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  • Chen, Jing  (4)
  • Linguistics  (4)
  • Biology  (4)
  • 1
    Online Resource
    Online Resource
    WDFY4 deficiency in NOD mice ameliorates autoimmune diabetes and insulitis
    Proceedings of the National Academy of Sciences ; 2023
    In:  Proceedings of the National Academy of Sciences Vol. 120, No. 13 ( 2023-03-28)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 120, No. 13 ( 2023-03-28)
    Abstract: The events that initiate autoimmune diabetes in nonobese diabetic (NOD) mice remain poorly understood. CD4 + and CD8 + T cells are both required to develop disease, but their relative roles in initiating disease are unclear. To test whether CD4 + T cell infiltration into islets requires damage to β cells induced by autoreactive CD8 + T cells, we inactivated Wdfy4 in nonobese diabetic (NOD) mice (NOD. Wdfy4 −/−- ) using CRISPR/Cas9 targeting to eliminate cross-presentation by type 1 conventional dendritic cells (cDC1s). Similar to C57BL/6 Wdfy4 −/− mice, cDC1 in NOD. Wdfy4 −/− mice are unable to cross-present cell-associated antigens to prime CD8 + T cells, while cDC1 from heterozygous NOD. Wdfy4 +/− mice cross-present normally. Further, NOD. Wdfy4 −/− mice fail to develop diabetes while heterozygous NOD. Wdfy4 +/− mice develop diabetes similarly to wild-type NOD mice. NOD. Wdfy4 −/− mice remain capable of processing and presenting major histocompatibility complex class II (MHC-II)-restricted autoantigens and can activate β cell-specific CD4 + T cells in lymph nodes. However, disease in these mice does not progress beyond peri-islet inflammation. These results indicate that the priming of autoreactive CD8 + T cells in NOD mice requires cross-presentation by cDC1. Further, autoreactive CD8 + T cells appear to be required not only to develop diabetes, but to recruit autoreactive CD4 + T cells into islets of NOD mice, perhaps in response to progressive β cell damage.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2219956120
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2023
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  • 2
    Online Resource
    Online Resource
    Maternal Huluwa dictates the embryonic body axis through β-catenin in vertebrates
    American Association for the Advancement of Science (AAAS) ; 2018
    In:  Science Vol. 362, No. 6417 ( 2018-11-23)
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 362, No. 6417 ( 2018-11-23)
    Abstract: The vertebrate body is formed by cell movements and shape change during embryogenesis. It remains undetermined which maternal signals govern the formation of the dorsal organizer and the body axis. We found that maternal depletion of huluwa , a previously unnamed gene, causes loss of the dorsal organizer, the head, and the body axis in zebrafish and Xenopus embryos. Huluwa protein is found on the plasma membrane of blastomeres in the future dorsal region in early zebrafish blastulas. Huluwa has strong dorsalizing and secondary axis–inducing activities, which require β-catenin but can function independent of Wnt ligand/receptor signaling. Mechanistically, Huluwa binds to and promotes the tankyrase-mediated degradation of Axin. Therefore, maternal Huluwa is an essential determinant of the dorsal organizer and body axis in vertebrate embryos.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aat1045
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2018
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 3
    Online Resource
    Online Resource
    The global succinylation of SARS-CoV-2–infected host cells reveals drug targets
    Proceedings of the National Academy of Sciences ; 2022
    In:  Proceedings of the National Academy of Sciences Vol. 119, No. 30 ( 2022-07-26)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 119, No. 30 ( 2022-07-26)
    Abstract: SARS-CoV-2, the causative agent of the COVID-19 pandemic, undergoes continuous evolution, highlighting an urgent need for development of novel antiviral therapies. Here we show a quantitative mass spectrometry-based succinylproteomics analysis of SARS-CoV-2 infection in Caco-2 cells, revealing dramatic reshape of succinylation on host and viral proteins. SARS-CoV-2 infection promotes succinylation of several key enzymes in the TCA, leading to inhibition of cellular metabolic pathways. We demonstrated that host protein succinylation is regulated by viral nonstructural protein (NSP14) through interaction with sirtuin 5 (SIRT5); overexpressed SIRT5 can effectively inhibit virus replication. We found succinylation inhibitors possess significant antiviral effects. We also found that SARS-CoV-2 nucleocapsid and membrane proteins underwent succinylation modification, which was conserved in SARS-CoV-2 and its variants. Collectively, our results uncover a regulatory mechanism of host protein posttranslational modification and cellular pathways mediated by SARS-CoV-2, which may become antiviral drug targets against COVID-19.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2123065119
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2022
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    Restraint of angiogenesis by zinc finger transcription factor CTCF-dependent chromatin insulation
    Proceedings of the National Academy of Sciences ; 2011
    In:  Proceedings of the National Academy of Sciences Vol. 108, No. 37 ( 2011-09-13), p. 15231-15236
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 108, No. 37 ( 2011-09-13), p. 15231-15236
    Abstract: Angiogenesis is meticulously controlled by a fine balance between positive and negative regulatory activities. Vascular endothelial growth factor (VEGF) is a predominant angiogenic factor and its dosage is precisely regulated during normal vascular formation. In cancer, VEGF is commonly overproduced, resulting in abnormal neovascularization. VEGF is induced in response to various stimuli including hypoxia; however, very little is known about the mechanisms that confine its induction to ensure proper angiogenesis. Chromatin insulation is a key transcription mechanism that prevents promiscuous gene activation by interfering with the action of enhancers. Here we show that the chromatin insulator-binding factor CTCF binds to the proximal promoter of VEGF . Consistent with the enhancer-blocking mode of chromatin insulators, CTCF has little effect on basal expression of VEGF but specifically affects its activation by enhancers. CTCF knockdown cells are sensitized for induction of VEGF and exhibit elevated proangiogenic potential. Cancer-derived CTCF missense mutants are mostly defective in blocking enhancers at the VEGF locus. Moreover, during mouse retinal development, depletion of CTCF causes excess angiogenesis. Therefore, CTCF-mediated chromatin insulation acts as a crucial safeguard against hyperactivation of angiogenesis.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1104662108
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2011
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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