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  1. 19761
    “…One of the proposed mechanisms of GGGGCC repeat expansion is their translation into non-canonical dipeptide repeats, which can then accumulate as aggregates and contribute to these pathologies. …”
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  2. 19762
    “…We here show that presence of IRF3 is crucial in this process, most likely through direct activation of pro-apoptotic factors rather than transcriptional induction of canonical downstream components, such as IFNs. Investigating genes reported to be involved in both DNA damage response and antiviral signaling, we demonstrate that IRF1 is an obligatory factor for DNA damage-induced cell death. …”
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  3. 19763
    “…Molecular analysis revealed that endothelial Heg deficiency decreased expression of Wnt ligands/agonists including Wnt2, Wnt9b, and Rspo3 in ECs, which limits Axin2 mediated canonical Wnt signaling and the expression of cytochrome P450 enzymes in hepatocytes. …”
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  4. 19764
    por Tessadori, Federico, Duran, Karen, Knapp, Karen, Fellner, Matthias, Smithson, Sarah, Beleza Meireles, Ana, Elting, Mariet W., Waisfisz, Quinten, O’Donnell-Luria, Anne, Nowak, Catherine, Douglas, Jessica, Ronan, Anne, Brunet, Theresa, Kotzaeridou, Urania, Svihovec, Shayna, Saenz, Margarita S., Thiffault, Isabelle, Del Viso, Florencia, Devine, Patrick, Rego, Shannon, Tenney, Jessica, van Haeringen, Arie, Ruivenkamp, Claudia A.L., Koene, Saskia, Robertson, Stephen P., Deshpande, Charulata, Pfundt, Rolph, Verbeek, Nienke, van de Kamp, Jiddeke M., Weiss, Janneke M.M., Ruiz, Anna, Gabau, Elisabeth, Banne, Ehud, Pepler, Alexander, Bottani, Armand, Laurent, Sacha, Guipponi, Michel, Bijlsma, Emilia, Bruel, Ange-Line, Sorlin, Arthur, Willis, Mary, Powis, Zoe, Smol, Thomas, Vincent-Delorme, Catherine, Baralle, Diana, Colin, Estelle, Revencu, Nicole, Calpena, Eduardo, Wilkie, Andrew O.M., Chopra, Maya, Cormier-Daire, Valerie, Keren, Boris, Afenjar, Alexandra, Niceta, Marcello, Terracciano, Alessandra, Specchio, Nicola, Tartaglia, Marco, Rio, Marlene, Barcia, Giulia, Rondeau, Sophie, Colson, Cindy, Bakkers, Jeroen, Mace, Peter D., Bicknell, Louise S., van Haaften, Gijs
    Publicado 2022
    “…Human histone H4 is encoded by fourteen canonical histone H4 genes, all differing at the nucleotide level but encoding an invariant protein. …”
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  5. 19765
    “…Inflammasomes are crucial gatekeepers of the immune response, but their maladaptive activation associates with inflammatory pathologies. Besides canonical activation, monocytes can trigger non-transcriptional or rapid inflammasome activation that has not been well defined in the context of acute myocardial infarction (AMI). …”
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  6. 19766
    “…Stimulation in areas that when used as network seed regions produced a network similar to the canonical DN was associated with reduction of creative fluency. …”
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  7. 19767
    “…Interleukin 10 (IL‐10)‐producing B cells (B10 cells) are a canonical cell fraction for regulating other activities of immune cells. …”
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  8. 19768
    “…Polysome profiling revealed that 35% of aberrantly spliced transcripts are more translated than their corresponding canonically spliced transcripts. This mostly occurs in genes with enriched metabolic functions. …”
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  9. 19769
    “…Promoter analysis also uncovered the existence of two canonical cold-related cis-acting elements, LTR and DRE/CRT, as well as stress-related phytohormone-responsive elements. …”
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  10. 19770
    “…Inhibition of Telomere repeat-binding factor 3 (TRB3)/Jagged Canonical Notch Ligand 1 (JAG1) signaling suppressed Notch signals activation induced by laminin-integrin axis. …”
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  11. 19771
    “…Due to a lack sample availability, however, many studies have been limited to characterizing T(FH) in mice or non-canonical tissue types, such as peripheral blood. Such constraints have resulted in a limited, and sometimes contradictory, understanding of this fundamental cell type. …”
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  12. 19772
    “…Identification of proteins by mass spectrometry showed F4 to contain several known “moonlighting proteins”—i.e., with additional activities to the canonical function, including enolase, Triosephosphate isomerase (TPI), Glyceraldehyde 3 phosphate dehydrogenase (G3P) and Elongation factor TU (EF-Tu). …”
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  13. 19773
    “…This tumor suppressor gene functions by negatively regulating the β-catenin protein and the majority of APC mutations disrupt the β-catenin degradation complex signalosome leading to the activation of the canonical Wnt pathway. Pathogenic APC mutations were reported in association to medulloblastoma. …”
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  14. 19774
    “…Morphological, pharmacological and genetic analyses showed that AQP4-IgG-induced axon injury involved osmotic stress and ionic overload, but does not appear to use canonical pathways of Wallerian-like degeneration. …”
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  15. 19775
    “…The covariation between symptom improvements and cytokine changes was calculated and validated by sparse canonical correlation analysis. Response patterns to bumetanide were revealed by clustering analysis. …”
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  16. 19776
  17. 19777
    “…By combining mutant and gene expression analysis we have determined that this protective effect depends on the activation of the Heat Shock Transcription Factor (HSF-1), whereas it is independent of other canonical cytoprotective molecules such as abnormal Dauer Formation-16 (DAF-16/FOXO) and Skinhead-1 (SKN-1/Nrf2). …”
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  18. 19778
    “…We previously found that upregulated E-cadherin in the epithelial micrometastases activated canonical survival pathways, including PI3K-Akt, that protected the tumor cells from death; however, the extent of protection from blocking the pathway in its entirety was modest, because different isoforms may have alternately affected cell functioning. …”
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  19. 19779
  20. 19780
    “…A quantification study using real-time polymerase chain reaction showed a significant reduction of the Na(V)1.7 canonical transcript. Collectively, these data widen the spectrum of SCN9A-related insensitivity to pain by describing a mutation causing Na(V)1.7 deficiency, underlying the nociceptor dysfunction, and highlight the importance of molecular investigation of U12 introns' mutations despite the silent prediction.…”
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