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  1. Article: The influence of mitochondrial-directed regulation of Wnt signaling on tumorigenesis.

    Delgado-Deida, Yaritza / Alula, Kibrom M / Theiss, Arianne L

    Gastroenterology report

    2020  Volume 8, Issue 3, Page(s) 215–223

    Abstract: Mitochondria are dynamic organelles that play a key role in integrating cellular signaling. Mitochondrial alterations are evident in all stages of tumorigenesis and targeting mitochondrial pathways has emerged as an anticancer therapeutic strategy. The ... ...

    Abstract Mitochondria are dynamic organelles that play a key role in integrating cellular signaling. Mitochondrial alterations are evident in all stages of tumorigenesis and targeting mitochondrial pathways has emerged as an anticancer therapeutic strategy. The Wnt-signaling pathway regulates many fundamental cellular functions such as proliferation, survival, migration, stem-cell maintenance, and mitochondrial metabolism and dynamics. Emerging evidence demonstrates that mitochondrial-induced regulation of Wnt signaling provides an additional mechanism to influence cell-fate decisions. Crosstalk between mitochondria and Wnt signaling presents a feedforward loop in which Wnt activation regulates mitochondrial function that, in turn, drives Wnt signaling. In this mini-review, we will discuss the recent evidence revealing the mitochondrial control of Wnt signaling and its implications for tumorigenesis and anticancer therapeutic targeting.
    Language English
    Publishing date 2020-06-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2710871-5
    ISSN 2052-0034
    ISSN 2052-0034
    DOI 10.1093/gastro/goaa025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Nuclear partitioning of Prohibitin 1 inhibits Wnt/β-catenin-dependent intestinal tumorigenesis.

    Alula, Kibrom M / Delgado-Deida, Yaritza / Jackson, Dakota N / Venuprasad, K / Theiss, Arianne L

    Oncogene

    2020  Volume 40, Issue 2, Page(s) 369–383

    Abstract: The Wnt/β-catenin signaling pathway is aberrantly activated in the majority of colorectal cancer cases due to somatic mutations in the adenomatous polyposis coli (APC) gene. Prohibitin 1 (PHB1) serves pleiotropic cellular functions with dynamic ... ...

    Abstract The Wnt/β-catenin signaling pathway is aberrantly activated in the majority of colorectal cancer cases due to somatic mutations in the adenomatous polyposis coli (APC) gene. Prohibitin 1 (PHB1) serves pleiotropic cellular functions with dynamic subcellular trafficking, facilitating signaling crosstalk between organelles. Nuclear-localized PHB1 is an important regulator of gene transcription. Using mice with inducible intestinal epithelial cell (IEC)-specific deletion of Phb1 (Phb1
    MeSH term(s) Animals ; Apoptosis ; Axin Protein/genetics ; Axin Protein/metabolism ; Carcinogenesis ; Cell Nucleus/metabolism ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intestinal Neoplasms/metabolism ; Intestinal Neoplasms/pathology ; Intestinal Neoplasms/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Prohibitins ; Repressor Proteins/physiology ; Tumor Cells, Cultured ; Wnt Proteins/antagonists & inhibitors ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; beta Catenin/antagonists & inhibitors ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances AXIN1 protein, human ; Axin Protein ; PHB protein, human ; Prohibitins ; Repressor Proteins ; Wnt Proteins ; beta Catenin
    Language English
    Publishing date 2020-11-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-020-01538-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2218: 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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  3. Article ; Online: Inner mitochondrial membrane protein Prohibitin 1 mediates Nix-induced, Parkin-independent mitophagy.

    Alula, Kibrom M / Delgado-Deida, Yaritza / Callahan, Rosemary / Till, Andreas / Underwood, Lucia / Thompson, Winston E / Souza, Rhonda F / Dassopoulos, Themistocles / Onyiah, Joseph / Venuprasad, K / Theiss, Arianne L

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 18

    Abstract: Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered ... ...

    Abstract Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered expression of the inner mitochondrial membrane (IMM) protein Prohibitin 1. The mechanisms whereby dysfunction occurring internally at the IMM and matrix activate events at the outer mitochondrial membrane (OMM) to induce mitophagy are not fully elucidated. Using the gastrointestinal epithelium as a model system highly susceptible to autophagy inhibition, we reveal a specific role of Prohibitin-induced mitophagy in maintaining intestinal homeostasis. We demonstrate that Prohibitin 1 induces mitophagy in response to increased mitochondrial reactive oxygen species (ROS) through binding to mitophagy receptor Nix/Bnip3L and independently of Parkin. Prohibitin 1 is required for ROS-induced Nix localization to mitochondria and maintaining homeostasis of epithelial cells highly susceptible to mitochondrial dysfunction.
    MeSH term(s) Mitochondrial Membranes/metabolism ; Mitophagy ; Prohibitins ; Reactive Oxygen Species/metabolism ; Mitochondria/metabolism ; Autophagy ; Membrane Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Mitochondrial Proteins/metabolism
    Chemical Substances Prohibitins ; Reactive Oxygen Species ; Membrane Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Mitochondrial Proteins
    Language English
    Publishing date 2023-01-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-26775-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The Synthetic Small Molecule FL3 Combats Intestinal Tumorigenesis via Axin1-Mediated Inhibition of Wnt/β-Catenin Signaling.

    Jackson, Dakota N / Alula, Kibrom M / Delgado-Deida, Yaritza / Tabti, Redouane / Turner, Kevin / Wang, Xuan / Venuprasad, K / Souza, Rhonda F / Désaubry, Laurent / Theiss, Arianne L

    Cancer research

    2020  Volume 80, Issue 17, Page(s) 3519–3529

    Abstract: Colorectal cancer exhibits aberrant activation of Wnt/β-catenin signaling. Many inhibitors of the Wnt/β-catenin pathway have been tested for Wnt-dependent cancers including colorectal cancer, but are unsuccessful due to severe adverse reactions. FL3 is a ...

    Abstract Colorectal cancer exhibits aberrant activation of Wnt/β-catenin signaling. Many inhibitors of the Wnt/β-catenin pathway have been tested for Wnt-dependent cancers including colorectal cancer, but are unsuccessful due to severe adverse reactions. FL3 is a synthetic derivative of natural products called flavaglines, which exhibit anti-inflammatory and cytoprotective properties in intestinal epithelial cells, but has not been previously tested in cell or preclinical models of intestinal tumorigenesis.
    MeSH term(s) Animals ; Axin Protein/metabolism ; Benzofurans/pharmacology ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Organoids/drug effects ; Repressor Proteins/metabolism ; Wnt Signaling Pathway/drug effects
    Chemical Substances (1R,3S,3aR,8bS)-3a-(4-Bromophenyl)-6,8-dimethoxy-3-phenyl-2,3,3a,8b-tetrahydro-1H-cyclopenta(b)benzofuran-1,8b-diol ; Axin Protein ; Benzofurans ; Repressor Proteins ; prohibitin
    Language English
    Publishing date 2020-07-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-20-0216
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: 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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