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  1. Article ; Online: Poly(ADP-Ribose) Polymerase 1: Cellular Pluripotency, Reprogramming, and Tumorogenesis.

    Jiang, Bo-Hua / Tseng, Wei-Lien / Li, Hsin-Yang / Wang, Mong-Lien / Chang, Yuh-Lih / Sung, Yen-Jen / Chiou, Shih-Hwa

    International journal of molecular sciences

    2015  Volume 16, Issue 7, Page(s) 15531–15545

    Abstract: Poly(ADP-ribos)ylation (PARylation) is the catalytic function of the Poly(ADP-ribose) polymerases (Parps) family for post-translational modification in cellular process. Being a major member of Parps, Parp1 is a crucial nuclear factor with biological ... ...

    Abstract Poly(ADP-ribos)ylation (PARylation) is the catalytic function of the Poly(ADP-ribose) polymerases (Parps) family for post-translational modification in cellular process. Being a major member of Parps, Parp1 is a crucial nuclear factor with biological significance in modulating DNA repair, DNA replication, transcription, DNA methylation and chromatin remodeling through PARylation of downstream proteins. In addition, high expression level and activity of Parp1 are correlated with pluripotent status, reprogramming, and cancer. Furthermore, epigenetic modulation of Parp1 is explored for regulating wide variety of gene expression. Genetic and pharmaceutical disruption of Parp1 further confirmed the importance of Parp1 in cell growth, DNA repair, and reprogramming efficiency. Taken together, the proximity toward the understanding of the modulation of Parp1 including interaction and modification in different fields will provide new insight for future studies. In this review, the biological significance of Parp1 in transcription and the epigenetic modulation of Parp1 in pluripotent status, reprogramming process and cancer will be summarized.
    MeSH term(s) Carcinogenesis ; Cellular Reprogramming ; Chromatin Assembly and Disassembly ; DNA Methylation ; DNA Repair ; Humans ; Poly(ADP-ribose) Polymerases/chemistry ; Poly(ADP-ribose) Polymerases/genetics ; Poly(ADP-ribose) Polymerases/metabolism
    Chemical Substances Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
    Language English
    Publishing date 2015-07-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms160715531
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: CHD1L Regulated PARP1-Driven Pluripotency and Chromatin Remodeling During the Early-Stage Cell Reprogramming.

    Jiang, Bo-Hua / Chen, Wei-Yi / Li, Hsin-Yang / Chien, Yueh / Chang, Wei-Chao / Hsieh, Pei-Chen / Wu, Ping / Chen, Chieh-Yu / Song, Hui-Yung / Chien, Chian-Shiu / Sung, Yen-Jen / Chiou, Shih-Hwa

    Stem cells (Dayton, Ohio)

    2015  Volume 33, Issue 10, Page(s) 2961–2972

    Abstract: PARP1 and poly(ADP-ribosyl)ation (PARylation) have been shown to be essential for the initial steps of cellular reprogramming. However, the mechanism underlying PARP1/PARylation-regulated activation of pluripotency loci remains undetermined. Here, we ... ...

    Abstract PARP1 and poly(ADP-ribosyl)ation (PARylation) have been shown to be essential for the initial steps of cellular reprogramming. However, the mechanism underlying PARP1/PARylation-regulated activation of pluripotency loci remains undetermined. Here, we demonstrate that CHD1L, a DNA helicase, possesses chromatin remodeling activity and interacts with PARP1/PARylation in regulating pluripotency during reprogramming. We found that this interaction is mediated through the interplay of the CHD1L macro-domain and the PAR moiety of PARylated-PARP1. Chromatin immunoprecipitation assays demonstrated the co-occupancy of CHD1L and PARP1 at Pou5f1, Nanog, and Esrrb pluripotency loci. Knockdown of CHD1L significantly blocked the binding activity of PARP1 at pluripotency loci and inhibited the efficiency of PARP1-driven reprogramming. Notably, we found that CHD1L-promoted reprogramming requires both a PARP1-interacting domain and DNA helicase activity, partly contributing to the chromatin-remodeling states of pluripotency loci. Taken together, these results identify CHD1L as a key chromatin remodeler involved in PARP1/PARylation-regulated early-stage reprogramming and pluripotency in stem cells.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Cellular Reprogramming/genetics ; Chromatin Assembly and Disassembly/genetics ; DNA Helicases/biosynthesis ; DNA Helicases/genetics ; DNA-Binding Proteins/biosynthesis ; DNA-Binding Proteins/genetics ; Gene Knockdown Techniques ; Homeodomain Proteins/biosynthesis ; Mice ; Nanog Homeobox Protein ; Octamer Transcription Factor-3/biosynthesis ; Pluripotent Stem Cells ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases/biosynthesis ; Poly(ADP-ribose) Polymerases/genetics ; Receptors, Estrogen/biosynthesis
    Chemical Substances DNA-Binding Proteins ; Esrrb protein, mouse ; Homeodomain Proteins ; Nanog Homeobox Protein ; Nanog protein, mouse ; Octamer Transcription Factor-3 ; Pou5f1 protein, mouse ; Receptors, Estrogen ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; DNA Helicases (EC 3.6.4.-) ; Chd1l protein, mouse (EC 3.6.4.12)
    Language English
    Publishing date 2015-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1143556-2
    ISSN 1549-4918 ; 1066-5099
    ISSN (online) 1549-4918
    ISSN 1066-5099
    DOI 10.1002/stem.2116
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1894: 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: Targeting autophagy enhances BO-1051-induced apoptosis in human malignant glioma cells.

