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  1. Artikel ; Online: Correction to 'Bias-minimized quantification of microRNA reveals widespread alternative processing and 3' end modification'.

    Kim, Haedong / Kim, Jimi / Kim, Kijun / Chang, Hyeshik / You, Kwontae / Kim, V Narry

    Nucleic acids research

    2022  Band 50, Heft 3, Seite(n) 1799–1800

    Sprache Englisch
    Erscheinungsdatum 2022-01-25
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkac078
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1067: Hefte anzeigen Standort:
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  2. Artikel ; Online: Gut bacterial metabolites modulate endoplasmic reticulum stress.

    Ke, Xiaobo / You, Kwontae / Pichaud, Matthieu / Haiser, Henry J / Graham, Daniel B / Vlamakis, Hera / Porter, Jeffrey A / Xavier, Ramnik J

    Genome biology

    2021  Band 22, Heft 1, Seite(n) 292

    Abstract: Background: The endoplasmic reticulum (ER) is a membranous organelle that maintains proteostasis and cellular homeostasis, controlling the fine balance between health and disease. Dysregulation of the ER stress response has been implicated in intestinal ...

    Abstract Background: The endoplasmic reticulum (ER) is a membranous organelle that maintains proteostasis and cellular homeostasis, controlling the fine balance between health and disease. Dysregulation of the ER stress response has been implicated in intestinal inflammation associated with inflammatory bowel disease (IBD), a chronic condition characterized by changes to the mucosa and alteration of the gut microbiota. While the microbiota and microbially derived metabolites have also been implicated in ER stress, examples of this connection remain limited to a few observations from pathogenic bacteria. Furthermore, the mechanisms underlying the effects of bacterial metabolites on ER stress signaling have not been well established.
    Results: Utilizing an XBP1s-GFP knock-in reporter colorectal epithelial cell line, we screened 399 microbiome-related metabolites for ER stress pathway modulation. We find both ER stress response inducers (acylated dipeptide aldehydes and bisindole methane derivatives) and suppressors (soraphen A) and characterize their activities on ER stress gene transcription and translation. We further demonstrate that these molecules modulate the ER stress pathway through protease inhibition or lipid metabolism interference.
    Conclusions: Our study identified novel links between classes of gut microbe-derived metabolites and the ER stress response, suggesting the potential for these metabolites to contribute to gut ER homeostasis and providing insight into the molecular mechanisms by which gut microbes impact intestinal epithelial cell homeostasis.
    Mesh-Begriff(e) Aldehydes/pharmacology ; Apoptosis ; Bacteria/metabolism ; Dipeptides/pharmacology ; Endoplasmic Reticulum Stress/drug effects ; Gastrointestinal Microbiome ; HT29 Cells ; Humans ; Indoles/pharmacology ; Macrolides/pharmacology ; Tunicamycin/pharmacology ; Unfolded Protein Response/drug effects
    Chemische Substanzen Aldehydes ; Dipeptides ; Indoles ; Macrolides ; Tunicamycin (11089-65-9) ; soraphen A (122547-72-2)
    Sprache Englisch
    Erscheinungsdatum 2021-10-15
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1474-760X
    ISSN (online) 1474-760X
    ISSN 1474-760X
    DOI 10.1186/s13059-021-02496-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Gut bacterial metabolites modulate endoplasmic reticulum stress

    Ke, Xiaobo / You, Kwontae / Pichaud, Matthieu / Haiser, Henry J. / Graham, Daniel B. / Vlamakis, Hera / Porter, Jeffrey A. / Xavier, Ramnik J.

    Genome biology. 2021 Dec., v. 22, no. 1

    2021  

    Abstract: BACKGROUND: The endoplasmic reticulum (ER) is a membranous organelle that maintains proteostasis and cellular homeostasis, controlling the fine balance between health and disease. Dysregulation of the ER stress response has been implicated in intestinal ... ...

    Abstract BACKGROUND: The endoplasmic reticulum (ER) is a membranous organelle that maintains proteostasis and cellular homeostasis, controlling the fine balance between health and disease. Dysregulation of the ER stress response has been implicated in intestinal inflammation associated with inflammatory bowel disease (IBD), a chronic condition characterized by changes to the mucosa and alteration of the gut microbiota. While the microbiota and microbially derived metabolites have also been implicated in ER stress, examples of this connection remain limited to a few observations from pathogenic bacteria. Furthermore, the mechanisms underlying the effects of bacterial metabolites on ER stress signaling have not been well established. RESULTS: Utilizing an XBP1s-GFP knock-in reporter colorectal epithelial cell line, we screened 399 microbiome-related metabolites for ER stress pathway modulation. We find both ER stress response inducers (acylated dipeptide aldehydes and bisindole methane derivatives) and suppressors (soraphen A) and characterize their activities on ER stress gene transcription and translation. We further demonstrate that these molecules modulate the ER stress pathway through protease inhibition or lipid metabolism interference. CONCLUSIONS: Our study identified novel links between classes of gut microbe-derived metabolites and the ER stress response, suggesting the potential for these metabolites to contribute to gut ER homeostasis and providing insight into the molecular mechanisms by which gut microbes impact intestinal epithelial cell homeostasis.
    Schlagwörter cell lines ; dipeptides ; endoplasmic reticulum ; endoplasmic reticulum stress ; epithelial cells ; genome ; homeostasis ; inflammation ; inflammatory bowel disease ; intestinal microorganisms ; lipid metabolism ; metabolites ; methane ; proteinases ; stress response ; transcription (genetics)
    Sprache Englisch
    Erscheinungsverlauf 2021-12
    Umfang p. 292.
    Erscheinungsort BioMed Central
    Dokumenttyp Artikel
    ZDB-ID 2040529-7
    ISSN 1474-760X
    ISSN 1474-760X
    DOI 10.1186/s13059-021-02496-8
    Datenquelle NAL Katalog (AGRICOLA)

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  4. Artikel ; Online: Bias-minimized quantification of microRNA reveals widespread alternative processing and 3' end modification.

