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  1. AU=Yoon Mee-Sup
  2. AU="Schmitt, L."
  3. AU="Clark, Roger"
  4. AU="Tütüncüoğlu, Atacan"
  5. AU=Onuigbo Macaulay Amechi Chukwukadibia
  6. AU="Ohanyerenwa, Chioma"
  7. AU=Kaur Kirandeep
  8. AU=Shrimal Shiteshu
  9. AU=Hamp Thomas
  10. AU="Fazila Aloweni"
  11. AU="Mitchel, Liz"
  12. AU="Aguirre González, Alejandra"
  13. AU="Abdelhak, Bensaid"

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  1. Artikel ; Online: Nanotechnology-Based Targeting of mTOR Signaling in Cancer.

    Yoon, Mee-Sup

    International journal of nanomedicine

    2020  Band 15, Seite(n) 5767–5781

    Abstract: Mammalian target of rapamycin (mTOR) is a master regulator of cell growth and metabolism, which is activated in response to intra- and extracellular signals, including nutrients, growth factors, and cellular energy levels. The frequent dysregulation of ... ...

    Abstract Mammalian target of rapamycin (mTOR) is a master regulator of cell growth and metabolism, which is activated in response to intra- and extracellular signals, including nutrients, growth factors, and cellular energy levels. The frequent dysregulation of mTOR signaling in cancer makes it an attractive therapeutic target, and several types of mTOR inhibitors have been developed. Nanoparticle-based mTOR modulators are predicted to target various cancers and deliver as well as release drugs in a controlled manner, resulting in enhanced bioavailability and reduced side effects. This mini-review is focused on the molecular mechanism of nanoparticle-based mTOR modulator action as well as the current development of mTOR inhibitors using nanoparticles. Understanding the biological function of nanoparticle-based mTOR modulators will contribute to the development of efficient nano-therapeutics for the treatment of cancers.
    Mesh-Begriff(e) Autophagy ; Humans ; Molecular Targeted Therapy ; Nanotechnology ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
    Chemische Substanzen TOR Serine-Threonine Kinases (EC 2.7.1.1)
    Sprache Englisch
    Erscheinungsdatum 2020-08-06
    Erscheinungsland New Zealand
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2364941-0
    ISSN 1178-2013 ; 1176-9114
    ISSN (online) 1178-2013
    ISSN 1176-9114
    DOI 10.2147/IJN.S254574
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Role of ARHGEF3 as a GEF and mTORC2 Regulator

    Sana Abdul Khaliq / Zobia Umair / Mee-Sup Yoon

    Frontiers in Cell and Developmental Biology, Vol

    2022  Band 9

    Abstract: Guanine nucleotide exchange factors (GEFs) activate GTPases by stimulating the release of guanosine diphosphate to permit the binding of guanosine triphosphate. ARHGEF3 or XPLN (exchange factor found in platelets, leukemic, and neuronal tissues) is a ... ...

    Abstract Guanine nucleotide exchange factors (GEFs) activate GTPases by stimulating the release of guanosine diphosphate to permit the binding of guanosine triphosphate. ARHGEF3 or XPLN (exchange factor found in platelets, leukemic, and neuronal tissues) is a selective guanine nucleotide exchange factor for Rho GTPases (RhoGEFs) that activates RhoA and RhoB but not RhoC, RhoG, Rac1, or Cdc42. ARHGEF3 contains the diffuse B-cell lymphoma homology and pleckstrin homology domains but lacks similarity with other known functional domains. ARHGEF3 also binds the mammalian target of rapamycin complex 2 (mTORC2) and subsequently inhibits mTORC2 and Akt. In vivo investigation has also indicated the communication between ARHGEF3 and autophagy-related muscle pathologies. Moreover, studies on genetic variation in ARHGEF3 and genome-wide association studies have predicted exciting novel roles of ARHGEF3 in controlling bone mineral density, platelet formation and differentiation, and Hirschsprung disease. In conclusion, we hypothesized that additional biochemical and functional studies are required to elucidate the detailed mechanism of ARHGEF3-related pathologies and therapeutics.
    Schlagwörter ARHGEF3 ; XPLN ; rho guanine nucleotide exchange factors ; mTORC2 ; Akt ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2022-01-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Author Correction: Age-dependent loss of Crls1 causes myopathy and skeletal muscle regeneration failure.

    Yoo, Youngbum / Yeon, MyeongHoon / Kim, Won-Kyung / Shin, Hyeon-Bin / Lee, Seung-Min / Yoon, Mee-Sup / Ro, Hyunju / Seo, Young-Kyo

    Experimental & molecular medicine

    2024  Band 56, Heft 4, Seite(n) 1031

    Sprache Englisch
    Erscheinungsdatum 2024-04-25
    Erscheinungsland United States
    Dokumenttyp Published Erratum
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-024-01238-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Role of ARHGEF3 as a GEF and mTORC2 Regulator.

