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  1. Article ; Online: Circadian transcriptome processing and analysis: a workflow for muscle stem cells.

    Sica, Valentina / Deryagin, Oleg / Smith, Jacob G / Muñoz-Canoves, Pura

    FEBS open bio

    2023  Volume 13, Issue 7, Page(s) 1228–1237

    Abstract: Circadian rhythms coordinate biological processes with Earth's 24-h daily light/dark cycle. In the last years, efforts in the field of chronobiology have sought to understand the ways in which the circadian clock controls transcription across tissues and ...

    Abstract Circadian rhythms coordinate biological processes with Earth's 24-h daily light/dark cycle. In the last years, efforts in the field of chronobiology have sought to understand the ways in which the circadian clock controls transcription across tissues and cells. This has been supported by the development of different bioinformatic approaches that allow the identification of 24-h oscillating transcripts. This workflow aims to describe how to isolate muscle stem cells for RNA sequencing analysis from a typical circadian experiment and introduces bioinformatic tools suitable for the analysis of circadian transcriptomes.
    MeSH term(s) Transcriptome/genetics ; Workflow ; Circadian Rhythm/genetics ; Satellite Cells, Skeletal Muscle ; Muscles
    Language English
    Publishing date 2023-05-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13629
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: A bidirectional crosstalk between autophagy and TP53 determines the pace of aging.

    Sica, Valentina / Kroemer, Guido

    Molecular & cellular oncology

    2020  Volume 7, Issue 5, Page(s) 1769434

    Abstract: When the orthologue of tumor suppressor protein p53 ( ...

    Abstract When the orthologue of tumor suppressor protein p53 (
    Language English
    Publishing date 2020-06-18
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2020.1769434
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Circadian transcriptome processing and analysis: a workflow for muscle stem cells

    Sica, Valentina / Deryagin, Oleg / Smith, Jacob G. / Muñoz‐Canoves, Pura

    FEBS Open Bio. 2023 July, v. 13, no. 7, p. 1228-1237

    2023  , Page(s) 1228–1237

    Abstract: Circadian rhythms coordinate biological processes with Earth's 24‐h daily light/dark cycle. In the last years, efforts in the field of chronobiology have sought to understand the ways in which the circadian clock controls transcription across tissues and ...

    Abstract Circadian rhythms coordinate biological processes with Earth's 24‐h daily light/dark cycle. In the last years, efforts in the field of chronobiology have sought to understand the ways in which the circadian clock controls transcription across tissues and cells. This has been supported by the development of different bioinformatic approaches that allow the identification of 24‐h oscillating transcripts. This workflow aims to describe how to isolate muscle stem cells for RNA sequencing analysis from a typical circadian experiment and introduces bioinformatic tools suitable for the analysis of circadian transcriptomes.
    Keywords RNA ; bioinformatics ; circadian clocks ; muscles ; transcriptome
    Language English
    Dates of publication 2023-07
    Size p. 1228-1237
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note JOURNAL ARTICLE
    ZDB-ID 2651702-4
    ISSN 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13629
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Running skeletal muscle clocks on time- the determining factors.

    Vaca-Dempere, Mireia / Kumar, Arun / Sica, Valentina / Muñoz-Cánoves, Pura

    Experimental cell research

    2022  Volume 413, Issue 1, Page(s) 112989

    Abstract: Circadian rhythms generate 24 h-long oscillations, which are key regulators of many aspects of behavior and physiology. Recent circadian transcriptome studies have discovered rhythmicity at the transcriptional level of hundreds of skeletal muscle genes, ... ...

    Abstract Circadian rhythms generate 24 h-long oscillations, which are key regulators of many aspects of behavior and physiology. Recent circadian transcriptome studies have discovered rhythmicity at the transcriptional level of hundreds of skeletal muscle genes, with roles in skeletal muscle growth, maintenance, and metabolic functions. These rhythms allow this tissue to perform molecular functions at the appropriate time of the day in order to anticipate environmental changes. However, while the last decade of research has characterized several aspects of the skeletal muscle molecular clock, many still are unexplored, including its functions, regulatory mechanisms, and interactions with other tissues. The central clock is believed to be located in the suprachiasmatic nucleus (SCN) of the brain hypothalamus, providing entrainment to peripheral organs through humoral and neuronal signals. However, these mechanisms of action are still unknown. Conversely, muscle tissue can be entrained through extrinsic, SCN-independent factors, such as feeding and physical activity. In this review, we provide an overview of the recent research about the extrinsic and intrinsic factors required for skeletal muscle clock regulation. Furthermore, we discuss the need for future studies to elucidate the mechanisms behind this regulation, which will in turn help dissect the role of circadian disruption at the onset of aging and diseases.
    Language English
    Publishing date 2022-01-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2021.112989
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 563: 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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  5. Article ; Online: IMMP2L: a mitochondrial protease suppressing cellular senescence.

