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  1. Article ; Online: From white to brown fat through the PGC-1α-dependent myokine irisin: implications for diabetes and obesity.

    Castillo-Quan, Jorge Iván

    Disease models & mechanisms

    2012  Volume 5, Issue 3, Page(s) 293–295

    MeSH term(s) Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/pathology ; Fibronectins/metabolism ; Mice ; Models, Biological ; Obesity/metabolism ; Obesity/pathology ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Physical Conditioning, Animal ; Trans-Activators/metabolism ; Transcription Factors
    Chemical Substances FNDC5 protein, mouse ; Fibronectins ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, mouse ; Trans-Activators ; Transcription Factors
    Language English
    Publishing date 2012-05-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.009894
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Parkin' control: regulation of PGC-1α through PARIS in Parkinson's disease.

    Castillo-Quan, Jorge Iván

    Disease models & mechanisms

    2011  Volume 4, Issue 4, Page(s) 427–429

    MeSH term(s) Animals ; Humans ; Parkinson Disease/metabolism ; Repressor Proteins/metabolism ; Trans-Activators/metabolism
    Chemical Substances Repressor Proteins ; Trans-Activators
    Language English
    Publishing date 2011-06-27
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.008227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: An antisteatosis response regulated by oleic acid through lipid droplet-mediated ERAD enhancement.

    Castillo-Quan, Jorge Iván / Steinbaugh, Michael J / Fernández-Cárdenas, Laura Paulette / Pohl, Nancy K / Wu, Ziyun / Zhu, Feimei / Moroz, Natalie / Teixeira, Veronica / Bland, Monet S / Lehrbach, Nicolas J / Moronetti, Lorenza / Teufl, Magdalena / Blackwell, T Keith

    Science advances

    2023  Volume 9, Issue 1, Page(s) eadc8917

    Abstract: Although excessive lipid accumulation is a hallmark of obesity-related pathologies, some lipids are beneficial. Oleic acid (OA), the most abundant monounsaturated fatty acid (FA), promotes health and longevity. Here, we show that OA ... ...

    Abstract Although excessive lipid accumulation is a hallmark of obesity-related pathologies, some lipids are beneficial. Oleic acid (OA), the most abundant monounsaturated fatty acid (FA), promotes health and longevity. Here, we show that OA benefits
    Language English
    Publishing date 2023-01-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adc8917
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Metformin: Restraining Nucleocytoplasmic Shuttling to Fight Cancer and Aging

    Castillo-Quan, Jorge Iván / T. Keith Blackwell

    Cell. 2016 Dec. 15, v. 167

    2016  

    Abstract: In this issue of Cell, Wu et al. employed C. elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, ACAD10, is activated when metformin induces nuclear ... ...

    Abstract In this issue of Cell, Wu et al. employed C. elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, ACAD10, is activated when metformin induces nuclear exclusion of the GTPase RagC, thereby inhibiting mTORC1 through an unexpected mechanism.
    Keywords guanosinetriphosphatase ; humans ; longevity ; metformin ; transcription (genetics)
    Language English
    Dates of publication 2016-1215
    Size p. 1670-1671.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2016.11.058
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  5. Article: Mitochondrial dysfunction and defects in lipid homeostasis as therapeutic targets in neurodegeneration with brain iron accumulation.

    Kinghorn, Kerri J / Castillo-Quan, Jorge Iván

    Rare diseases (Austin, Tex.)

    2016  Volume 4, Issue 1, Page(s) e1128616

    Abstract: The PLA2G6 gene encodes a group VIA calcium independent phospholipase A2 (iPLA2β), which hydrolyses glycerophospholipids to release fatty acids and lysophospholipids. Mutations in PLA2G6 are associated with a number of neurodegenerative disorders ... ...

