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  • 1
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    Online Resource
    Expression of 11β-Hydroxylase (CYP11B1) and Aldosterone Synthase (CYP11B2) in the Human Fetal Adrenal
    Springer Science and Business Media LLC ; 1997
    In:  Journal of the Society for Gynecologic Investigation Vol. 4, No. 6 ( 1997-11), p. 305-309
    Details
    In: Journal of the Society for Gynecologic Investigation, Springer Science and Business Media LLC, Vol. 4, No. 6 ( 1997-11), p. 305-309
    Type of Medium: Online Resource
    ISSN: 1071-5576
    URL: Article
    DOI: 10.1177/107155769700400607
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1997
    detail.hit.zdb_id: 2266096-3
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  • 2
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    Developmental changes in steroidogenic enzymes in human postnatal adrenal cortex: immunohistochemical studies : Developmental changes in adrenal steroidogenesis
    Wiley ; 2000
    In:  Clinical Endocrinology Vol. 53, No. 6 ( 2000-12-19), p. 739-747
    Details
    In: Clinical Endocrinology, Wiley, Vol. 53, No. 6 ( 2000-12-19), p. 739-747
    Type of Medium: Online Resource
    ISSN: 0300-0664
    URL: Article
    DOI: 10.1046/j.1365-2265.2000.01144.x
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2000
    detail.hit.zdb_id: 2004597-9
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  • 3
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    Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cells
    Wiley ; 2008
    In:  Journal of Neuroscience Research Vol. 86, No. 1 ( 2008-01), p. 48-60
    Details
    In: Journal of Neuroscience Research, Wiley, Vol. 86, No. 1 ( 2008-01), p. 48-60
    Abstract: Emerging evidence suggests that neural stem cells and brain tumors regulate their proliferation via similar pathways. In a previous study, we demonstrated that maternal embryonic leucine zipper kinase (Melk) is highly expressed in murine neural stem cells and regulates their proliferation. Here we describe how MELK expression is correlated with pathologic grade of brain tumors, and its expression levels are significantly correlated with shorter survival, particularly in younger glioblastoma patients. In normal human astrocytes, MELK is only faintly expressed, and MELK knockdown does not significantly influence their growth, whereas Ras and Akt overexpressing astrocytes have up‐regulated MELK expression, and the effect of MELK knockdown is more prominent in these transformed astrocytes. In primary cultures from human glioblastoma and medulloblastoma, MELK knockdown by siRNA results in inhibition of the proliferation and survival of these tumors. Furthermore, we show that MELK siRNA dramatically inhibits proliferation and, to some extent, survival of stem cells isolated from glioblastoma in vitro. These results demonstrate a critical role for MELK in the proliferation of brain tumors, including their stem cells, and suggest that MELK may be a compelling molecular target for treatment of high‐grade brain tumors. © 2007 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    URL: Article
    DOI: 10.1002/jnr.v86:1
    DOI: 10.1002/jnr.21471
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 1474904-X
    SSG: 12
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  • 4
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    Maternal embryonic leucine zipper kinase (MELK) regulates multipotent neural progenitor proliferation
    Rockefeller University Press ; 2005
    In:  The Journal of Cell Biology Vol. 170, No. 3 ( 2005-08-01), p. 413-427
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 170, No. 3 ( 2005-08-01), p. 413-427
    Abstract: Maternal embryonic leucine zipper kinase (MELK) was previously identified in a screen for genes enriched in neural progenitors. Here, we demonstrate expression of MELK by progenitors in developing and adult brain and that MELK serves as a marker for self-renewing multipotent neural progenitors (MNPs) in cultures derived from the developing forebrain and in transgenic mice. Overexpression of MELK enhances (whereas knockdown diminishes) the ability to generate neurospheres from MNPs, indicating a function in self-renewal. MELK down-regulation disrupts the production of neurogenic MNP from glial fibrillary acidic protein (GFAP)–positive progenitors in vitro. MELK expression in MNP is cell cycle regulated and inhibition of MELK expression down-regulates the expression of B-myb, which is shown to also mediate MNP proliferation. These findings indicate that MELK is necessary for proliferation of embryonic and postnatal MNP and suggest that it regulates the transition from GFAP-expressing progenitors to rapid amplifying progenitors in the postnatal brain.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.200412115
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2005
    detail.hit.zdb_id: 1421310-2
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  • 5
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    The Hepatic Transcriptome of Young Suckling and Aging Intrauterine Growth Restricted Male Rats
    Wiley ; 2015
    In:  Journal of Cellular Biochemistry Vol. 116, No. 4 ( 2015-04), p. 566-579
    Details
    In: Journal of Cellular Biochemistry, Wiley, Vol. 116, No. 4 ( 2015-04), p. 566-579
