Publications by authors named "Eun Ji E Kim"

Article Synopsis
  • - Aging affects gene expression differently, with two main types: chronological (actual time lived) and physiological (biological condition), both presenting challenges in analysis due to their complexity.
  • - Research indicates that as people age chronologically, there is an increase in noncoding RNAs and certain transcript elements, while physiological aging leads to a decrease in mRNAs linked to various biological functions.
  • - An important finding is the age-related rise in using distal 3' splice sites in mRNA as a potential biomarker for physiological aging, which may help differentiate between the two aging types at the transcriptomic level.
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The Golgi apparatus plays a central role in trafficking cargoes such as proteins and lipids. Defects in the Golgi apparatus lead to various diseases, but its role in organismal longevity is largely unknown. Using a quantitative proteomic approach, we found that a Golgi protein, MON-2, was up-regulated in long-lived mutants with mitochondrial respiration defects and was required for their longevity.

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Y RNA is a conserved small non-coding RNA whose functions in aging remain unknown. Here, we sought to determine the role of Y RNA homologs, CeY RNA (CeY) and stem-bulge RNAs (sbRNAs), in aging. We found that the levels of CeY and sbRNAs generally increased during aging.

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Article Synopsis
  • - Nonsense-mediated mRNA decay (NMD) is a cellular process that helps maintain RNA quality by removing faulty mRNA, which supports longevity in organisms.
  • - Researchers identified key factors influencing NMD, finding that deactivating certain proteins led to an increase in faulty mRNA levels, suggesting a link to lifespan.
  • - Specifically, the protein ALGN-2 was shown to decrease with age and was necessary for extending lifespan, particularly when insulin/IGF-1 signaling was inhibited, highlighting NMD's role in longevity.
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Excessive glucose causes various diseases and decreases lifespan by altering metabolic processes, but underlying mechanisms remain incompletely understood. Here, we show that Lipin 1/LPIN-1, a phosphatidic acid phosphatase and a putative transcriptional coregulator, prevents life-shortening effects of dietary glucose on Caenorhabditis elegans. We found that depletion of lpin-1 decreased overall lipid levels, despite increasing the expression of genes that promote fat synthesis and desaturation, and downregulation of lipolysis.

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PDZ domain-containing proteins (PDZ proteins) act as scaffolds for protein-protein interactions and are crucial for a variety of signal transduction processes. However, the role of PDZ proteins in organismal lifespan and aging remains poorly understood. Here, we demonstrate that KIN-4, a PDZ domain-containing microtubule-associated serine-threonine (MAST) protein kinase, is a key longevity factor acting through binding PTEN phosphatase in Caenorhabditis elegans.

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Caenorhabditis elegans is an exceptionally valuable model for aging research because of many advantages, including its genetic tractability, short lifespan, and clear age-dependent physiological changes. Aged C. elegans display a decline in their anatomical and functional features, including tissue integrity, motility, learning and memory, and immunity.

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Article Synopsis
  • Mitochondria are vital for producing energy and metabolites, but they also play significant roles in regulating the immune system against infections.
  • Recent findings highlight various mitochondrial processes, such as mitochondrial surveillance, the unfolded protein response (UPRmt), and mitophagy, that enhance immune responses in the model organism Caenorhabditis elegans.
  • Insights gained from studying C. elegans could help us understand similar mitochondrial defense mechanisms in more complex organisms, including mammals.
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