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The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Translational regulation in prokaryotes ensures efficient protein synthesis by controlling ribosome access to mRNA. This regulation is mediated by secondary RNA structures, including translational riboswitches, RNA thermometers, and small RNAs (sRNAs), which respond to intracellular and environmental signals to modulate gene expression.Translational RiboswitchesRiboswitches in the leader region of mRNAs can regulate translation by altering the accessibility of the Shine-Dalgarno (SD) sequence,...
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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
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Pseudouridilación mediada por DKC1 de las dianas de rRNA hnRNP A1 para mantener la traducción dependiente de IRES y

Anamika Gupta1,2, Mohit Bansal1,2, Jane Ding1,2

  • 1Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

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Resumen

La pseudouridina sintasa DKC1, regulada al alza en los cánceres, mantiene la supervivencia de las células cancerosas promoviendo la expresión de ATF4 y la adaptación metabólica a través del mediador hnRNP A1. Esto pone de relieve una vía clave en la progresión del cáncer.

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Área de la Ciencia:

  • Biología molecular
  • Biología del cáncer
  • La bioquímica

Sus antecedentes:

  • La pseudouridina sintasa DKC1 es regulada al alza en los cánceres por los oncogenes MYC.
  • No se comprende bien el papel de DKC1 en la traducción dependiente del sitio de entrada del ribosoma interno (IRES) y su conexión con la pseudouridilación.
  • Comprender esta vía es crucial para la terapia del cáncer.

Objetivo del estudio:

  • Para aclarar la importancia funcional de la regulación del DKC1 en el cáncer.
  • Investigar el vínculo mecanicista entre la DKC1, la pseudouridilación y la traducción mediada por el IRES.
  • Identificar los mediadores posteriores de DKC1 en la adaptación de las células cancerosas.

Principales métodos:

  • Investigó el papel de DKC1 en los programas de transcripción.
  • Se ha identificado a hnRNP A1 como un mediador posterior.
  • Se analizó la pseudouridilación mediada por DKC1 del ARN ribosomal.
  • Se examinó el efecto de hnRNP A1 en la estabilidad y la traducción del ARNm ATF4.
  • Se evaluó el papel de hnRNP A1 en la expresión de ATF4 inducida por el estrés.

Principales resultados:

  • DKC1 impulsa un programa de transcripción mediado por ATF4 que apoya el metabolismo de los aminoácidos y la adaptación al estrés.
  • hnRNP A1 es un mediador crítico, que mantiene la expresión de ATF4 y la traducción dependiente de IRES.
  • La pseudouridilación mediada por DKC1 del ARNr 28S es esencial para la expresión de la proteína hnRNP A1.
  • hnRNP A1 estabiliza el ARNm ATF4, promoviendo su traducción dependiente del IRES.
  • El estrés celular induce hnRNP A1, que es necesario para la expresión de ATF4 inducida por el estrés.

Conclusiones:

  • Se descubrió un eje DKC1-hnRNP A1 impulsado por MYC que vincula la traducción dependiente de IRES y la adaptación metabólica mediada por ATF4.
  • Esta vía apoya la supervivencia de las células cancerosas bajo estrés metabólico.
  • DKC1 y hnRNP A1 son objetivos terapéuticos potenciales en el cáncer.