    Sica, Valentina / Kroemer, Guido

    Cell research

    2018  Volume 28, Issue 6, Page(s) 607–608

    MeSH term(s) Cell Death ; Cellular Senescence ; Endopeptidases ; Mitochondria
    Chemical Substances Endopeptidases (EC 3.4.-)
    Language English
    Publishing date 2018-05-29
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-018-0051-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5283: 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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  6. Article ; Online: Author Correction: IMMP2L: a mitochondrial protease suppressing cellular senescence.

    Sica, Valentina / Kroemer, Guido

    Cell research

    2018  Volume 28, Issue 7, Page(s) 782

    Abstract: We apologize for an error we just found in the paper published online on 29 May 2018. The protein SERPINB4 is mistakenly indicated as SERPIN4B for three times in the main text and once in Fig. 1. The corrected sentences and Fig. 1 are provided below. ... ...

    Abstract We apologize for an error we just found in the paper published online on 29 May 2018. The protein SERPINB4 is mistakenly indicated as SERPIN4B for three times in the main text and once in Fig. 1. The corrected sentences and Fig. 1 are provided below.   This paragraph is the same with the one below. Is it redundant? The pdf file is correct.
    Language English
    Publishing date 2018-06-12
    Publishing country England
    Document type Journal Article ; Published Erratum
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-018-0059-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5283: 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: Quantification of intracellular ACBP/DBI levels.

    Sica, Valentina / Martins, Isabelle / Pietrocola, Federico / Bravo-San Pedro, José Manuel

    Methods in cell biology

    2021  Volume 165, Page(s) 111–122

    Abstract: Acyl-CoA binding protein (ACBP), also called diazepam-binding inhibitor (DBI), is a ubiquitous protein that can be secreted from cells by an unconventional pathway. Depending on its levels and on its subcellular localization, ACBP/DBI can regulate lipid ... ...

    Abstract Acyl-CoA binding protein (ACBP), also called diazepam-binding inhibitor (DBI), is a ubiquitous protein that can be secreted from cells by an unconventional pathway. Depending on its levels and on its subcellular localization, ACBP/DBI can regulate lipid metabolism. Several studies have shown that ACBP/DBI is secreted by an autophagy-dependent mechanism, positioning this catabolic pathway as the mechanism that controls lipid metabolism through the intracellular modulation of the levels of this protein. Autophagy is activated, among other stimuli, when cells have increased energy requirements; this causes a drop in the intracellular ACBP/DBI levels due to its release into the extracellular space and triggers an increase in the lipid catabolism. Conversely, when autophagy is inhibited, during pathological (obesity) or physiological (after-meal) situations, the intracellular levels of ACBP/DBI increase resulting in the activation of lipid anabolism, this effect has been demonstrated to be the link between obesity and autophagy inhibition. Here, we detail three different protocols for the detection of the ACBP/DBI levels by immunofluorescence, image flow cytometry or immunoblot techniques, which allow the quantification of ACBP/DBI levels and, indirectly, its autophagy-dependent release.
    MeSH term(s) Autophagy ; Diazepam Binding Inhibitor/metabolism ; Humans ; Lipid Metabolism ; Obesity
    Chemical Substances Diazepam Binding Inhibitor
    Language English
    Publishing date 2021-01-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2020.12.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Acyl-CoA-binding protein (ACBP): the elusive 'hunger factor' linking autophagy to food intake.

    Pedro, José Manuel Bravo-San / Sica, Valentina / Madeo, Frank / Kroemer, Guido

    Cell stress

    2019  Volume 3, Issue 10, Page(s) 312–318

    Abstract: The best-known appetite-regulating factors identified in rodents are leptin, an appetite inhibitor, and ghrelin, an appetite stimulator. Rare cases of loss-of-functions mutations affecting leptin and its receptor, as well as polymorphisms concerning ... ...