    Abstract The PLA2G6 gene encodes a group VIA calcium independent phospholipase A2 (iPLA2β), which hydrolyses glycerophospholipids to release fatty acids and lysophospholipids. Mutations in PLA2G6 are associated with a number of neurodegenerative disorders including neurodegeneration with brain iron accumulation (NBIA), infantile neuroaxonal dystrophy (INAD), and dystonia parkinsonism, collectively known as PLA2G6-associated neurodegeneration (PLAN). Recently Kinghorn et al. demonstrated in Drosophila and PLA2G6 mutant fibroblasts that loss of normal PLA2G6 activity is associated with mitochondrial dysfunction and mitochondrial lipid peroxidation. Furthermore, they were able to show the beneficial effects of deuterated polyunsaturated fatty acids (D-PUFAs), which reduce lipid peroxidation. D-PUFAs were able to rescue the locomotor deficits of flies lacking the fly ortholog of PLA2G6 (iPLA2-VIA), as well as the mitochondrial abnormalities in PLA2G6 mutant fibroblasts. This work demonstrated that the iPLA2-VIA knockout fly is a useful organism to dissect the mechanisms of pathogenesis of PLAN, and that further investigation is required to determine the therapeutic potential of D-PUFAs in patients with PLA2G6 mutations. The fruit fly has also been used to study some of the other genetic causes of NBIA, and here we also describe what is known about the mechanisms of pathogenesis of these NBIA variants. Mitochondrial dysfunction, defects in lipid metabolism, as well as defective Coenzyme A (CoA) biosynthesis, have all been implicated in some genetic forms of NBIA, including PANK2, CoASY, C12orf19 and FA2H.
    Language English
    Publishing date 2016-01-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2817861-0
    ISSN 2167-5511
    ISSN 2167-5511
    DOI 10.1080/21675511.2015.1128616
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: The emerging role of autophagic-lysosomal dysfunction in Gaucher disease and Parkinson's disease.

    Kinghorn, Kerri J / Asghari, Amir M / Castillo-Quan, Jorge Iván

    Neural regeneration research

    2017  Volume 12, Issue 3, Page(s) 380–384

    Abstract: Gaucher disease (GD), the commonest lysosomal storage disorder, results from the lack or functional deficiency of glucocerebrosidase (GCase) secondary to mutations in ... ...

    Abstract Gaucher disease (GD), the commonest lysosomal storage disorder, results from the lack or functional deficiency of glucocerebrosidase (GCase) secondary to mutations in the
    Language English
    Publishing date 2017-04-19
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.202934
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Untangling Longevity, Dauer, and Healthspan in Caenorhabditis elegans Insulin/IGF-1-Signalling.

    Ewald, Collin Yvès / Castillo-Quan, Jorge Iván / Blackwell, T Keith

    Gerontology

    2017  Volume 64, Issue 1, Page(s) 96–104

    Abstract: The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other ... ...

    Abstract The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other genes in this pathway can double lifespan. Subsequent work has revealed that reduced IIS (rIIS) extends lifespan across diverse species, possibly including humans. In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism. Considerable progress has been made uncovering mechanisms that are affected by C. elegans rIIS. However, from the beginning it has remained unclear to what extent rIIS extends C. elegans lifespan by mobilizing dauer-associated mechanisms in adults. As we discuss, recent work has shed light on this question by determining that rIIS can extend C. elegans lifespan comparably through downstream processes that are either dauer-related or -independent. Importantly, these two lifespan extension programs can be distinguished genetically. It will now be critical to tease apart these programs, because each may involve different longevity-promoting mechanisms that may be relevant to higher organisms. A recent analysis of organismal "healthspan" has questioned the value of C. elegans rIIS as a paradigm for understanding healthy aging, as opposed to simply extending life. We discuss other work that argues strongly that C. elegans rIIS is indeed an invaluable model and consider the likely possibility that dauer-related processes affect parameters associated with health under rIIS conditions. Together, these studies indicate that C. elegans and analyses of rIIS in this organism will continue to provide unexpected and exciting results, and new paradigms that will be valuable for understanding healthy aging in humans.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/physiology ; Diapause/genetics ; Diapause/physiology ; Insulin/genetics ; Insulin/physiology ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/physiology ; Longevity/genetics ; Longevity/physiology ; Models, Biological ; Mutation ; Receptor, Insulin/genetics ; Receptor, Insulin/physiology ; Signal Transduction
    Chemical Substances Caenorhabditis elegans Proteins ; Insulin ; Insulin-Like Growth Factor I (67763-96-6) ; DAF-2 protein, C elegans (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1)
    Language English
    Publishing date 2017-09-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000480504
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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.201: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article: Genetics and pharmacology of longevity: the road to therapeutics for healthy aging.

    Castillo-Quan, Jorge Iván / Kinghorn, Kerri J / Bjedov, Ivana

    Advances in genetics

    2015  Volume 90, Page(s) 1–101

    Abstract: Aging can be defined as the progressive decline in tissue and organismal function and the ability to respond to stress that occurs in association with homeostatic failure and the accumulation of molecular damage. Aging is the biggest risk factor for ... ...

