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  • 1
    In: Cell Motility and the Cytoskeleton, Wiley, Vol. 64, No. 1 ( 2007-01), p. 19-48
    Type of Medium: Online Resource
    ISSN: 0886-1544 , 1097-0169
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 1473796-6
    detail.hit.zdb_id: 2536522-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2013
    In:  Cytoskeleton Vol. 70, No. 6 ( 2013-06), p. 328-348
    In: Cytoskeleton, Wiley, Vol. 70, No. 6 ( 2013-06), p. 328-348
    Abstract: Myosins comprise a highly conserved superfamily of eukaryotic actin‐dependent motor proteins implicated in a large repertoire of functions in both the cytoplasm and the nucleus. Class XVI myosin, MYO16, reveals expression in most somatic as well as meiotic cells with prominent localization in the nucleus, excepting the nucleolus; however, the role(s) of Myo16 in the nucleus remain unknown. In this report, we investigated Myo16 abundance during transit through the cell cycle. Immunolocalization, immunoblot, flow cytometric and quantitative RT‐PCR studies performed in Rat2 cells indicate that Myo16 mRNA and protein abundance are cell cycle regulated: in the unperturbed cell cycle, each rises to peak levels in late G 1 and thereon through S‐phase and each decays as cells enter M‐phase. Notably, RNA interference‐induced Myo16 depletion results in altered cell cycle distribution as well as in large‐scale cell death. In response to DNA replication stress (impaired replication fork progression as a consequence of DNA damage, lack of sufficient deoxynucleotides, or inhibition of DNA polymerases), Myo16 protein shows substantial loss. Attenuation of replication stress (aphidicolin or hydroxyurea) is followed by a recovery of Myo16 expression and resumption of S‐phase progression. Collectively, these observations suggest that Myo16 may play a regulatory role in cell cycle progression. © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 1949-3584 , 1949-3592
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 2536522-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 176, No. 4 ( 2006-02-15), p. 2122-2133
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 176, No. 4 ( 2006-02-15), p. 2122-2133
    Abstract: We investigated the role of B cell Ag presentation in homeostasis of the memory B cell compartment in a mouse model where a conditional allele for the β-chain of MHC class II (MHC-II) is deleted in the vast majority of all B cells by cd19 promoter-mediated expression of Cre recombinase (IA-B mice). Upon T cell-dependent immunization, a small number of MHC-II+ B cells in IA-B mice dramatically expanded and restored normal albeit delayed levels of germinal center (GC) B cells with an affinity-enhancing somatic mutation to Ag. IA-B mice also established normal levels of MHC-II+ memory B cells, which, however, subsequently lost MHC-II expression by ongoing deletion of the conditional iab allele without significant loss in their number. Furthermore, in vivo Ag restimulation of MHC-II− memory B cells of IA-B mice failed to cause differentiation into plasma cells (PCs), even in the presence of Ag-specific CD4+ T cells. In addition, both numbers and Ag-specific affinity of long-lived PCs during the late post-GC phase, as well as post-GC serum affinity maturation, were significantly reduced in IA-B mice. These results support a notion that MHC-II-dependent T cell help during post-GC phase is not absolutely required for the maintenance of memory B cell frequency but is important for their differentiation into PCs and for the establishment of the long-lived PC compartment.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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