    Abstract The best-known appetite-regulating factors identified in rodents are leptin, an appetite inhibitor, and ghrelin, an appetite stimulator. Rare cases of loss-of-functions mutations affecting leptin and its receptor, as well as polymorphisms concerning ghrelin and its receptor, have been documented in human obesity, apparently validating the relevance of leptin and ghrelin for human physiology. Paradoxically, however, the overwhelming majority of obese individuals manifest high leptin and low ghrelin plasma levels, suggesting that both factors are not directly disease-relevant. We recently discovered that acyl-CoA-binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), acts as an efficient lipogenic and appetite stimulator in mice. Indeed, in response to starvation, ACBP/DBI is released from tissues in an autophagy-dependent fashion and increases in the plasma. Intravenous injection of ACBP/DBI stimulates feeding behavior through a reduction of circulating glucose levels, and consequent activation of orexigenic neurons in the hypothalamus. In contrast, neutralization of ACBP/DBI abolishes the hyperphagia observed after starvation of mice. Of note, ACBP/DBI is increased in the plasma of obese persons and mice, pointing to a convergence (rather than divergence) between its role in appetite stimulation and human obesity. Based on our results, we postulate a novel 'hunger reflex' in which starvation induces a surge in extracellular ACBP/DBI, which in turn stimulates feeding behavior. Thus, ACBP/DBI might be the elusive 'hunger factor' that explains increased food uptake in obesity.
    Language English
    Publishing date 2019-09-24
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 2523-0204
    ISSN (online) 2523-0204
    DOI 10.15698/cst2019.10.200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Pseudodiabetes-not a contraindication for metabolic interventions.

    Bravo-San Pedro, José Manuel / Sica, Valentina / Kroemer, Guido

    Cell death & disease

    2019  Volume 10, Issue 10, Page(s) 765

    Abstract: Type-2 diabetes is characterized by glycosuria, hyperglycemia, glucose intolerance, hyperinsulinemia, and insulin resistance. One or several among these alterations are also found after starvation, ketogenic diet, and pharmacological treatment with ... ...

    Abstract Type-2 diabetes is characterized by glycosuria, hyperglycemia, glucose intolerance, hyperinsulinemia, and insulin resistance. One or several among these alterations are also found after starvation, ketogenic diet, and pharmacological treatment with rapamycin or antibody-mediated neutralization of the obesogenic factor ACBP/DBI. Thus, a variety of metabolic interventions that improve metabolic health can induce a transient state of "pseudo-diabetes".
    MeSH term(s) Animals ; Autophagy/physiology ; Caloric Restriction/adverse effects ; Diabetes Mellitus, Type 2/diet therapy ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/therapy ; Glucose Intolerance/complications ; Glycosuria/complications ; Humans ; Hyperglycemia/complications ; Hyperinsulinism/complications ; Insulin Resistance ; Obesity/metabolism
    Language English
    Publishing date 2019-10-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-019-2007-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: The elusive "hunger protein": an appetite-stimulatory factor that is overabundant in human obesity.

    Bravo-San Pedro, José Manuel / Sica, Valentina / Kroemer, Guido

    Molecular & cellular oncology

    2019  Volume 6, Issue 6, Page(s) e1667193

    Abstract: Paradoxically, most if not all previously known appetite-stimulatory hormones are downregulated in human obesity, reflecting failing homeostatic circuitries. Recently, we discovered that acyl-coenzyme-A binding protein/diazepam-binding inhibitor (ACBP/ ... ...

    Abstract Paradoxically, most if not all previously known appetite-stimulatory hormones are downregulated in human obesity, reflecting failing homeostatic circuitries. Recently, we discovered that acyl-coenzyme-A binding protein/diazepam-binding inhibitor (ACBP/DBI) acts as a lipogenic and appetite stimulator, when systemically injected into mice. ACBP/DBI plasma levels are also elevated in obese subjects, supporting the notion that it may represent the elusive "hunger protein" that explains overeating in human obesity.
    Language English
    Publishing date 2019-10-15
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2019.1667193
    Database MEDical Literature Analysis and Retrieval System OnLINE

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