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  1. Article ; Online: Rapid DNA Synthesis During Early

    Lesly, Shera / Bandura, Jennifer L / Calvi, Brian R

    Genetics

    2017  Volume 207, Issue 3, Page(s) 935–947

    Abstract: Problems with DNA replication cause cancer and developmental malformations. It is not fully understood how DNA replication is coordinated with development and perturbed in disease. We had previously identified ... ...

    Abstract Problems with DNA replication cause cancer and developmental malformations. It is not fully understood how DNA replication is coordinated with development and perturbed in disease. We had previously identified the
    MeSH term(s) Animals ; Chromosomal Instability ; DNA Replication ; Drosophila ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Embryonic Development/genetics ; Female ; Homozygote ; Male ; Maternal Inheritance ; Meiosis ; Mutation, Missense ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Ovary/metabolism
    Chemical Substances Drosophila Proteins ; Nuclear Proteins ; hd protein, Drosophila
    Language English
    Publishing date 2017-09-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2167-2
    ISSN 1943-2631 ; 0016-6731
    ISSN (online) 1943-2631
    ISSN 0016-6731
    DOI 10.1534/genetics.117.300318
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 767: Show issues Location:
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  2. Article ; Online: Yorkie and Scalloped: partners in growth activation.

    Bandura, Jennifer L / Edgar, Bruce A

    Developmental cell

    2008  Volume 14, Issue 3, Page(s) 315–316

    Abstract: The Hippo (Hpo) signaling pathway limits organ growth in organisms from Drosophila to mammals by suppressing the activity of the transcriptional coactivator Yorkie (Yki)/YAP. The TEAD/TEF factor Scalloped (Sd) has been identified as the first known ... ...

    Abstract The Hippo (Hpo) signaling pathway limits organ growth in organisms from Drosophila to mammals by suppressing the activity of the transcriptional coactivator Yorkie (Yki)/YAP. The TEAD/TEF factor Scalloped (Sd) has been identified as the first known transcription factor to partner with Yki as a downstream target of Hpo signaling.
    MeSH term(s) Animals ; Drosophila/growth & development ; Drosophila/physiology ; Drosophila Proteins/physiology ; Intracellular Signaling Peptides and Proteins/physiology ; Models, Biological ; Nuclear Proteins/physiology ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction ; Trans-Activators/physiology ; Transcription Factors/physiology
    Chemical Substances Drosophila Proteins ; Intracellular Signaling Peptides and Proteins ; Nuclear Proteins ; Trans-Activators ; Transcription Factors ; Yki protein, Drosophila ; sd protein, Drosophila ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; hpo protein, Drosophila (EC 2.7.11.1)
    Language English
    Publishing date 2008-02-28
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2008.02.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5742: Show issues Location:
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    Zs.MG 76: Show issues

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  3. Article ; Online: The molecular chaperone Hsp90 is required for cell cycle exit in Drosophila melanogaster.

    Bandura, Jennifer L / Jiang, Huaqi / Nickerson, Derek W / Edgar, Bruce A

    PLoS genetics

    2013  Volume 9, Issue 9, Page(s) e1003835

    Abstract: The coordination of cell proliferation and differentiation is crucial for proper development. In particular, robust mechanisms exist to ensure that cells permanently exit the cell cycle upon terminal differentiation, and these include restraining the ... ...

