome through time, albeit at different speeds. Human satDNA families present a high degree of sub-variability, leading to the definition of various subfamilies with different organization and clustered localization. Evolution of satDNA analysis has enabled the progressive characterization of satDNA features. Despite recent advances in the sequencing of centromeric arrays, comprehensive genomic studies to assess their variability are still required to provide accurate and proportional representation of satDNA (peri)centromeric/acrocentric short arm sequences. Approaches combining multiple techniques have been successfully applied and seem to be the path to follow for generating integrated knowledge in the promising field of human satDNA biology.},
  copyright = {http://creativecommons.org/licenses/by/3.0/},
  langid = {english},
  keywords = {genomics,satellite DNA characterization,satellite DNA families,technique interdependency,variability},
  file = {/home/gil/Zotero/storage/FA7UE8NW/Lopes et al. - 2021 - Genomic Tackling of Human Satellite DNA Breaking .pdf}
}

@article{marques2022a,
  title = {Network {{Approaches}} to {{Study Endogenous RNA Competition}} and {{Its Impact}} on {{Tissue-Specific microRNA Functions}}},
  author = {Marques, T{\^a}nia Monteiro and {Gama-Carvalho}, Margarida},
  year = {2022},
  month = feb,
  journal = {Biomolecules},
  volume = {12},
  number = {2},
  pages = {332},
  publisher = {{Multidisciplinary Digital Publishing Institute}},
  issn = {2218-273X},
  doi = {10.3390/biom12020332},
  abstract = {microRNAs are small non-coding RNAs that play a key role in regulating gene expression. These molecules exert their function through sequence complementarity with microRNA responsive elements and are typically located in the 3{${'}$} untranslated region of mRNAs, negatively regulating expression. Even though the relevant role of miRNA-dependent regulation is broadly recognized, the principles governing their ability to lead to specific functional outcomes in distinct cell types are still not well understood. In recent years, an intriguing hypothesis proposed that miRNA-responsive elements act as communication links between different RNA species, making the investigation of microRNA function even more complex than previously thought. The competing endogenous RNA hypothesis suggests the presence of a new level of regulation, whereby a specific RNA transcript can indirectly influence the abundance of other transcripts by limiting the availability of a common miRNA, acting as a ``molecular sponge''. Since this idea has been proposed, several studies have tried to pinpoint the interaction networks that have been established between different RNA species and whether they contribute to normal cell function and disease. The focus of this review is to highlight recent developments and achievements made towards the process of characterizing competing endogenous RNA networks and their role in cellular function.},
  copyright = {http://creativecommons.org/licenses/by/3.0/},
  langid = {english},
  keywords = {ceRNA networks,microRNAs,post-transcriptional regulation},
  file = {/home/gil/Zotero/storage/HKQCALJK/Marques and Gama-Carvalho - 2022 - Network Approaches to Study Endogenous RNA Competi.pdf}
}