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  1. Article: P2 receptors in macrophage fusion and osteoclast formation.

    Steinberg, Thomas H / Hiken, Jeffrey F

    Purinergic signalling

    2007  Volume 3, Issue 1-2, Page(s) 53–57

    Abstract: Cells of the mononuclear phagocyte lineage fuse to form multinucleated giant cells and osteoclasts. Several lines of evidence suggest that P2 receptors, in particular P2X₇, are involved in this process, although P2X₇ is not absolutely required for fusion ...

    Abstract Cells of the mononuclear phagocyte lineage fuse to form multinucleated giant cells and osteoclasts. Several lines of evidence suggest that P2 receptors, in particular P2X₇, are involved in this process, although P2X₇ is not absolutely required for fusion because P2X₇-null mice form multinucleated osteoclasts. Extracellular ATP may be an important regulator of macrophage fusion.
    Language English
    Publishing date 2007-02-06
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2172143-9
    ISSN 1573-9546 ; 1573-9538
    ISSN (online) 1573-9546
    ISSN 1573-9538
    DOI 10.1007/s11302-006-9036-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Discovering high-resolution patterns of differential DNA methylation that correlate with gene expression changes.

    Vanderkraats, Nathan D / Hiken, Jeffrey F / Decker, Keith F / Edwards, John R

    Nucleic acids research

    2013  Volume 41, Issue 14, Page(s) 6816–6827

    Abstract: Methylation of the CpG-rich region (CpG island) overlapping a gene's promoter is a generally accepted mechanism for silencing expression. While recent technological advances have enabled measurement of DNA methylation and expression changes genome-wide, ... ...

    Abstract Methylation of the CpG-rich region (CpG island) overlapping a gene's promoter is a generally accepted mechanism for silencing expression. While recent technological advances have enabled measurement of DNA methylation and expression changes genome-wide, only modest correlations between differential methylation at gene promoters and expression have been found. We hypothesize that stronger associations are not observed because existing analysis methods oversimplify their representation of the data and do not capture the diversity of existing methylation patterns. Recently, other patterns such as CpG island shore methylation and long partially hypomethylated domains have also been linked with gene silencing. Here, we detail a new approach for discovering differential methylation patterns associated with expression change using genome-wide high-resolution methylation data: we represent differential methylation as an interpolated curve, or signature, and then identify groups of genes with similarly shaped signatures and corresponding expression changes. Our technique uncovers a diverse set of patterns that are conserved across embryonic stem cell and cancer data sets. Overall, we find strong associations between these methylation patterns and expression. We further show that an extension of our method also outperforms other approaches by generating a longer list of genes with higher quality associations between differential methylation and expression.
    MeSH term(s) DNA Methylation ; Gene Expression Regulation ; Genomics/methods ; Humans ; Promoter Regions, Genetic ; Transcription Initiation Site
    Language English
    Publishing date 2013-06-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkt482
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1067: Show issues Location:
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  3. Article: ATP downregulates P2X7 and inhibits osteoclast formation in RAW cells.

    Hiken, Jeffrey F / Steinberg, Thomas H

    American journal of physiology. Cell physiology

    2004  Volume 287, Issue 2, Page(s) C403–12

    Abstract: Multinucleated giant cells derive from fusion of precursor cells of the macrophage lineage. It has been proposed that the purinoreceptor P2X(7) is involved in this fusion process. Prolonged exposure of macrophages to ATP, the ligand for P2X(7), induces ... ...