    Abstract The coordination of cell proliferation and differentiation is crucial for proper development. In particular, robust mechanisms exist to ensure that cells permanently exit the cell cycle upon terminal differentiation, and these include restraining the activities of both the E2F/DP transcription factor and Cyclin/Cdk kinases. However, the full complement of mechanisms necessary to restrain E2F/DP and Cyclin/Cdk activities in differentiating cells are not known. Here, we have performed a genetic screen in Drosophila melanogaster, designed to identify genes required for cell cycle exit. This screen utilized a PCNA-miniwhite(+) reporter that is highly E2F-responsive and results in a darker red eye color when crossed into genetic backgrounds that delay cell cycle exit. Mutation of Hsp83, the Drosophila homolog of mammalian Hsp90, results in increased E2F-dependent transcription and ectopic cell proliferation in pupal tissues at a time when neighboring wild-type cells are postmitotic. Further, these Hsp83 mutant cells have increased Cyclin/Cdk activity and accumulate proteins normally targeted for proteolysis by the anaphase-promoting complex/cyclosome (APC/C), suggesting that APC/C function is inhibited. Indeed, reducing the gene dosage of an inhibitor of Cdh1/Fzr, an activating subunit of the APC/C that is required for timely cell cycle exit, can genetically suppress the Hsp83 cell cycle exit phenotype. Based on these data, we propose that Cdh1/Fzr is a client protein of Hsp83. Our results reveal that Hsp83 plays a heretofore unappreciated role in promoting APC/C function during cell cycle exit and suggest a mechanism by which Hsp90 inhibition could promote genomic instability and carcinogenesis.
    MeSH term(s) Anaphase-Promoting Complex-Cyclosome/genetics ; Animals ; Cdh1 Proteins/genetics ; Cdh1 Proteins/metabolism ; Cell Cycle Checkpoints/genetics ; Cell Cycle Proteins/genetics ; Cell Differentiation/genetics ; Cell Proliferation ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster/genetics ; E2F Transcription Factors/genetics ; E2F Transcription Factors/metabolism ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Mitosis/genetics ; Transcription Factors ; Ubiquitin-Protein Ligase Complexes/genetics
    Chemical Substances Cdh1 Proteins ; Cell Cycle Proteins ; Drosophila Proteins ; E2F Transcription Factors ; E2f1 protein, Drosophila ; Heat-Shock Proteins ; Hsp83 protein, Drosophila ; Transcription Factors ; fzr protein, Drosophila ; Ubiquitin-Protein Ligase Complexes (EC 2.3.2.23) ; Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27)
    Language English
    Publishing date 2013-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1003835
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Duplication of the genome in normal and cancer cell cycles.

    Bandura, Jennifer L / Calvi, Brian R

    Cancer biology & therapy

    2002  Volume 1, Issue 1, Page(s) 8–13

    Abstract: It is critical to discover the mechanisms of normal cell cycle regulation if we are to fully understand what goes awry in cancer cells. The normal eukaryotic cell tightly regulates the activity of origins of DNA replication so that the genome is ... ...

    Abstract It is critical to discover the mechanisms of normal cell cycle regulation if we are to fully understand what goes awry in cancer cells. The normal eukaryotic cell tightly regulates the activity of origins of DNA replication so that the genome is duplicated exactly once per cell cycle. Over the last ten years much has been learned concerning the cell cycle regulation of origin activity. It is now clear that the proteins and cell cycle mechanisms that control origin activity are largely conserved from yeast to humans. Despite this conservation, the composition of origins of DNA replication in higher eukaryotes remains ill defined. A DNA consensus for predicting origins has yet to emerge, and it is of some debate whether primary DNA sequence determines where replication initiates. In this review we outline what is known about origin structure and the mechanism of once per cell cycle DNA replication with an emphasis on recent advances in mammalian cells. We discuss the possible relevance of these regulatory pathways for cancer biology and therapy.
    MeSH term(s) Animals ; Cell Cycle Proteins/physiology ; DNA Replication ; DNA, Fungal/biosynthesis ; DNA, Fungal/genetics ; DNA, Neoplasm/biosynthesis ; DNA, Neoplasm/genetics ; Eukaryotic Cells/cytology ; Eukaryotic Cells/metabolism ; Fungal Proteins/physiology ; Gene Duplication ; Genome ; Humans ; Insect Proteins/physiology ; Macromolecular Substances ; Mammals/genetics ; Models, Genetic ; Neoplasms/genetics ; Replication Origin ; S Phase/genetics ; Yeasts/genetics
    Chemical Substances Cell Cycle Proteins ; DNA, Fungal ; DNA, Neoplasm ; Fungal Proteins ; Insect Proteins ; Macromolecular Substances
    Language English
    Publishing date 2002-07-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2146305-0
    ISSN 1538-4047
    ISSN 1538-4047
    DOI 10.4161/cbt.1.1.31
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5887: Show issues Location:
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  5. Article: humpty dumpty is required for developmental DNA amplification and cell proliferation in Drosophila.

    Bandura, Jennifer L / Beall, Eileen L / Bell, Maren / Silver, Hannah R / Botchan, Michael R / Calvi, Brian R

    Current biology : CB

    2005  Volume 15, Issue 8, Page(s) 755–759

    Abstract: The full complement of proteins required for the proper regulation of genome duplication are yet to be described. We employ a genetic DNA-replication model system based on developmental amplification of Drosophila eggshell (chorion) genes [1]. ... ...