    Abstract: Intrauterine growth restriction leads to the development of adult onset obesity/metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non‐alcoholic fatty liver disease/steatohepatitis. Continued postnatal growth restriction has been shown to ameliorate many of these sequelae. To further our understanding of the mechanism of how intrauterine and early postnatal growth affects adult health we have employed Affymetrix microarray‐based expression profiling to characterize hepatic gene expression of male offspring in a rat model of maternal nutrient restriction in early and late life. At day 21 of life (p21) combined intrauterine and postnatal calorie restriction treatment led to expression changes in circadian, metabolic, and insulin‐like growth factor genes as part of a larger transcriptional response that encompasses 144 genes. Independent and controlled experiments at p21 confirm the early life circadian, metabolic, and growth factor perturbations. In contrast to the p21 transcriptional response, at day 450 of life (d450) only seven genes, largely uncharacterized, were differentially expressed. This lack of a transcriptional response identifies non‐transcriptional mechanisms mediating the adult sequelae of intrauterine growth restriction. Independent experiments at d450 identify a circadian defect as well as validate expression changes to four of the genes identified by the microarray screen which have a novel association with growth restriction. Emerging from this rich dataset is a portrait of how the liver responds to growth restriction through circadian dysregulation, energy/substrate management, and growth factor modulation. J. Cell. Biochem. 9999: 1–15, 2015. © 2014 Wiley Periodicals, Inc. J. Cell. Biochem. 116: 566–579, 2015. © 2014 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0730-2312 , 1097-4644
    URL: Issue
    URL: Article
    DOI: 10.1002/jcb.v116.4
    DOI: 10.1002/jcb.25008
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 1479976-5
    SSG: 12
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  • 6
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    Abstract 313: Perinatal Growth Restriction Decreases Hepatic RNA Editing of Apolipoprotein B in Male Rat Offspring
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 35, No. suppl_1 ( 2015-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. suppl_1 ( 2015-05)
    Abstract: Introduction: Individuals born with intrauterine growth restriction develop cardiovascular disease. We employed hepatic microarray-based expression profiling of male rat offspring born to mothers subjected to combined intrauterine and postnatal calorie restriction (IPCR) as a discovery driven experiment to interrogate intrauterine growth restriction. These studies identified that the expression of Apobec1 and Apobec1 complementation factor (A1CF), genes known to edit apolipoprotein B (ApoB) mRNA through the epigenetic process of cytosine deamination, are decreased in IPCR. Editing of ApoB mRNA at position 666 changes the ribonucleotide base from a cytosine to a uracil (U) and controls the production of ApoB100 and ApoB48 lipoproteins. Hypothesis: IPCR decreases hepatic ApoB mRNA editing in male offspring through transcriptional regulation of Apobec1 and A1CF. Methods: Pyrosequencing designed to interrogate ApoB mRNA editing was used to quantify hepatic ApoB100 and ApoB48 transcripts in an experiment employing the male offspring (litters culled to 6 male offspring for each mother) from 4 control fed mothers and 4 mothers subjected to 50% calorie restriction from embryonic day 11 to postnatal day 21 (IPCR). RT-qPCR and western blotting were employed to quantify the hepatic expression of Apobec1 and A1CF. Serum ApoB100 and Apo48 were quantified by ELISA. Results: ApoB transcripts in the control fed offspring were edited, with a U base call of 55 ± 2% at position 666, whereas IPCR offspring possessed decreased editing with a U base call of 12 ± 1% (n=12 for each group; F=368; p 〈 0.0001). The RT-qPCR relative quotient (RQ) in the IPCR group was 0.2 ± 0.1 (F=107;p 〈 0.0001) and 0.4 ± 0.1 (F=25;p 〈 0.0001) for Apobec1 and A1CF, respectively (RQ=1 in the control fed offspring for both Apobec1 and A1CF). Relative to control, IPCR treatment significantly decreased hepatic Apobec1 and A1CF proteins by 45% ± 10 and 27 % ± 9.2 respectively. IPCR treatment increased serum ApoB100 by 1.5 fold ± 0.43 (p= 0.051) and significantly decreased ApoB48 by 0.8 fold ± 0.1 (n=6) compared to control. Conclusion: These data define a novel association of IPCR and ApoB editing through a nutritionally controlled epigenetic process working through transcriptional control of Apobec1 and A1CF.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.35.suppl_1.313
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1494427-3
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  • 7
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    Expression Profiling of Attenuated Mitochondrial Function Identifies Retrograde Signals in Drosophila
    Oxford University Press (OUP) ; 2012
    In:  G3 Genes|Genomes|Genetics Vol. 2, No. 8 ( 2012-08-01), p. 843-851
    Details
    In: G3 Genes|Genomes|Genetics, Oxford University Press (OUP), Vol. 2, No. 8 ( 2012-08-01), p. 843-851
    Abstract: Mitochondria are able to modulate cell state and fate during normal and pathophysiologic conditions through a nuclear-mediated mechanism collectively termed as a retrograde response. Our previous studies in Drosophila melanogaster have clearly established that progress through the cell cycle is precisely regulated by the intrinsic activity of the mitochondrion by specific signaling cascades mounted by the cell. As a means to further our understanding of how mitochondrial energy status affects nuclear control of basic cell decisions, we have employed Affymetrix microarray-based transcriptional profiling of Drosophila S2 cells knocked down for the gene encoding subunit Va of the complex IV of the mitochondrial electron transport chain. The profiling data identify transcriptional upregulation of glycolytic genes, and metabolic studies confirm this increase in glycolysis. The data provide a model of the shift of metabolism from a predominately oxidative state toward a predominately aerobic glycolytic state mediated through transcriptional control. The transcriptional changes alter many signaling systems, including p53, insulin, hypoxia-induced factor α, and conserved mitochondrial retrograde responses. This rich dataset provides many novel targets for further understanding the mechanism whereby the mitochondrion manages energy substrate disposition and directs cellular fate decisions.