    Abstract Multinucleated giant cells derive from fusion of precursor cells of the macrophage lineage. It has been proposed that the purinoreceptor P2X(7) is involved in this fusion process. Prolonged exposure of macrophages to ATP, the ligand for P2X(7), induces the formation of plasma membrane pores and eventual cell death. We took advantage of this cytolytic property to select RAW 264.7 (RAW) cells that lacked P2X(7) function by maintaining them in ATP (RAW ATP-R cells). RAW ATP-R cells failed to fuse to form multinucleated osteoclasts in response to receptor activator nuclear factor-kappaB ligand, although they did become positive for the osteoclast marker enzyme tartrate-resistant acid phosphatase, and upregulated expression of other osteoclast marker genes. RAW ATP-R cells and wild-type RAW cells expressed similar amounts of P2X(7) protein, but little P2X(7) was present on the surface of RAW ATP-R cells. After ATP was removed from the medium of RAW ATP-R cells, the cells reexpressed P2X(7) on the cell surface, regained sensitivity to ATP, and formed multinucleated osteoclasts. These results suggest that P2X(7) or another protein that is downregulated in concert with P2X(7) is involved either in the mechanics of cell fusion to form osteoclasts or in a signaling pathway proximal to this event. These results also suggest that P2X(7) may be regulated by ligand-mediated internalization and that extracellular ATP may regulate the formation of osteoclasts and other multinucleated giant cells.
    MeSH term(s) Adenosine Diphosphate/pharmacology ; Adenosine Monophosphate/pharmacology ; Adenosine Triphosphate/pharmacology ; Animals ; Carrier Proteins/metabolism ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Line ; Extracellular Space/metabolism ; Fluorescent Antibody Technique ; Giant Cells/cytology ; Giant Cells/metabolism ; Macrophages/cytology ; Macrophages/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; NF-kappa B/metabolism ; Osteoclasts/cytology ; Osteoclasts/metabolism ; Platelet Aggregation Inhibitors/pharmacology ; Pyridoxal Phosphate/analogs & derivatives ; Pyridoxal Phosphate/pharmacology ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7 ; Up-Regulation
    Chemical Substances Carrier Proteins ; Membrane Glycoproteins ; NF-kappa B ; P2rx7 protein, mouse ; Platelet Aggregation Inhibitors ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; Receptors, Purinergic P2 ; Receptors, Purinergic P2X7 ; Tnfrsf11a protein, mouse ; Tnfsf11 protein, mouse ; pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (149017-66-3) ; Adenosine Monophosphate (415SHH325A) ; Pyridoxal Phosphate (5V5IOJ8338) ; Adenosine Diphosphate (61D2G4IYVH) ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2004-04-07
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00361.2003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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  4. Article ; Online: DNMT gene expression and methylome in Marek's disease resistant and susceptible chickens prior to and following infection by MDV.

    Tian, Fei / Zhan, Fei / VanderKraats, Nathan D / Hiken, Jeffrey F / Edwards, John R / Zhang, Huanmin / Zhao, Keji / Song, Jiuzhou

    Epigenetics

    2013  Volume 8, Issue 4, Page(s) 431–444

    Abstract: Marek's disease (MD) is characterized as a T cell lymphoma induced by a cell-associated α-herpesvirus, Marek's disease virus type 1 (MDV1). As with many viral infectious diseases, DNA methylation variations were observed in the progression of MD; these ... ...

    Abstract Marek's disease (MD) is characterized as a T cell lymphoma induced by a cell-associated α-herpesvirus, Marek's disease virus type 1 (MDV1). As with many viral infectious diseases, DNA methylation variations were observed in the progression of MD; these variations are thought to play an important role in host-virus interactions. We observed that DNA methyltransferase 3a (DNMT3a) and 3b (DNMT3b) were differentially expressed in chicken MD-resistant line 6 3 and MD-susceptible line 7 2 at 21 d after MDV infection. To better understand the role of methylation variation induced by MDV infection in both chicken lines, we mapped the genome-wide DNA methylation profiles in each line using Methyl-MAPS (methylation mapping analysis by paired-end sequencing). Collectively, the data sets collected in this study provide a more comprehensive picture of the chicken methylome. Overall, methylation levels were reduced in chickens from the resistant line 6 3 after MDV infection. We identified 11,512 infection-induced differential methylation regions (iDMRs). The number of iDMRs was larger in line 7 2 than in line 6 3, and most of iDMRs found in line 6 3 were overlapped with the iDMRs found in line 7 2. We further showed that in vitro methylation levels were associated with MDV replication, and found that MDV propagation in the infected cells was restricted by pharmacological inhibition of DNA methylation. Our results suggest that DNA methylation in the host may be associated with disease resistance or susceptibility. The methylation variations induced by viral infection may consequentially change the host transcriptome and result in diverse disease outcomes.
    MeSH term(s) Animals ; Azacitidine/pharmacology ; Cell Line ; Chick Embryo ; Chickens ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Methylation ; Disease Resistance ; Disease Susceptibility ; Herpesvirus 2, Gallid ; Marek Disease/genetics ; Marek Disease/metabolism ; Marek Disease/virology
    Chemical Substances DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Azacitidine (M801H13NRU)
    Language English
    Publishing date 2013-03-28
    Publishing country United States
    Document type Journal Article
    ISSN 1559-2308
    ISSN (online) 1559-2308
    DOI 10.4161/epi.24361
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The predominant mechanism of intercellular calcium wave propagation changes during long-term culture of human osteoblast-like cells.