    Abstract The full complement of proteins required for the proper regulation of genome duplication are yet to be described. We employ a genetic DNA-replication model system based on developmental amplification of Drosophila eggshell (chorion) genes [1]. Hypomorphic mutations in essential DNA replication genes result in a distinct thin-eggshell phenotype owing to reduced amplification [2]. Here, we molecularly identify the gene, which we have named humpty dumpty (hd), corresponding to the thin-eggshell mutant fs(3)272-9 [3]. We confirm that hd is essential for DNA amplification in the ovary and show that it also is required for cell proliferation during development. Mosaic analysis of hd mutant cells during development and RNAi in Kc cells reveal that depletion of Hd protein results in severe defects in genomic replication and DNA damage. Most Hd protein is found in nuclear foci, and some may traverse the nuclear envelope. Consistent with a role in DNA replication, expression of Hd protein peaks during late G1 and S phase, and it responds to the E2F1/Dp transcription factor. Hd protein sequence is conserved from plants to humans, and published microarrays indicate that expression of its putative human ortholog also peaks at G1/S [4]. Our data suggest that hd defines a new gene family likely required for cell proliferation in all multicellular eukaryotes.
    MeSH term(s) Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Southern ; Brain/metabolism ; Cell Proliferation ; Cells, Cultured ; Chorion/cytology ; Cloning, Molecular ; DNA Primers ; DNA Replication/genetics ; Drosophila/genetics ; Drosophila/physiology ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Female ; Flow Cytometry ; Microscopy, Fluorescence ; Molecular Sequence Data ; Multigene Family/genetics ; Ovary/metabolism ; RNA Interference ; Sequence Alignment ; Sequence Analysis, DNA ; Transgenes/genetics
    Chemical Substances DNA Primers ; Drosophila Proteins
    Language English
    Publishing date 2005-04-26
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2005.02.063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3208: Show issues Location:
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  6. Article: A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells.

    Kwiatkowski, David J / Zhang, Hongbing / Bandura, Jennifer L / Heiberger, Kristina M / Glogauer, Michael / el-Hashemite, Nisreen / Onda, Hiroaki

    Human molecular genetics

    2002  Volume 11, Issue 5, Page(s) 525–534

    Abstract: Tuberous sclerosis (TSC) is a autosomal dominant genetic disorder caused by mutations in either TSC1 or TSC2, and characterized by benign hamartoma growth. We developed a murine model of Tsc1 disease by gene targeting. Tsc1 null embryos die at mid- ... ...

    Abstract Tuberous sclerosis (TSC) is a autosomal dominant genetic disorder caused by mutations in either TSC1 or TSC2, and characterized by benign hamartoma growth. We developed a murine model of Tsc1 disease by gene targeting. Tsc1 null embryos die at mid-gestation from a failure of liver development. Tsc1 heterozygotes develop kidney cystadenomas and liver hemangiomas at high frequency, but the incidence of kidney tumors is somewhat lower than in Tsc2 heterozygote mice. Liver hemangiomas were more common, more severe and caused higher mortality in female than in male Tsc1 heterozygotes. Tsc1 null embryo fibroblast lines have persistent phosphorylation of the p70S6K (S6K) and its substrate S6, that is sensitive to treatment with rapamycin, indicating constitutive activation of the mTOR-S6K pathway due to loss of the Tsc1 protein, hamartin. Hyperphosphorylation of S6 is also seen in kidney tumors in the heterozygote mice, suggesting that inhibition of this pathway may have benefit in control of TSC hamartomas.
    MeSH term(s) Animals ; Cells, Cultured ; Clone Cells ; Cystadenoma/genetics ; Cystadenoma/pathology ; Disease Models, Animal ; Female ; Genes, Tumor Suppressor ; Genotype ; Germ-Line Mutation ; Hemangioma/genetics ; Hemangioma/mortality ; Hemangioma/pathology ; Heterozygote ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/mortality ; Liver Neoplasms/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Phenotype ; Proteins/genetics ; Ribosomal Protein S6 Kinases/metabolism ; Sex Factors ; Stem Cells ; Survival Rate ; Tuberous Sclerosis Complex 1 Protein ; Tumor Suppressor Proteins ; Up-Regulation
    Chemical Substances Proteins ; Tsc1 protein, mouse ; Tuberous Sclerosis Complex 1 Protein ; Tumor Suppressor Proteins ; Ribosomal Protein S6 Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2002-03-01
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/11.5.525
    Database MEDical Literature Analysis and Retrieval System OnLINE

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