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  1. Article ; Online: Meeting report: BioMolViz workshops for developing assessments of biomolecular visual literacy.

    Procko, Kristen / Engelman, Shelly / Jakubowski, Henry / Beckham, Josh T / Dean, Diane M / Franzen, Margaret A / Novak, Walter R P / Roberts, Rebecca / Roca, Alberto I / Shor, Audrey C / Terrell, Cassidy R / Dries, Daniel R

    Biochemistry and molecular biology education : a bimonthly publication of the International Union of Biochemistry and Molecular Biology

    2020  Volume 49, Issue 2, Page(s) 278–286

    Abstract: While molecular visualization has been recognized as a threshold concept in biology education, the explicit assessment of students' visual literacy skills is rare. To facilitate the evaluation of this fundamental ability, a series of NSF-IUSE-sponsored ... ...

    Abstract While molecular visualization has been recognized as a threshold concept in biology education, the explicit assessment of students' visual literacy skills is rare. To facilitate the evaluation of this fundamental ability, a series of NSF-IUSE-sponsored workshops brought together a community of faculty engaged in creating instruments to assess students' biomolecular visualization skills. These efforts expanded our earlier work in which we created a rubric describing overarching themes, learning goals, and learning objectives that address student progress toward biomolecular visual literacy. Here, the BioMolViz Steering Committee (BioMolViz.org) documents the results of those workshops and uses social network analysis to examine the growth of a community of practice. We also share many of the lessons we learned as our workshops evolved, as they may be instructive to other members of the scientific community as they organize workshops of their own.
    MeSH term(s) Biochemistry/education ; Humans ; Learning ; Literacy ; Students
    Language English
    Publishing date 2020-09-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2039717-3
    ISSN 1539-3429 ; 1470-8175
    ISSN (online) 1539-3429
    ISSN 1470-8175
    DOI 10.1002/bmb.21440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sleep in children with cancer.

    Rosen, Gerald M / Shor, Audrey C / Geller, Thomas J

    Current opinion in pediatrics

    2008  Volume 20, Issue 6, Page(s) 676–681

    Abstract: Purpose of review: Advances in cancer treatment have improved the 5-year survival rate for childhood cancers to over 78%, resulting in a large population of pediatric cancer survivors. There is increasing recognition that sleep intersects with cancer ... ...

    Abstract Purpose of review: Advances in cancer treatment have improved the 5-year survival rate for childhood cancers to over 78%, resulting in a large population of pediatric cancer survivors. There is increasing recognition that sleep intersects with cancer through the circadian control of the cell cycle and that sleep problems are one of the 'effects' of cancer, its treatments, or both. Recognition of these intersections will facilitate new areas of treatment and the use of proven clinical interventions for sleep problems in cancer survivors.
    Recent findings: Discoveries in circadian biology have revealed that the biologic clocks, which control sleep/wake rhythms, are present in all cells and exert considerable control over the cell cycle. This has opened new opportunities for improving efficacy, decreasing toxicity, or both of cancer therapy through circadian timing of chemotherapy. Excessive daytime sleepiness has emerged as one of the most common, but often unrecognized, sleep symptoms in cancer survivors.
    Summary: Sleep complaints are especially common in survivors of childhood cancer who have sustained an injury to the hypothalamus or brainstem, have evidence of endocrine dysfunction, are obese, or have been treated with cranial radiation. If recognized and treated appropriately, sleep problems can be successfully managed.
    MeSH term(s) Brain Neoplasms/complications ; Central Nervous System Neoplasms/complications ; Child ; Chronobiology Disorders/etiology ; Chronobiology Disorders/therapy ; Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications ; Sleep Wake Disorders/etiology ; Sleep Wake Disorders/therapy
    Language English
    Publishing date 2008-10-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1049374-8
    ISSN 1531-698X ; 1040-8703
    ISSN (online) 1531-698X
    ISSN 1040-8703
    DOI 10.1097/mop.0b013e328312c7ad
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3049: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  3. Article ; Online: Histone deacetylase 5 represses the transcription of cyclin D3.

    Roy, Sangita / Shor, Audrey C / Bagui, Tapan K / Seto, Edward / Pledger, W Jackson

    Journal of cellular biochemistry

    2008  Volume 104, Issue 6, Page(s) 2143–2154

    Abstract: ... the cell cycle-regulatory protein cyclin D3. When overexpressed in Balb/c-3T3 cells or mouse embryo fibroblasts, HDAC5 substantially ...