    Khaliq, Sana Abdul / Umair, Zobia / Yoon, Mee-Sup

    Frontiers in cell and developmental biology

    2022  Band 9, Seite(n) 806258

    Abstract: Guanine nucleotide exchange factors (GEFs) activate GTPases by stimulating the release of guanosine diphosphate to permit the binding of guanosine triphosphate. ARHGEF3 or XPLN (exchange factor found in platelets, leukemic, and neuronal tissues) is a ... ...

    Abstract Guanine nucleotide exchange factors (GEFs) activate GTPases by stimulating the release of guanosine diphosphate to permit the binding of guanosine triphosphate. ARHGEF3 or XPLN (exchange factor found in platelets, leukemic, and neuronal tissues) is a selective guanine nucleotide exchange factor for Rho GTPases (RhoGEFs) that activates RhoA and RhoB but not RhoC, RhoG, Rac1, or Cdc42. ARHGEF3 contains the diffuse B-cell lymphoma homology and pleckstrin homology domains but lacks similarity with other known functional domains. ARHGEF3 also binds the mammalian target of rapamycin complex 2 (mTORC2) and subsequently inhibits mTORC2 and Akt.
    Sprache Englisch
    Erscheinungsdatum 2022-01-31
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.806258
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: mTOR as a Key Regulator in Maintaining Skeletal Muscle Mass.

    Yoon, Mee-Sup

    Frontiers in physiology

    2017  Band 8, Seite(n) 788

    Abstract: Maintenance of skeletal muscle mass is regulated by the balance between anabolic and catabolic processes. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase, and is known to play vital roles in protein synthesis. ... ...

    Abstract Maintenance of skeletal muscle mass is regulated by the balance between anabolic and catabolic processes. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase, and is known to play vital roles in protein synthesis. Recent findings have continued to refine our understanding of the function of mTOR in maintaining skeletal muscle mass. mTOR controls the anabolic and catabolic signaling of skeletal muscle mass, resulting in the modulation of muscle hypertrophy and muscle wastage. This review will highlight the fundamental role of mTOR in skeletal muscle growth by summarizing the phenotype of skeletal-specific mTOR deficiency. In addition, the evidence that mTOR is a dual regulator of anabolism and catabolism in skeletal muscle mass will be discussed. A full understanding of mTOR signaling in the maintenance of skeletal muscle mass could help to develop mTOR-targeted therapeutics to prevent muscle wasting.
    Sprache Englisch
    Erscheinungsdatum 2017-10-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2017.00788
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: The Role of Mammalian Target of Rapamycin (mTOR) in Insulin Signaling.

    Yoon, Mee-Sup

    Nutrients

    2017  Band 9, Heft 11

    Abstract: The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that controls a wide spectrum of cellular processes, including cell growth, differentiation, and metabolism. mTOR forms two distinct multiprotein complexes known as mTOR complex 1 ( ... ...

    Abstract The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that controls a wide spectrum of cellular processes, including cell growth, differentiation, and metabolism. mTOR forms two distinct multiprotein complexes known as mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2), which are characterized by the presence of raptor and rictor, respectively. mTOR controls insulin signaling by regulating several downstream components such as growth factor receptor-bound protein 10 (Grb10), insulin receptor substrate (IRS-1), F-box/WD repeat-containing protein 8 (Fbw8), and insulin like growth factor 1 receptor/insulin receptor (IGF-IR/IR). In addition, mTORC1 and mTORC2 regulate each other through a feedback loop to control cell growth. This review outlines the current understanding of mTOR regulation in insulin signaling in the context of whole body metabolism.
    Sprache Englisch
    Erscheinungsdatum 2017-10-27
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu9111176
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Premature Ovarian Insufficiency

    Seung Joo Chon / Zobia Umair / Mee-Sup Yoon

    Frontiers in Cell and Developmental Biology, Vol

    Past, Present, and Future

    2021  Band 9

    Abstract: Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by ... ...

    Abstract Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by amenorrhea with hypoestrogenic and hypergonadotropic conditions, in some cases, causing loss of fertility. Heterogeneity of POI is registered by genetic and non-genetic causes, such as autoimmunity, environmental toxins, and chemicals. The identification of possible causative genes and selection of candidate genes for POI confirmation remain to be elucidated in cases of idiopathic POI. This review discusses the current understanding and future prospects of heterogeneous POI. We focus on the genetic basis of POI and the recent studies on non-coding RNA in POI pathogenesis as well as on animal models of POI pathogenesis, which help unravel POI mechanisms and potential targets. Despite the latest discoveries, the crosstalk among gene regulatory networks and the possible therapies targeting the same needs to explore in near future.
    Schlagwörter premature ovarian insufficiency ; premature ovarian failure ; early menopause ; ovarian aging ; ovary ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2021-05-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: The Emerging Role of Branched-Chain Amino Acids in Insulin Resistance and Metabolism.

    Yoon, Mee-Sup

    Nutrients

    2016  Band 8, Heft 7

    Abstract: Insulin is required for maintenance of glucose homeostasis. Despite the importance of insulin sensitivity to metabolic health, the mechanisms that induce insulin resistance remain unclear. Branched-chain amino acids (BCAAs) belong to the essential amino ... ...