    Henriksen, Zanne / Hiken, Jeffrey F / Steinberg, Thomas H / Jørgensen, Niklas R

    Cell calcium

    2006  Volume 39, Issue 5, Page(s) 435–444

    Abstract: Intercellular calcium waves (ICW) are calcium transients that spread from cell to cell in response to different stimuli. We previously demonstrated that human osteoblast-like cells in culture propagate ICW in response to mechanical stimulation by two ... ...

    Abstract Intercellular calcium waves (ICW) are calcium transients that spread from cell to cell in response to different stimuli. We previously demonstrated that human osteoblast-like cells in culture propagate ICW in response to mechanical stimulation by two mechanisms. One mechanism involves autocrine activation of P2Y receptors, and the other requires gap junctional communication. In the current work we ask whether long-term culture of osteoblast-like cells affects the propagation of ICW by these two mechanisms. Human osteoblast-like cells were isolated from bone marrow. Mechanically induced ICW were assessed by video imaging of Fura-2 loaded cells after 1, 2 and 4 months culture. The P2Y2 receptor and the gap junction protein Cx43 were assessed by Western blot and real-time PCR. In resting conditions, P2Y mediated ICW prevailed and spread rapidly to about 13 cells. P2Y receptor desensitization by ATP disclosed gap junction-mediated ICW which diffused more slowly and involved not more than five to six cells. After 2 months in culture, ICW appeared slower and wave propagation was much less inhibited by P2Y desensitization, suggesting an increase in gap junction-mediated ICW. After 4 months in culture cells still responded to addition of ATP, but P2Y desensitization did not inhibit ICW propagation. Our data indicate that the relative role of P2Y-mediated and gap junction-mediated ICW changes during osteoblast differentiation in vitro. In less differentiated cells, P2Y-mediated ICW predominate, but as cells differentiate in culture, gap-junction-mediated ICW become more prominent. These results suggest that P2Y receptor-mediated and gap junction-mediated mechanisms of intercellular calcium signaling may play different roles during differentiation of bone-forming cells.
    MeSH term(s) Adult ; Alkaline Phosphatase/metabolism ; Bone Marrow/metabolism ; Calcium/metabolism ; Calcium Signaling/physiology ; Cell Communication ; Cell Culture Techniques ; Cell Differentiation ; Cells, Cultured ; Connexin 43/metabolism ; Connexins/metabolism ; Culture Media ; Female ; Gap Junctions/metabolism ; Humans ; Male ; Osteoblasts/cytology ; Osteoblasts/metabolism ; RNA, Messenger/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2
    Chemical Substances Connexin 43 ; Connexins ; Culture Media ; P2RY2 protein, human ; RNA, Messenger ; Receptors, Purinergic P2 ; Receptors, Purinergic P2Y2 ; connexin 45 ; Alkaline Phosphatase (EC 3.1.3.1) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2006-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2006.01.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1596: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article: DNMT gene expression and methylome in Marek's disease resistant and susceptible chickens prior to and following infection by MDV

    Tian, Fei / Zhan, Fei / VanderKraats, Nathan D / Hiken, Jeffrey F / Edwards, John R / Zhang, Huanmin / Zhao, Keji / Song, Jiuzhou

    Epigenetics. 2013, v. 8, no. 4

    2013  

    Abstract: Marek's disease (MD) is characterized as a T cell lymphoma induced by a cell-associated α-herpesvirus, Marek's disease virus type 1 (MDV1). As with many viral infectious diseases, DNA methylation variations were observed in the progression of MD; these ... ...

