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  1. Article ; Online: Distinct Signaling Pathways for Autophagy-Driven Cell Death and Survival in Adult Hippocampal Neural Stem Cells.

    Jeong, Seol-Hwa / An, Hyun-Kyu / Ha, Shinwon / Yu, Seong-Woon

    International journal of molecular sciences

    2023  Volume 24, Issue 9

    Abstract: Autophagy is a cellular catabolic process that degrades and recycles cellular materials. Autophagy is considered to be beneficial to the cell and organism by preventing the accumulation of toxic protein aggregates, removing damaged organelles, and ... ...

    Abstract Autophagy is a cellular catabolic process that degrades and recycles cellular materials. Autophagy is considered to be beneficial to the cell and organism by preventing the accumulation of toxic protein aggregates, removing damaged organelles, and providing bioenergetic substrates that are necessary for survival. However, autophagy can also cause cell death depending on cellular contexts. Yet, little is known about the signaling pathways that differentially regulate the opposite outcomes of autophagy. We have previously reported that insulin withdrawal (IW) or corticosterone (CORT) induces autophagic cell death (ACD) in adult hippocampal neural stem (HCN) cells. On the other hand, metabolic stresses caused by 2-deoxy-D-glucose (2DG) and glucose-low (GL) induce autophagy without death in HCN cells. Rather, we found that 2DG-induced autophagy was cytoprotective. By comparing IW and CORT conditions with 2DG treatment, we revealed that ERK and JNK are involved with 2DG-induced protective autophagy, whereas GSK-3β regulates death-inducing autophagy. These data suggest that cell death and survival-promoting autophagy undergo differential regulation with distinct signaling pathways in HCN cells.
    MeSH term(s) Apoptosis ; Glycogen Synthase Kinase 3 beta/metabolism ; Neural Stem Cells/metabolism ; Cell Death ; Signal Transduction ; Autophagy ; Insulin/metabolism ; Insulin, Regular, Human ; Hippocampus/metabolism
    Chemical Substances Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Insulin ; Insulin, Regular, Human
    Language English
    Publishing date 2023-05-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24098289
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Presenilin 2 N141I Mutation Induces Hyperimmunity by Immune Cell-specific Suppression of REV-ERBα without Altering Central Circadian Rhythm.

    Nam, Hyeri / Kim, Boil / Lee, Younghwan / Choe, Han Kyoung / Yu, Seong-Woon

    Experimental neurobiology

    2023  Volume 32, Issue 4, Page(s) 259–270

    Abstract: Circadian rhythm is a 24-hour cycle of behavioral and physiological changes. Disrupted sleep-wake patterns and circadian dysfunction are common in patients of Alzheimer Disease (AD) and are closely related with neuroinflammation. However, it is not well ... ...

    Abstract Circadian rhythm is a 24-hour cycle of behavioral and physiological changes. Disrupted sleep-wake patterns and circadian dysfunction are common in patients of Alzheimer Disease (AD) and are closely related with neuroinflammation. However, it is not well known how circadian rhythm of immune cells is altered during the progress of AD. Previously, we found presenilin 2 (
    Language English
    Publishing date 2023-09-26
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2639017-6
    ISSN 2093-8144 ; 1226-2560
    ISSN (online) 2093-8144
    ISSN 1226-2560
    DOI 10.5607/en23012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Autophagy as a decisive process for cell death.

    Jung, Seonghee / Jeong, Hyeonjeong / Yu, Seong-Woon

    Experimental & molecular medicine

    2020  Volume 52, Issue 6, Page(s) 921–930

    Abstract: Autophagy is an intracellular catabolic pathway in which cellular constituents are engulfed by autophagosomes and degraded upon autophagosome fusion with lysosomes. Autophagy serves as a major cytoprotective process by maintaining cellular homeostasis ... ...