    Kim, Haedong / Kim, Jimi / Kim, Kijun / Chang, Hyeshik / You, Kwontae / Kim, V Narry

    Nucleic acids research

    2018  Band 47, Heft 5, Seite(n) 2630–2640

    Abstract: MicroRNAs (miRNAs) modulate diverse biological and pathological processes via post-transcriptional gene silencing. High-throughput small RNA sequencing (sRNA-seq) has been widely adopted to investigate the functions and regulatory mechanisms of miRNAs. ... ...

    Abstract MicroRNAs (miRNAs) modulate diverse biological and pathological processes via post-transcriptional gene silencing. High-throughput small RNA sequencing (sRNA-seq) has been widely adopted to investigate the functions and regulatory mechanisms of miRNAs. However, accurate quantification of miRNAs has been limited owing to the severe ligation bias in conventional sRNA-seq methods. Here, we quantify miRNAs and their variants (known as isomiRs) by an improved sRNA-seq protocol, termed AQ-seq (accurate quantification by sequencing), that utilizes adapters with terminal degenerate sequences and a high concentration of polyethylene glycol (PEG), which minimize the ligation bias during library preparation. Measurement using AQ-seq allows us to correct the previously misannotated 5' end usage and strand preference in public databases. Importantly, the analysis of 5' terminal heterogeneity reveals widespread alternative processing events which have been underestimated. We also identify highly uridylated miRNAs originating from the 3p strands, indicating regulations mediated by terminal uridylyl transferases at the pre-miRNA stage. Taken together, our study reveals the complexity of the miRNA isoform landscape, allowing us to refine miRNA annotation and to advance our understanding of miRNA regulation. Furthermore, AQ-seq can be adopted to improve other ligation-based sequencing methods including crosslinking-immunoprecipitation-sequencing (CLIP-seq) and ribosome profiling (Ribo-seq).
    Mesh-Begriff(e) Base Sequence ; High-Throughput Nucleotide Sequencing/methods ; Immunoprecipitation ; MicroRNAs/genetics ; Molecular Sequence Annotation/methods ; Polyethylene Glycols/chemistry ; RNA Interference ; Sequence Analysis, RNA
    Chemische Substanzen MicroRNAs ; Polyethylene Glycols (3WJQ0SDW1A)
    Sprache Englisch
    Erscheinungsdatum 2018-01-04
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gky1293
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1067: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Artikel ; Online: QRICH1 dictates the outcome of ER stress through transcriptional control of proteostasis.

    You, Kwontae / Wang, Lingfei / Chou, Chih-Hung / Liu, Kai / Nakata, Toru / Jaiswal, Alok / Yao, Junmei / Lefkovith, Ariel / Omar, Abdifatah / Perrigoue, Jacqueline G / Towne, Jennifer E / Regev, Aviv / Graham, Daniel B / Xavier, Ramnik J

    Science (New York, N.Y.)

    2021  Band 371, Heft 6524

    Abstract: Tissue homeostasis is perturbed in a diversity of inflammatory pathologies. These changes can elicit endoplasmic reticulum (ER) stress, protein misfolding, and cell death. ER stress triggers the unfolded protein response (UPR), which can promote recovery ...

    Abstract Tissue homeostasis is perturbed in a diversity of inflammatory pathologies. These changes can elicit endoplasmic reticulum (ER) stress, protein misfolding, and cell death. ER stress triggers the unfolded protein response (UPR), which can promote recovery of ER proteostasis and cell survival or trigger programmed cell death. Here, we leveraged single-cell RNA sequencing to define dynamic transcriptional states associated with the adaptive versus terminal UPR in the mouse intestinal epithelium. We integrated these transcriptional programs with genome-scale CRISPR screening to dissect the UPR pathway functionally. We identified QRICH1 as a key effector of the PERK-eIF2α axis of the UPR. QRICH1 controlled a transcriptional program associated with translation and secretory networks that were specifically up-regulated in inflammatory pathologies. Thus, QRICH1 dictates cell fate in response to pathological ER stress.
    Mesh-Begriff(e) Animals ; Apoptosis ; Cells, Cultured ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Endoplasmic Reticulum Stress/genetics ; Eukaryotic Initiation Factor-2/metabolism ; Gene Expression Regulation ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Mice ; Organoids ; Proteostasis/genetics ; RNA-Seq ; Single-Cell Analysis ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Unfolded Protein Response/genetics ; eIF-2 Kinase/metabolism
    Chemische Substanzen DNA-Binding Proteins ; Eukaryotic Initiation Factor-2 ; QRICH1 protein, human ; Transcription Factors ; PERK kinase (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2021-02-07
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abb6896
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 77: Hefte anzeigen

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