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  1. Article: Prenatal phenotype analysis and mutation identification of a fetus with meckel gruber syndrome.

    Moreno-Leon, Laura / Quezada-Ramirez, Marco A / Bilsbury, Evan / Kiss, Courtney / Guerin, Andrea / Khanna, Hemant

    Frontiers in genetics

    2022  Volume 13, Page(s) 982127

    Abstract: Ciliopathies are a class of inherited severe human disorders that occur due to defective formation or function of cilia. ... ...

    Abstract Ciliopathies are a class of inherited severe human disorders that occur due to defective formation or function of cilia. The
    Language English
    Publishing date 2022-08-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2022.982127
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Curcumin downregulates Smad pathways and reduces hepatic stellate cells activation in experimental fibrosis.

    Hernández-Aquino, Erika / Quezada-Ramírez, Marco A / Silva-Olivares, Angélica / Ramos-Tovar, Erika / Flores-Beltrán, Rosa E / Segovia, José / Shibayama, Mineko / Muriel, Pablo

    Annals of hepatology

    2020  Volume 19, Issue 5, Page(s) 497–506

    Abstract: Introduction and objectives: Curcumin, a polyphenol, is a natural compound that has been widely studied as a hepatoprotector; however, only a few studies have examined its ability to reduce fibrosis in previously established cirrhosis. The objective of ... ...

    Abstract Introduction and objectives: Curcumin, a polyphenol, is a natural compound that has been widely studied as a hepatoprotector; however, only a few studies have examined its ability to reduce fibrosis in previously established cirrhosis. The objective of this study was to investigate whether curcumin could reduce carbon tetrachloride (CCl
    Materials and methods: CCl
    Results and conclusions: Curcumin reduced liver damage, oxidative stress, fibrosis, and restored normal activity of MMP-9 and MMP-2. Besides, curcumin restored NF-κB, IL-1, IL-10, TGF-β, CTGF, Col-I, MMP-13, and Smad7 protein levels. On the other hand, curcumin decreased JNK and Smad3 phosphorylation. Furthermore, curcumin treatment decreased α-SMA and Smad3 protein and mRNA levels. Curcumin normalized GSH, and NF-κB, JNK-Smad3, and TGF-β-Smad3 pathways, leading to a decrement in activated hepatic stellate cells, thereby producing its antifibrotic effects.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Antioxidants/pharmacology ; Carbon Tetrachloride ; Cell Transdifferentiation/drug effects ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Chemical and Drug Induced Liver Injury/prevention & control ; Curcumin/pharmacology ; Cytokines/metabolism ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/ultrastructure ; Liver/drug effects ; Liver/metabolism ; Liver/ultrastructure ; Liver Cirrhosis, Experimental/chemically induced ; Liver Cirrhosis, Experimental/metabolism ; Liver Cirrhosis, Experimental/pathology ; Liver Cirrhosis, Experimental/prevention & control ; Male ; Oxidative Stress/drug effects ; Phosphorylation ; Protective Agents/pharmacology ; Rats, Wistar ; Signal Transduction ; Smad3 Protein/metabolism ; Smad7 Protein/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Antioxidants ; Cytokines ; Protective Agents ; Smad3 Protein ; Smad3 protein, rat ; Smad7 Protein ; Smad7 protein, rat ; Carbon Tetrachloride (CL2T97X0V0) ; Curcumin (IT942ZTH98)
    Language English
    Publishing date 2020-07-14
    Publishing country Mexico
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2188733-0
    ISSN 1665-2681
    ISSN 1665-2681
    DOI 10.1016/j.aohep.2020.05.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6221: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Naringenin attenuates the progression of liver fibrosis via inactivation of hepatic stellate cells and profibrogenic pathways.

    Hernández-Aquino, Erika / Quezada-Ramírez, Marco A / Silva-Olivares, Angélica / Casas-Grajales, Sael / Ramos-Tovar, Erika / Flores-Beltrán, Rosa E / Segovia, José / Shibayama, Mineko / Muriel, Pablo

    European journal of pharmacology

    2019  Volume 865, Page(s) 172730

    Abstract: There is no effective treatment for hepatic fibrosis. Previously, we demonstrated that naringenin possesses the ability to prevent experimental chronic liver damage. Therefore, the objective of this work was to investigate whether naringenin could ... ...