    Abstract Aging can be defined as the progressive decline in tissue and organismal function and the ability to respond to stress that occurs in association with homeostatic failure and the accumulation of molecular damage. Aging is the biggest risk factor for human disease and results in a wide range of aging pathologies. Although we do not completely understand the underlying molecular basis that drives the aging process, we have gained exceptional insights into the plasticity of life span and healthspan from the use of model organisms such as the worm Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Single-gene mutations in key cellular pathways that regulate environmental sensing, and the response to stress, have been identified that prolong life span across evolution from yeast to mammals. These genetic manipulations also correlate with a delay in the onset of tissue and organismal dysfunction. While the molecular genetics of aging will remain a prosperous and attractive area of research in biogerontology, we are moving towards an era defined by the search for therapeutic drugs that promote healthy aging. Translational biogerontology will require incorporation of both therapeutic and pharmacological concepts. The use of model organisms will remain central to the quest for drug discovery, but as we uncover molecular processes regulated by repurposed drugs and polypharmacy, studies of pharmacodynamics and pharmacokinetics, drug-drug interactions, drug toxicity, and therapeutic index will slowly become more prevalent in aging research. As we move from genetics to pharmacology and therapeutics, studies will not only require demonstration of life span extension and an underlying molecular mechanism, but also the translational relevance for human health and disease prevention.
    MeSH term(s) Aging/drug effects ; Aging/genetics ; Animals ; Antioxidants/administration & dosage ; Humans ; Longevity/drug effects ; Models, Animal ; Population Forecast ; Quality of Life ; United Nations
    Chemical Substances Antioxidants
    Language English
    Publishing date 2015-07-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 148-x
    ISSN 0065-2660
    ISSN 0065-2660
    DOI 10.1016/bs.adgen.2015.06.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Se 836: Show issues Location:
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  9. Article ; Online: Metformin: Restraining Nucleocytoplasmic Shuttling to Fight Cancer and Aging.

    Castillo-Quan, Jorge Iván / Blackwell, T Keith

    Cell

    2015  Volume 167, Issue 7, Page(s) 1670–1671

    Abstract: In this issue of Cell, Wu et al. employed C. elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, ACAD10, is activated when metformin induces nuclear ... ...

    Abstract In this issue of Cell, Wu et al. employed C. elegans and human cell experiments to identify a pathway through which metformin increases lifespan and inhibits growth. A key transcriptional target, ACAD10, is activated when metformin induces nuclear exclusion of the GTPase RagC, thereby inhibiting mTORC1 through an unexpected mechanism.
    MeSH term(s) Active Transport, Cell Nucleus ; Aging/drug effects ; Animals ; Caenorhabditis elegans/drug effects ; Humans ; Metformin/pharmacology ; Neoplasms/drug therapy
    Chemical Substances Metformin (9100L32L2N)
    Language English
    Publishing date 2015-06-08
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2016.11.058
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
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  10. Article: Gerontología molecular: hacia un envejecimiento saludable.

    Castillo-Quan, Jorge Iván / Kinghorn, Kerri J

    Gaceta medica de Mexico

    2013  Volume 149, Issue 6, Page(s) 680–685

    Abstract: For many years aging research was confined to statistics, psychology, and socioeconomic aspects of old age. However, today the study of aging is one of the most attractive and prosperous fields in biology. This change followed on from observations that ... ...

    Title translation Molecular gerontology: towards healthy aging.
    Abstract For many years aging research was confined to statistics, psychology, and socioeconomic aspects of old age. However, today the study of aging is one of the most attractive and prosperous fields in biology. This change followed on from observations that single gene mutations can modulate the aging process, demonstrating the dynamic and plastic nature of the pathways involved. The field of aging is continually being fuelled by the discovery of new genes and pathways that extend lifespan when manipulated in organisms ranging from unicellular yeast to the more complex round worm C. elegans and the fruit fly Drosophila melanogaster. Such interventions have also been successful in mammals, proving the principle that discoveries in invertebrates can be evolutionarily relevant to humans. The most successful and evolutionary conserved interventions are those related to nutrient sensing pathways, the effector pathways upon which dietary restriction operates to promote health and longevity. To validate the existence of genes that modify the aging process in humans, biogerontologists have opted for a genome-wide approach to studying centenarians, those fortunate to live beyond 100 years of age. By studying these individuals, they hope to unravel the genetic signatures that promote healthy ageing and long life.
    MeSH term(s) Aging/genetics ; Geriatrics ; Humans ; Insulin/physiology ; Insulin-Like Growth Factor I/physiology
    Chemical Substances Insulin ; Insulin-Like Growth Factor I (67763-96-6)
    Language Spanish
    Publishing date 2013-11
    Publishing country Mexico
    Document type English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 425456-9
    ISSN 0016-3813
    ISSN 0016-3813
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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