ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Stability of metal-rich very massive stars (2015)
    Oxford University Press
    Details
    Publication Date: 2015-12-18
    Description: We revisit the stability of very massive non-rotating main-sequence stars at solar metallicity, with the goal of understanding whether radial pulsations set a physical upper limit to stellar mass. Models of up to 938 solar masses are constructed with the mesa code, and their linear stability in the fundamental mode, assumed to be the most dangerous, is analysed with a fully non-adiabatic method. Models above 100 M have extended tenuous atmospheres (‘shelves’) that affect the stability of the fundamental. Even when positive, this growth rate is small, in agreement with previous results. We argue that small growth rates lead to saturation at small amplitudes that are not dangerous to the star. A mechanism for saturation is demonstrated involving non-linear parametric coupling to short-wavelength g-modes and the damping of the latter by radiative diffusion. The shelves are subject to much more rapidly growing strange modes. This also agrees with previous results but is extended here to higher masses. The strange modes probably saturate via shocks rather than mode coupling but have very small amplitudes in the core, where almost all of the stellar mass resides. Although our stellar models are hydrostatic, the structure of their outer parts suggests that optically thick winds, driven by some combination of radiation pressure, transonic convection, and strange modes, are more likely than pulsation in the fundamental mode to limit the main-sequence lifetime.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Role of the Polymerase {epsilon} sub-unit DPB2 in DNA replication, cell cycle regulation and DNA damage response in Arabidopsis (2016)
    Oxford University Press
    Details
    Publication Date: 2016-09-03
    Description: Faithful DNA replication maintains genome stability in dividing cells and from one generation to the next. This is particularly important in plants because the whole plant body and reproductive cells originate from meristematic cells that retain their proliferative capacity throughout the life cycle of the organism. DNA replication involves large sets of proteins whose activity is strictly regulated, and is tightly linked to the DNA damage response to detect and respond to replication errors or defects. Central to this interconnection is the replicative polymerase DNA Polymerase (Pol ) which participates in DNA replication per se , as well as replication stress response in animals and in yeast. Surprisingly, its function has to date been little explored in plants, and notably its relationship with DNA Damage Response (DDR) has not been investigated. Here, we have studied the role of the largest regulatory sub-unit of Arabidopsis DNA Pol : DPB2, using an over-expression strategy. We demonstrate that excess accumulation of the protein impairs DNA replication and causes endogenous DNA stress. Furthermore, we show that Pol dysfunction has contrasting outcomes in vegetative and reproductive cells and leads to the activation of distinct DDR pathways in the two cell types.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Rheumatoid arthritis-associated RBPJ polymorphism alters memory CD4+ T cells (2016)
    Oxford University Press
    Details
    Publication Date: 2016-01-09
    Description: Notch signaling has recently emerged as an important regulator of immune responses in autoimmune diseases. The recombination signal-binding protein for immunoglobulin kappa J region (RBPJ) is a transcriptional repressor, but converts into a transcriptional activator upon activation of the canonical Notch pathway. Genome-wide association studies of rheumatoid arthritis (RA) identified a susceptibility locus, rs874040 CC , which implicated the RBPJ gene. Here, chromatin state mapping generated using the chromHMM algorithm reveals strong enhancer regions containing DNase I hypersensitive sites overlapping the rs874040 linkage disequilibrium block in human memory, but not in naïve CD4 + T cells. The rs874040 overlapping this chromatin state was associated with increased RBPJ expression in stimulated memory CD4 + T cells from healthy subjects homozygous for the risk allele (CC) compared with memory CD4 + T cells bearing the protective allele (GG). Transcriptomic analysis of rs874040 CC memory T cells showed a repression of canonical Notch target genes IL (interleukin)-9, IL-17 and interferon (IFN) in the basal state. Interestingly, activation of the Notch pathway using soluble Notch ligand, Jagged2-Fc, induced IL-9 and IL-17A while delta-like 4Fc, another Notch ligand, induced higher IFN expression in the rs874040 CC memory CD4 + T cells compared with their rs874040 GG counterparts. In RA, RBPJ expression is elevated in memory T cells from RA patients compared with control subjects, and this was associated with induced inflammatory cytokines IL-9, IL-17A and IFN in response to Notch ligation in vitro . These findings demonstrate that the rs874040 CC allele skews memory T cells toward a pro-inflammatory phenotype involving Notch signaling, thus increasing the susceptibility to develop RA.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    eIF2{beta} is critical for eIF5-mediated GDP-dissociation inhibitor activity and translational control (2016)
    Oxford University Press
    Details
    Publication Date: 2016-12-01
    Description: In protein synthesis translation factor eIF2 binds initiator tRNA to ribosomes and facilitates start codon selection. eIF2 GDP/GTP status is regulated by eIF5 (GAP and GDI functions) and eIF2B (GEF and GDF activities), while eIF2α phosphorylation in response to diverse signals is a major point of translational control. Here we characterize a growth suppressor mutation in eIF2β that prevents eIF5 GDI and alters cellular responses to reduced eIF2B activity, including control of GCN4 translation. By monitoring the binding of fluorescent nucleotides and initiator tRNA to purified eIF2 we show that the eIF2β mutation does not affect intrinsic eIF2 affinities for these ligands, neither does it interfere with eIF2 binding to 43S pre-initiation complex components. Instead we show that the eIF2β mutation prevents eIF5 GDI stabilizing nucleotide binding to eIF2, thereby altering the off-rate of GDP from eIF2•GDP/eIF5 complexes. This enables cells to grow with reduced eIF2B GEF activity but impairs activation of GCN4 targets in response to amino acid starvation. These findings provide support for the importance of eIF5 GDI activity in vivo and demonstrate that eIF2β acts in concert with eIF5 to prevent premature release of GDP from eIF2 and thereby ensure tight control of protein synthesis initiation.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...