    Abstract There is no effective treatment for hepatic fibrosis. Previously, we demonstrated that naringenin possesses the ability to prevent experimental chronic liver damage. Therefore, the objective of this work was to investigate whether naringenin could reverse carbon tetrachloride (CCl
    MeSH term(s) Animals ; Biomarkers/metabolism ; Cell Differentiation/drug effects ; Collagen/metabolism ; Disease Progression ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Flavanones/pharmacology ; Flavanones/therapeutic use ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/pathology ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/pathology ; Male ; Proteolysis/drug effects ; Rats ; Rats, Wistar ; Signal Transduction/drug effects
    Chemical Substances Biomarkers ; Flavanones ; Collagen (9007-34-5) ; naringenin (HN5425SBF2)
    Language English
    Publishing date 2019-10-13
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2019.172730
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 522: 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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  4. Article ; Online: Annexin A1, Annexin A2, and Dyrk 1B are upregulated during GAS1-induced cell cycle arrest.

    Pérez-Sánchez, Gilberto / Jiménez, Adriana / Quezada-Ramírez, Marco A / Estudillo, Enrique / Ayala-Sarmiento, Alberto E / Mendoza-Hernández, Guillermo / Hernández-Soto, Justino / Hernández-Hernández, Fidel C / Cázares-Raga, Febe E / Segovia, Jose

    Journal of cellular physiology

    2017  Volume 233, Issue 5, Page(s) 4166–4182

    Abstract: GAS1 is a pleiotropic protein that has been investigated because of its ability to induce cell proliferation, cell arrest, and apoptosis, depending on the cellular or the physiological context in which it is expressed. At this point, we have information ... ...

    Abstract GAS1 is a pleiotropic protein that has been investigated because of its ability to induce cell proliferation, cell arrest, and apoptosis, depending on the cellular or the physiological context in which it is expressed. At this point, we have information about the molecular mechanisms by which GAS1 induces proliferation and apoptosis; but very few studies have been focused on elucidating the mechanisms by which GAS1 induces cell arrest. With the aim of expanding our knowledge on this subject, we first focused our research on finding proteins that were preferentially expressed in cells arrested by serum deprivation. By using a proteomics approach and mass spectrometry analysis, we identified 17 proteins in the 2-DE protein profile of serum deprived NIH3T3 cells. Among them, Annexin A1 (Anxa1), Annexin A2 (Anxa2), dual specificity tyrosine-phosphorylation-regulated kinase 1B (Dyrk1B), and Eukaryotic translation initiation factor 3, F (eIf3f) were upregulated at transcriptional the level in proliferative NIH3T3 cells. Moreover, we demonstrated that Anxa1, Anxa2, and Dyrk1b are upregulated at both the transcriptional and translational levels by the overexpression of GAS1. Thus, our results suggest that the upregulation of Anxa1, Anxa2, and Dyrk1b could be related to the ability of GAS1 to induce cell arrest and maintain cell viability. Finally, we provided further evidence showing that GAS1 through Dyrk 1B leads not only to the arrest of NIH3T3 cells but also maintains cell viability.
    MeSH term(s) Animals ; Annexin A1/genetics ; Annexin A2/genetics ; Apoptosis/genetics ; Cell Cycle Checkpoints/genetics ; Cell Cycle Proteins/genetics ; Cell Proliferation/genetics ; Eukaryotic Initiation Factor-3/genetics ; GPI-Linked Proteins/genetics ; Gene Expression Regulation/genetics ; Humans ; Mice ; NIH 3T3 Cells ; Protein Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/genetics ; Transcriptional Activation ; Dyrk Kinases
    Chemical Substances Annexin A1 ; Annexin A2 ; Cell Cycle Proteins ; Eukaryotic Initiation Factor-3 ; GPI-Linked Proteins ; Gas1 protein, mouse ; annexin A1, mouse ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017-12-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.26226
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.212: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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