    Abstract Autophagy is an intracellular catabolic pathway in which cellular constituents are engulfed by autophagosomes and degraded upon autophagosome fusion with lysosomes. Autophagy serves as a major cytoprotective process by maintaining cellular homeostasis and recycling cytoplasmic contents. However, emerging evidence suggests that autophagy is a primary mechanism of cell death (autophagic cell death, ACD) and implicates ACD in several aspects of mammalian physiology, including tumor suppression and psychological disorders. However, little is known about the physiological roles and molecular mechanisms of ACD. In this review, we document examples of ACD and discuss recent progress in our understanding of its molecular mechanisms.
    MeSH term(s) Animals ; Autophagosomes/metabolism ; Autophagy/physiology ; Cell Death/physiology ; Humans ; Lysosomes/metabolism
    Language English
    Publishing date 2020-06-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-020-0455-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4775: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Cx3cr1

    Lee, Younghwan / Lee, Ji-Won / Nam, Hyeri / Yu, Seong-Woon

    Molecular brain

    2020  Volume 13, Issue 1, Page(s) 88

    Abstract: Microglia are macrophages resident in the central nervous system. C-X3-C motif chemokine receptor 1 (CX3CR1) is a ... ...

    Abstract Microglia are macrophages resident in the central nervous system. C-X3-C motif chemokine receptor 1 (CX3CR1) is a G
    MeSH term(s) Animals ; Autophagy-Related Protein 7/metabolism ; CX3C Chemokine Receptor 1/metabolism ; Gene Deletion ; Integrases/metabolism ; Intestines/pathology ; Mice ; Tamoxifen/pharmacology ; Tissue Adhesions/genetics
    Chemical Substances Atg7 protein, mouse ; CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Tamoxifen (094ZI81Y45) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
    Language English
    Publishing date 2020-06-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2436057-0
    ISSN 1756-6606 ; 1756-6606
    ISSN (online) 1756-6606
    ISSN 1756-6606
    DOI 10.1186/s13041-020-00630-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Translocator protein 18 kDa (TSPO): old dogma, new mice, new structure, and new questions for neuroprotection.

    Kim, Eun-Jung / Yu, Seong-Woon

    Neural regeneration research

    2015  Volume 10, Issue 6, Page(s) 878–880

    Language English
    Publishing date 2015-06-25
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.158338
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interplay between autophagy and programmed cell death in mammalian neural stem cells.

    Chung, Kyung Min / Yu, Seong-Woon

    BMB reports

    2013  Volume 46, Issue 8, Page(s) 383–390

    Abstract: Mammalian neural stem cells (NSCs) are of particular interest because of their role in brain development and function. Recent findings suggest the intimate involvement of programmed cell death (PCD) in the turnover of NSCs. However, the underlying ... ...

    Abstract Mammalian neural stem cells (NSCs) are of particular interest because of their role in brain development and function. Recent findings suggest the intimate involvement of programmed cell death (PCD) in the turnover of NSCs. However, the underlying mechanisms of PCD are largely unknown. Although apoptosis is the best-defined form of PCD, accumulating evidence has revealed a wide spectrum of PCD encompassing apoptosis, autophagic cell death (ACD) and necrosis. This mini-review aims to illustrate a unique regulation of PCD in NSCs. The results of our recent studies on autophagic death of adult hippocampal neural stem (HCN) cells are also discussed. HCN cell death following insulin withdrawal clearly provides a reliable model that can be used to analyze the molecular mechanisms of ACD in the larger context of PCD. More research efforts are needed to increase our understanding of the molecular basis of NSC turnover under degenerating conditions, such as aging, stress and neurological diseases. Efforts aimed at protecting and harnessing endogenous NSCs will offer novel opportunities for the development of new therapeutic strategies for neuropathologies.
    MeSH term(s) Aging ; Animals ; Apoptosis ; Autophagy ; Hippocampus/cytology ; Humans ; Insulin/metabolism ; Necrosis ; Neural Stem Cells/cytology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurogenesis
    Chemical Substances Insulin
    Language English
    Publishing date 2013-08-27
    Publishing country Korea (South)
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2410389-5
    ISSN 1976-670X ; 1976-6696
    ISSN (online) 1976-670X
    ISSN 1976-6696
    DOI 10.5483/bmbrep.2013.46.8.164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4202: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: Systematic Analysis of Translocator Protein 18 kDa (TSPO) Ligands on Toll-like Receptors-mediated Pro-inflammatory Responses in Microglia and Astrocytes.