    Abstract Insulin is required for maintenance of glucose homeostasis. Despite the importance of insulin sensitivity to metabolic health, the mechanisms that induce insulin resistance remain unclear. Branched-chain amino acids (BCAAs) belong to the essential amino acids, which are both direct and indirect nutrient signals. Even though BCAAs have been reported to improve metabolic health, an increased BCAA plasma level is associated with a high risk of metabolic disorder and future insulin resistance, or type 2 diabetes mellitus (T2DM). The activation of mammalian target of rapamycin complex 1 (mTORC1) by BCAAs has been suggested to cause insulin resistance. In addition, defective BCAA oxidative metabolism might occur in obesity, leading to a further accumulation of BCAAs and toxic intermediates. This review provides the current understanding of the mechanism of BCAA-induced mTORC1 activation, as well as the effect of mTOR activation on metabolic health in terms of insulin sensitivity. Furthermore, the effects of impaired BCAA metabolism will be discussed in detail.
    Mesh-Begriff(e) Amino Acids, Branched-Chain/blood ; Amino Acids, Branched-Chain/metabolism ; Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/blood ; Disease Models, Animal ; Humans ; Insulin/blood ; Insulin Resistance ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes/genetics ; Multiprotein Complexes/metabolism ; Obesity/blood ; Risk Factors ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemische Substanzen Amino Acids, Branched-Chain ; Blood Glucose ; Insulin ; Multiprotein Complexes ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2016-07-01
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu8070405
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  9. Artikel ; Online: Age-dependent loss of Crls1 causes myopathy and skeletal muscle regeneration failure.

    Yoo, Youngbum / Yeon, MyeongHoon / Kim, Won-Kyung / Shin, Hyeon-Bin / Lee, Seung-Min / Yoon, Mee-Sup / Ro, Hyunju / Seo, Young-Kyo

    Experimental & molecular medicine

    2024  Band 56, Heft 4, Seite(n) 922–934

    Abstract: Skeletal muscle aging results in the gradual suppression of myogenesis, leading to muscle mass loss. However, the specific role of cardiolipin in myogenesis has not been determined. This study investigated the crucial role of mitochondrial cardiolipin ... ...

    Abstract Skeletal muscle aging results in the gradual suppression of myogenesis, leading to muscle mass loss. However, the specific role of cardiolipin in myogenesis has not been determined. This study investigated the crucial role of mitochondrial cardiolipin and cardiolipin synthase 1 (Crls1) in age-related muscle deterioration and myogenesis. Our findings demonstrated that cardiolipin and Crls1 are downregulated in aged skeletal muscle. Moreover, the knockdown of Crls1 in myoblasts reduced mitochondrial mass, activity, and OXPHOS complex IV expression and disrupted the structure of the mitochondrial cristae. AAV9-shCrls1-mediated downregulation of Crls1 impaired muscle regeneration in a mouse model of cardiotoxin (CTX)-induced muscle damage, whereas AAV9-mCrls1-mediated Crls1 overexpression improved regeneration. Overall, our results highlight that the age-dependent decrease in CRLS1 expression contributes to muscle loss by diminishing mitochondrial quality in skeletal muscle myoblasts. Hence, modulating CRLS1 expression is a promising therapeutic strategy for mitigating muscle deterioration associated with aging, suggesting potential avenues for developing interventions to improve overall muscle health and quality of life in elderly individuals.
    Mesh-Begriff(e) Animals ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Mice ; Regeneration ; Muscular Diseases/metabolism ; Muscular Diseases/etiology ; Muscular Diseases/pathology ; Muscular Diseases/genetics ; Aging/metabolism ; Muscle Development ; Mitochondria/metabolism ; Disease Models, Animal ; Humans ; Cardiolipins/metabolism ; Mitochondrial Proteins/metabolism ; Mitochondrial Proteins/genetics ; Male ; Myoblasts/metabolism
    Chemische Substanzen Cardiolipins ; Mitochondrial Proteins
    Sprache Englisch
    Erscheinungsdatum 2024-04-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-024-01199-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Premature Ovarian Insufficiency: Past, Present, and Future.

    Chon, Seung Joo / Umair, Zobia / Yoon, Mee-Sup

    Frontiers in cell and developmental biology

    2021  Band 9, Seite(n) 672890

    Abstract: Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by ... ...

    Abstract Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by amenorrhea with hypoestrogenic and hypergonadotropic conditions, in some cases, causing loss of fertility. Heterogeneity of POI is registered by genetic and non-genetic causes, such as autoimmunity, environmental toxins, and chemicals. The identification of possible causative genes and selection of candidate genes for POI confirmation remain to be elucidated in cases of idiopathic POI. This review discusses the current understanding and future prospects of heterogeneous POI. We focus on the genetic basis of POI and the recent studies on non-coding RNA in POI pathogenesis as well as on animal models of POI pathogenesis, which help unravel POI mechanisms and potential targets. Despite the latest discoveries, the crosstalk among gene regulatory networks and the possible therapies targeting the same needs to explore in near future.
    Sprache Englisch
    Erscheinungsdatum 2021-05-10
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.672890
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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