    Abstract Marek's disease (MD) is characterized as a T cell lymphoma induced by a cell-associated α-herpesvirus, Marek's disease virus type 1 (MDV1). As with many viral infectious diseases, DNA methylation variations were observed in the progression of MD; these variations are thought to play an important role in host-virus interactions. We observed that DNA methyltransferase 3a (DNMT3a) and 3b (DNMT3b) were differentially expressed in chicken MD-resistant line 6 3 and MD-susceptible line 7 2 at 21 d after MDV infection. To better understand the role of methylation variation induced by MDV infection in both chicken lines, we mapped the genome-wide DNA methylation profiles in each line using Methyl-MAPS (methylation mapping analysis by paired-end sequencing). Collectively, the data sets collected in this study provide a more comprehensive picture of the chicken methylome. Overall, methylation levels were reduced in chickens from the resistant line 6 3 after MDV infection. We identified 11,512 infection-induced differential methylation regions (iDMRs). The number of iDMRs was larger in line 7 2 than in line 6 3, and most of iDMRs found in line 6 3 were overlapped with the iDMRs found in line 7 2. We further showed that in vitro methylation levels were associated with MDV replication, and found that MDV propagation in the infected cells was restricted by pharmacological inhibition of DNA methylation. Our results suggest that DNA methylation in the host may be associated with disease resistance or susceptibility. The methylation variations induced by viral infection may consequentially change the host transcriptome and result in diverse disease outcomes.
    Keywords DNA ; DNA fingerprinting ; DNA methylation ; Gallid herpesvirus 2 ; Marek disease ; T-lymphocytes ; chickens ; disease resistance ; gene expression ; hosts ; lymphoma ; sequence analysis ; transcriptome
    Language English
    Size p. 431-444.
    Document type Article
    ISSN 1559-2308
    DOI 10.4161/epi.24361
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts.

    Li, Shunqiang / Shen, Dong / Shao, Jieya / Crowder, Robert / Liu, Wenbin / Prat, Aleix / He, Xiaping / Liu, Shuying / Hoog, Jeremy / Lu, Charles / Ding, Li / Griffith, Obi L / Miller, Christopher / Larson, Dave / Fulton, Robert S / Harrison, Michelle / Mooney, Tom / McMichael, Joshua F / Luo, Jingqin /
    Tao, Yu / Goncalves, Rodrigo / Schlosberg, Christopher / Hiken, Jeffrey F / Saied, Laila / Sanchez, Cesar / Giuntoli, Therese / Bumb, Caroline / Cooper, Crystal / Kitchens, Robert T / Lin, Austin / Phommaly, Chanpheng / Davies, Sherri R / Zhang, Jin / Kavuri, Megha Shyam / McEachern, Donna / Dong, Yi Yu / Ma, Cynthia / Pluard, Timothy / Naughton, Michael / Bose, Ron / Suresh, Rama / McDowell, Reida / Michel, Loren / Aft, Rebecca / Gillanders, William / DeSchryver, Katherine / Wilson, Richard K / Wang, Shaomeng / Mills, Gordon B / Gonzalez-Angulo, Ana / Edwards, John R / Maher, Christopher / Perou, Charles M / Mardis, Elaine R / Ellis, Matthew J

    Cell reports

    2013  Volume 4, Issue 6, Page(s) 1116–1130

    Abstract: To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained ... ...

    Abstract To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Alleles ; Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Drug Resistance, Neoplasm ; Estradiol/pharmacology ; Estrogen Receptor alpha/genetics ; Female ; Gene Amplification ; Genomic Instability ; Heterografts ; Humans ; Mice ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Neoplasm Staging ; Phosphoproteins/genetics ; Point Mutation ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics ; Transcription Factors ; Translocation, Genetic
    Chemical Substances Adaptor Proteins, Signal Transducing ; ESR1 protein, human ; Estrogen Receptor alpha ; Neoplasm Proteins ; Phosphoproteins ; RNA, Neoplasm ; Transcription Factors ; YAP1 protein, human ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2013-09-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2013.08.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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