    Lee, Ji-Won / Nam, Hyeri / Yu, Seong-Woon

    Experimental neurobiology

    2016  Volume 25, Issue 5, Page(s) 262–268

    Abstract: Translocator protein 18 kDa (TSPO) is a mitochondrial protein highly expressed on reactive microglia and astrocytes, and is considered as a biomarker for neurodegeneration and brain damage, especially neuroinflammation. Toll-like receptors (TLRs) are ... ...

    Abstract Translocator protein 18 kDa (TSPO) is a mitochondrial protein highly expressed on reactive microglia and astrocytes, and is considered as a biomarker for neurodegeneration and brain damage, especially neuroinflammation. Toll-like receptors (TLRs) are closely related with inflammatory responses of microglia and astrocytes and these signaling pathways regulate neuroinflammation. Previous reports have identified the anti-inflammatory effects of TSPO ligands, however study of their effects in relation to the TLR signaling was limited. Here, we investigated the effects of five representative TSPO ligands on microglia and astrocytes following activation by various TLR ligands. Our results show that TSPO ligands reduce the pro-inflammatory response elicited by the TLR ligands with more profound effects on microglia than astrocytes.
    Language English
    Publishing date 2016-10-18
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2639017-6
    ISSN 2093-8144 ; 1226-2560
    ISSN (online) 2093-8144
    ISSN 1226-2560
    DOI 10.5607/en.2016.25.5.262
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  8. Article ; Online: Autophagy for the quality control of adult hippocampal neural stem cells.

    Hong, Caroline Jeeyeon / Park, Hyunhee / Yu, Seong-Woon

    Brain research

    2016  Volume 1649, Issue Pt B, Page(s) 166–172

    Abstract: Autophagy plays an important role in neurodegeneration, as well as in normal brain development and function. Recent studies have also implicated autophagy in the regulation of stemness and neurogenesis in neural stem cells (NSCs). However, little is ... ...

    Abstract Autophagy plays an important role in neurodegeneration, as well as in normal brain development and function. Recent studies have also implicated autophagy in the regulation of stemness and neurogenesis in neural stem cells (NSCs). However, little is known regarding the roles of autophagy in NSC biology. It has been shown that in addition to cytoprotective roles of autophagy, pro-death autophagy, or ׳autophagic cell death (ACD),' regulates the quantity of adult NSCs. A tight regulation of survival and death of NSCs residing in the neurogenic niches through programmed cell death (PCD) is critical for maintenance of adult neurogenesis. ACD plays a primary role in the death of adult hippocampal neural stem (HCN) cells following insulin withdrawal. Despite the normal apoptotic capability of HCN cells, they are committed to death by autophagy following insulin withdrawal, suggesting the existence of a unique regulatory program that controls the mode of cell death. We propose that dual roles of autophagy for maintenance of NSC pluripotency, as well as for elimination of defective NSCs, may serve as a combined NSC quality control mechanism. This article is part of a Special Issue entitled SI:Autophagy.
    MeSH term(s) Adult Stem Cells/physiology ; Animals ; Apoptosis ; Autophagy ; Hippocampus/metabolism ; Hippocampus/pathology ; Hippocampus/physiology ; Humans ; Insulin/metabolism ; Insulin/physiology ; Mice ; Necrosis ; Neural Stem Cells/metabolism ; Neural Stem Cells/pathology ; Neural Stem Cells/physiology ; Neurogenesis
    Chemical Substances Insulin
    Language English
    Publishing date 2016-10-15
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2016.02.048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 161: Show issues Location:
    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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  9. Article ; Online: Translocator protein (TSPO): the new story of the old protein in neuroinflammation.