    Chu, Pei-Ming / Chen, Li-Hsin / Chen, Ming-Teh / Ma, Hsin-I / Su, Tsann-Long / Hsieh, Pei-Chen / Chien, Chian-Shiu / Jiang, Bo-Hua / Chen, Yu-Chih / Lin, Yi-Hui / Shih, Yang-Hsin / Tu, Pang-Hsien / Chiou, Shih-Hwa

    Cancer chemotherapy and pharmacology

    2012  Volume 69, Issue 3, Page(s) 621–633

    Abstract: Purpose: BO-1051 is an N-mustard derivative that is conjugated with DNA-affinic 9-anilinoacridine. Since BO-1051 was reported to have strong anticancer activity, we investigated the effect and underlying mechanism of BO-1051 in human glioma cell lines.!# ...

    Abstract Purpose: BO-1051 is an N-mustard derivative that is conjugated with DNA-affinic 9-anilinoacridine. Since BO-1051 was reported to have strong anticancer activity, we investigated the effect and underlying mechanism of BO-1051 in human glioma cell lines.
    Methods: Human glioma cell lines U251MG and U87MG were studied with BO-1051 or the combination of BO-1051 and autophagic inhibitors. Growth inhibition was assessed by MTT assay. Apoptosis was measured by annexin V staining followed by flow cytometry and immunoblotting for apoptosis-related molecules. Induction of autophagy was detected by acridine orange labeling, electron microscopy, LC3 localization and its conversion. Transfection of shRNA was used to determine the involvement of Beclin1 in apoptotic cell death.
    Results: MTT assay showed that BO-1051 suppressed the viability of four glioma cell lines (U251MG, U87MG, GBM-3 and DBTRG-05MG) in a dose-dependent manner. The IC(50) values of BO-1051 for the glioma cells were significantly lower than the values for primary neurons cultures and normal fibroblast cells. Moreover, BO-1051 not only induced apoptotic cell death, but also enhanced autophagic flux via inhibition of Akt/mTOR and activation of Erk1/2. Importantly, suppression of autophagy by 3-methyladenine or bafilomycin A1 significantly increased BO-1051-induced apoptotic cell death in U251MG and U87MG cells. In addition, the proportion of apoptotic cells after BO-1051 treatment was enhanced by co-treatment with shRNA against Beclin1.
    Conclusions: BO-1051 induced both apoptosis and autophagy, and inhibition of autophagy significantly augmented the cytotoxic effect of BO-1051. Thus, a combination of BO-1051 and autophagic inhibitors offers a potentially new therapeutic modality for the treatment of malignant glioma.
    MeSH term(s) Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Autophagy/drug effects ; Blotting, Western ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Culture Techniques ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Glioma/drug therapy ; Glioma/metabolism ; Glioma/pathology ; Humans ; MAP Kinase Signaling System/drug effects ; Membrane Potential, Mitochondrial/drug effects ; Microscopy, Electron, Transmission ; Microscopy, Fluorescence ; Microscopy, Phase-Contrast ; Molecular Structure ; Nitrogen Mustard Compounds/chemistry ; Nitrogen Mustard Compounds/pharmacology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; TOR Serine-Threonine Kinases/antagonists & inhibitors
    Chemical Substances Antineoplastic Agents ; BO-1051 ; Nitrogen Mustard Compounds ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2012-03
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 6820-2
    ISSN 1432-0843 ; 0344-5704 ; 0943-9404
    ISSN (online) 1432-0843
    ISSN 0344-5704 ; 0943-9404
    DOI 10.1007/s00280-011-1747-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1420: 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)

    Order via subito

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