    Type of Medium: Online Resource
    ISSN: 2160-1836
    URL: Article
    DOI: 10.1534/g3.112.002584
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
    detail.hit.zdb_id: 2629978-1
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  • 8
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    Genome biology and gynecology: the application of oligonucleotide microarrays to leiomyomata
    Elsevier BV ; 2003
    In:  Fertility and Sterility Vol. 80, No. 2 ( 2003-08), p. 277-278
    Details
    In: Fertility and Sterility, Elsevier BV, Vol. 80, No. 2 ( 2003-08), p. 277-278
    Type of Medium: Online Resource
    ISSN: 0015-0282
    URL: Article
    DOI: 10.1016/S0015-0282(03)00729-5
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2003
    detail.hit.zdb_id: 1500469-7
    SSG: 12
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  • 9
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    Gene Expression Profiling of Gliomas Strongly Predicts Survival
    American Association for Cancer Research (AACR) ; 2004
    In:  Cancer Research Vol. 64, No. 18 ( 2004-09-15), p. 6503-6510
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 64, No. 18 ( 2004-09-15), p. 6503-6510
    Abstract: In current clinical practice, histology-based grading of diffuse infiltrative gliomas is the best predictor of patient survival time. Yet histology provides little insight into the underlying biology of gliomas and is limited in its ability to identify and guide new molecularly targeted therapies. We have performed large-scale gene expression analysis using the Affymetrix HG U133 oligonucleotide arrays on 85 diffuse infiltrating gliomas of all histologic types to assess whether a gene expression-based, histology-independent classifier is predictive of survival and to determine whether gene expression signatures provide insight into the biology of gliomas. We found that gene expression-based grouping of tumors is a more powerful survival predictor than histologic grade or age. The poor prognosis samples could be grouped into three different poor prognosis groups, each with distinct molecular signatures. We further describe a list of 44 genes whose expression patterns reliably classify gliomas into previously unrecognized biological and prognostic groups: these genes are outstanding candidates for use in histology-independent classification of high-grade gliomas. The ability of the large scale and 44 gene set expression signatures to group tumors into strong survival groups was validated with an additional external and independent data set from another institution composed of 50 additional gliomas. This demonstrates that large-scale gene expression analysis and subset analysis of gliomas reveals unrecognized heterogeneity of tumors and is efficient at selecting prognosis-related gene expression differences which are able to be applied across institutions.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-04-0452
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2004
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Metabolic control of G1–S transition: cyclin E degradation by p53-induced activation of the ubiquitin–proteasome system
    Rockefeller University Press ; 2010
    In:  Journal of Cell Biology Vol. 188, No. 4 ( 2010-02-22), p. 473-479
    Details
    In: Journal of Cell Biology, Rockefeller University Press, Vol. 188, No. 4 ( 2010-02-22), p. 473-479
    Abstract: Cell cycle progression is precisely regulated by diverse extrinsic and intrinsic cellular factors. Previous genetic analysis in Drosophila melanogaster has shown that disruption of the mitochondrial electron transport chain activates a G1–S checkpoint as a result of a control of cyclin E by p53. This regulation does not involve activation of the p27 homologue dacapo in flies. We demonstrate that regulation of cyclin E is not at the level of transcription or translation. Rather, attenuated mitochondrial activity leads to transcriptional upregulation of the F-box protein archipelago, the Fbxw7 homologue in flies. We establish that archipelago and the proteasomal machinery contribute to degradation of cyclin E in response to mitochondrial dysfunction. Our work provides in vivo genetic evidence for p53-mediated integration of metabolic stress signals, which modulate the activity of the ubiquitin–proteasome system to degrade cyclin E protein and thereby impose cell cycle arrest.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.200912024
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2010
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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