    Lee, Younghwan / Park, Youngjin / Nam, Hyeri / Lee, Ji-Won / Yu, Seong-Woon

    BMB reports

    2019  Volume 53, Issue 1, Page(s) 20–27

    Abstract: Translocator protein (TSPO), also known as peripheral benzodiazepine receptor, is a transmembrane protein located on the outer mitochondria membrane (OMM) and mainly expressed in glial cells in the brain. Because of the close correlation of its ... ...

    Abstract Translocator protein (TSPO), also known as peripheral benzodiazepine receptor, is a transmembrane protein located on the outer mitochondria membrane (OMM) and mainly expressed in glial cells in the brain. Because of the close correlation of its expression level with neuropathology and therapeutic efficacies of several TSPO binding ligands under many neurological conditions, TSPO has been regarded as both biomarker and therapeutic target, and the biological functions of TSPO have been a major research focus. However, recent genetic studies with animal and cellular models revealed unexpected results contrary to the anticipated biological importance of TSPO and cast doubt on the action modes of the TSPO-binding drugs. In this review, we summarize recent controversial findings on the discrepancy between pharmacological and genetic studies of TSPO and suggest some future direction to understand this old and mysterious protein. [BMB Reports 2020; 53(1): 20-27].
    MeSH term(s) Animals ; Brain/immunology ; Brain/metabolism ; Brain/pathology ; Humans ; Inflammation/immunology ; Ligands ; Mice ; Mitochondria/metabolism ; Nervous System Diseases/diagnostic imaging ; Nervous System Diseases/metabolism ; Nervous System Diseases/therapy ; Neuroglia/immunology ; Neuroglia/metabolism ; Neurons/immunology ; Neurons/metabolism ; Receptors, GABA/chemistry ; Receptors, GABA/genetics ; Receptors, GABA/metabolism
    Chemical Substances Ligands ; Receptors, GABA ; TSPO protein, human
    Language English
    Publishing date 2019-12-09
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 2410389-5
    ISSN 1976-670X ; 1976-6696
    ISSN (online) 1976-670X
    ISSN 1976-6696
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4202: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  10. Article ; Online: Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERBα.

    Nam, Hyeri / Lee, Younghwan / Kim, Boil / Lee, Ji-Won / Hwang, Seohyeon / An, Hyun-Kyu / Chung, Kyung Min / Park, Youngjin / Hong, Jihyun / Kim, Kyungjin / Kim, Eun-Kyoung / Choe, Han Kyoung / Yu, Seong-Woon

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 1972

    Abstract: Hyperimmunity drives the development of Alzheimer disease (AD). The immune system is under the circadian control, and circadian abnormalities aggravate AD progress. Here, we investigate how an AD-linked mutation deregulates expression of circadian genes ... ...

    Abstract Hyperimmunity drives the development of Alzheimer disease (AD). The immune system is under the circadian control, and circadian abnormalities aggravate AD progress. Here, we investigate how an AD-linked mutation deregulates expression of circadian genes and induces cognitive decline using the knock-in (KI) mice heterozygous for presenilin 2 N141I mutation. This mutation causes selective overproduction of clock gene-controlled cytokines through the DNA hypermethylation-mediated repression of REV-ERBα in innate immune cells. The KI/+ mice are vulnerable to otherwise innocuous, mild immune challenges. The antipsychotic chlorpromazine restores the REV-ERBα level by normalizing DNA methylation through the inhibition of PI3K/AKT1 pathway, and prevents the overexcitation of innate immune cells and cognitive decline in KI/+ mice. These results highlight a pathogenic link between this AD mutation and immune cell overactivation through the epigenetic suppression of REV-ERBα.
    MeSH term(s) Animals ; Circadian Rhythm/physiology ; Epigenetic Repression ; Immunity ; Mice ; Mutation ; Nuclear Receptor Subfamily 1, Group D, Member 1/metabolism ; Presenilin-2/genetics
    Chemical Substances Nuclear Receptor Subfamily 1, Group D, Member 1 ; Presenilin-2 ; Psen2 protein, mouse
    Language English
    Publishing date 2022-04-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-29653-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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