    Abstract Histone deacetylases (HDACs) modulate the transcription of a subset of genes by various means. HDAC5 is a class II HDAC whose subcellular location is signal-dependent. At present, its known gene targets are few in number. Here we identify a new HDAC5 target: the gene encoding the cell cycle-regulatory protein cyclin D3. When overexpressed in Balb/c-3T3 cells or mouse embryo fibroblasts, HDAC5 substantially reduced the activity of the cyclin D3 promoter and the abundance of endogenous cyclin D3 protein. Conversely, conditions that blocked HDAC5 function increased cyclin D3 expression: treatment of cells with the class I/II HDAC inhibitor trichostatin A (TSA), depletion of HDAC5 from cells by RNA interference, and cytoplasmic sequestration of HDAC5 by co-expression of catalytically active calcium/calmodulin-dependent protein kinase. HDAC5 interacted with the cyclin D3 promoter in vivo, and the HDAC5-responsive element was within 118 base pairs upstream of the transcription start site. Mutation of the Sp1 site and the cyclic AMP response element within this region did not affect the responsiveness of the cyclin D3 promoter to HDAC5 or TSA.
    MeSH term(s) 3T3 Cells ; Animals ; Binding Sites ; Cyclin D3 ; Cyclins/genetics ; Histone Deacetylases/metabolism ; Hydroxamic Acids/pharmacology ; Mice ; Mice, Inbred BALB C ; Mutation/genetics ; Repressor Proteins/metabolism ; Response Elements/genetics ; Sp1 Transcription Factor/metabolism ; Transcription, Genetic/drug effects
    Chemical Substances Ccnd3 protein, mouse ; Cyclin D3 ; Cyclins ; Hydroxamic Acids ; Repressor Proteins ; Sp1 Transcription Factor ; trichostatin A (3X2S926L3Z) ; Hdac5 protein, mouse (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2008-08-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.21771
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1114: Show issues Location:
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  4. Article: Therapeutic potential of directed tyrosine kinase inhibitor therapy in sarcomas.

    Shor, Audrey C / Agresta, Samuel V / D'Amato, Gina Z / Sondak, Vernon K

    Cancer control : journal of the Moffitt Cancer Center

    2008  Volume 15, Issue 1, Page(s) 47–54

    Abstract: Background: Sarcomas are rare mesenchymally derived tumors for which there are limited treatment options. This paper discusses the current therapeutic potential of directed tyrosine kinase inhibitors (TKIs) in sarcoma.: Methods: The authors review ... ...

    Abstract Background: Sarcomas are rare mesenchymally derived tumors for which there are limited treatment options. This paper discusses the current therapeutic potential of directed tyrosine kinase inhibitors (TKIs) in sarcoma.
    Methods: The authors review antibody-based strategies and small molecular inhibitors of TKIs, with specific emphasis placed on the potential use of these targeted agents as therapeutic options for the treatment of sarcomas that are not gastrointestinal stromal tumors.
    Results: Many TKs have been shown to be mutated or overexpressed in human sarcoma tumors and cell lines and may serve as potential targets for promising new sarcoma therapies. Furthermore, the novel mechanism of targeting TKs may complement the antitumor activity of existing sarcoma treatment options.
    Conclusions: TKIs such as imatinib, sunitinib, and sorefanib are promising new therapeutic options for the management of patients with soft tissue sarcoma.
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Humans ; Protein Kinase Inhibitors/therapeutic use ; Protein-Tyrosine Kinases/drug effects ; Protein-Tyrosine Kinases/metabolism ; Sarcoma/drug therapy ; Sarcoma/enzymology
    Chemical Substances Antineoplastic Agents ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2008-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1328503-8
    ISSN 1526-2359 ; 1073-2748
    ISSN (online) 1526-2359
    ISSN 1073-2748
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4467: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Inhibition of p27Kip1 gene transcription by mitogens.

    Bagui, Tapan K / Cui, Dongming / Roy, Sangita / Mohapatra, Subhra / Shor, Audrey C / Ma, Le / Pledger, W Jackson

    Cell cycle (Georgetown, Tex.)

    2009  Volume 8, Issue 1, Page(s) 115–124

    Abstract: ... protein synthesis and histone deacetylase activity but not Akt or ERK activity. PDGF increased the expression of c ... Myc in the absence but not presence of a histone deacetylase inhibitor, and c-Myc inhibited p27(Kip1 ... promoter activity when ectopically expressed in fibroblasts. c-Myc targeted the same region of the p27(Kip1 ...

    Abstract How mitogens reduce the abundance of the cell cycle inhibitor p27(Kip1) is an important question, and regulation of p27(Kip1) translation and turnover has been described. Here we show that platelet-derived growth factor (PDGF) reduces the activity of the p27(Kip1) promoter and the abundance of the p27(Kip1) transcript in density-arrested mouse fibroblasts. Inhibition of p27(Kip1) gene expression by PDGF required protein synthesis and histone deacetylase activity but not Akt or ERK activity. PDGF increased the expression of c-Myc in the absence but not presence of a histone deacetylase inhibitor, and c-Myc inhibited p27(Kip1) promoter activity when ectopically expressed in fibroblasts. c-Myc targeted the same region of the p27(Kip1) promoter as did PDGF (deletion analysis) and interacted with this region in vivo (chromatin immunoprecipitation assay). Collectively, these findings suggest that c-Myc mediates the inhibitory effects of PDGF on the p27(Kip1) promoter. We also demonstrate reductions in p27(Kip1) mRNA abundance in primary splenocytes exposed to concanavalin A and in T cells exposed to interleukin-2 (IL-2). In contrast to PDGF in fibroblasts, IL-2 required Akt activity for maximal reductions in p27(Kip1) promoter activity and mRNA abundance in T cells. Thus, mitogens repress p27(Kip1) gene transcription in multiple systems and by multiple mechanisms.
    MeSH term(s) Animals ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/enzymology ; Gene Expression Regulation/drug effects ; Histone Deacetylases/metabolism ; Hydroxamic Acids/pharmacology ; Mice ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Mitogens/pharmacology ; NIH 3T3 Cells ; Phosphoinositide-3 Kinase Inhibitors ; Platelet-Derived Growth Factor/pharmacology ; Promoter Regions, Genetic/genetics ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Stability/drug effects ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/drug effects ; T-Lymphocytes/enzymology ; Transcription, Genetic/drug effects
    Chemical Substances Hydroxamic Acids ; Mitogens ; Phosphoinositide-3 Kinase Inhibitors ; Platelet-Derived Growth Factor ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-myc ; RNA, Messenger ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; trichostatin A (3X2S926L3Z) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2009-01-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.8.1.7527
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article: Dasatinib inhibits migration and invasion in diverse human sarcoma cell lines and induces apoptosis in bone sarcoma cells dependent on SRC kinase for survival.

    Shor, Audrey C / Keschman, Elizabeth A / Lee, Francis Y / Muro-Cacho, Carlos / Letson, G Douglas / Trent, Jonathan C / Pledger, W Jack / Jove, Richard

    Cancer research

    2007  Volume 67, Issue 6, Page(s) 2800–2808

    Abstract: Sarcomas are rare malignant mesenchymal tumors for which there are limited treatment options. One potential molecular target for sarcoma treatment is the Src tyrosine kinase. Dasatinib (BMS-354825), a small-molecule inhibitor of Src kinase activity, is a ...

    Abstract Sarcomas are rare malignant mesenchymal tumors for which there are limited treatment options. One potential molecular target for sarcoma treatment is the Src tyrosine kinase. Dasatinib (BMS-354825), a small-molecule inhibitor of Src kinase activity, is a promising cancer therapeutic agent with p.o. bioavailability. Dasatinib exhibits antitumor effects in cultured human cell lines derived from epithelial tumors, including prostate and lung carcinomas. However, the action of dasatinib in mesenchymally derived tumors has yet to be shown. Based on our previous findings of Src activation in human sarcomas, we evaluated the effects of dasatinib in 12 cultured human sarcoma cell lines derived from bone and soft tissue sarcomas. Dasatinib inhibited Src kinase activity at nanomolar concentrations in these sarcoma cell lines. Downstream components of Src signaling, including focal adhesion kinase and Crk-associated substrate (p130(CAS)), were also inhibited at similar concentrations. This inhibition of Src signaling was accompanied by blockade of cell migration and invasion. Moreover, apoptosis was induced in the osteosarcoma and Ewing's subset of bone sarcomas at nanomolar concentrations of dasatinib. Inhibition of Src protein expression by small interfering RNA also induced apoptosis, indicating that these bone sarcoma cell lines are dependent on Src activity for survival. These results show that dasatinib inhibits migration and invasion of diverse sarcoma cell types and selectively blocks the survival of bone sarcoma cells. Therefore, dasatinib may provide therapeutic benefit by preventing the growth and metastasis of sarcomas in patients.
    MeSH term(s) Apoptosis/drug effects ; Apoptosis/physiology ; Bone Neoplasms/drug therapy ; Bone Neoplasms/enzymology ; Bone Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Dasatinib ; Enzyme Activation ; Humans ; Neoplasm Invasiveness ; Osteosarcoma/drug therapy ; Osteosarcoma/enzymology ; Osteosarcoma/pathology ; Protein Kinase Inhibitors/pharmacology ; Pyrimidines/pharmacology ; Rhabdomyosarcoma/drug therapy ; Rhabdomyosarcoma/enzymology ; Rhabdomyosarcoma/pathology ; Sarcoma, Ewing/drug therapy ; Sarcoma, Ewing/enzymology ; Sarcoma, Ewing/pathology ; Signal Transduction/drug effects ; Thiazoles/pharmacology ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/metabolism
    Chemical Substances Protein Kinase Inhibitors ; Pyrimidines ; Thiazoles ; src-Family Kinases (EC 2.7.10.2) ; Dasatinib (RBZ1571X5H)
    Language English
    Publishing date 2007-03-15
    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-06-3469
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.135/5: Show issues Location:
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