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
    Transcriptomic Analysis of Octanoic Acid Response in Drosophila sechellia Using RNA-Sequencing (2017)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2017-12-05
    Description: The dietary specialist fruit fly Drosophila sechellia has evolved to specialize on the toxic fruit of its host plant Morinda citrifolia . Toxicity of Morinda fruit is primarily due to high levels of octanoic acid (OA). Using RNA interference (RNAi), prior work found that knockdown of Osiris family genes Osiris 6 ( Osi6 ), Osi7 , and Osi8 led to increased susceptibility to OA in adult D. melanogaster flies, likely representing genes underlying a Quantitative Trait Locus (QTL) for OA resistance in D. sechellia . While genes in this major effect locus are beginning to be revealed, prior work has shown at least five regions of the genome contribute to OA resistance. Here, we identify new candidate OA resistance genes by performing differential gene expression analysis using RNA-sequencing (RNA-seq) on control and OA-exposed D. sechellia flies. We found 104 significantly differentially expressed genes with annotated orthologs in D. melanogaster , including six Osiris gene family members, consistent with previous functional studies and gene expression analyses. Gene ontology (GO) term enrichment showed significant enrichment for cuticle development in upregulated genes and significant enrichment of immune and defense responses in downregulated genes, suggesting important aspects of the physiology of D. sechellia that may play a role in OA resistance. In addition, we identified five candidate OA resistance genes that potentially underlie QTL peaks outside of the major effect region, representing promising new candidate genes for future functional studies.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Discovery of a viral NLR homolog that inhibits the inflammasome (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-22
    Description: The NLR (nucleotide binding and oligomerization, leucine-rich repeat) family of proteins senses microbial infections and activates the inflammasome, a multiprotein complex that promotes microbial clearance. Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to several human malignancies. We found that KSHV Orf63 is a viral homolog of human NLRP1. Orf63 blocked NLRP1-dependent innate immune responses, including caspase-1 activation and processing of interleukins IL-1beta and IL-18. KSHV Orf63 interacted with NLRP1, NLRP3, and NOD2. Inhibition of Orf63 expression resulted in increased expression of IL-1beta during the KSHV life cycle. Furthermore, inhibition of NLRP1 was necessary for efficient reactivation and generation of progeny virus. The viral homolog subverts the function of cellular NLRs, which suggests that modulation of NLR-mediated innate immunity is important for the lifelong persistence of herpesviruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072027/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregory, Sean M -- Davis, Beckley K -- West, John A -- Taxman, Debra J -- Matsuzawa, Shu-ichi -- Reed, John C -- Ting, Jenny P Y -- Damania, Blossom -- 5R21CA131645/CA/NCI NIH HHS/ -- AI057157/AI/NIAID NIH HHS/ -- AI077437/AI/NIAID NIH HHS/ -- AI56324/AI/NIAID NIH HHS/ -- AI91967/AI/NIAID NIH HHS/ -- CA096500/CA/NCI NIH HHS/ -- CA156330/CA/NCI NIH HHS/ -- DE018281/DE/NIDCR NIH HHS/ -- F32-AI78735/AI/NIAID NIH HHS/ -- R01 AI091967/AI/NIAID NIH HHS/ -- R01 CA096500/CA/NCI NIH HHS/ -- R01 CA096500-10/CA/NCI NIH HHS/ -- R01 DE018281/DE/NIDCR NIH HHS/ -- R01 DE018281-05/DE/NIDCR NIH HHS/ -- T32-AI007001/AI/NIAID NIH HHS/ -- T32-AI007419/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):330-4. doi: 10.1126/science.1199478.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21252346" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Amino Acid Sequence ; Apoptosis ; Apoptosis Regulatory Proteins/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Carrier Proteins/metabolism ; Caspase 1/metabolism ; Caspase Inhibitors ; Cell Line ; Cell Line, Tumor ; Herpesvirus 8, Human/genetics/immunology/*physiology ; Humans ; *Immune Evasion ; *Immunity, Innate ; Inflammasomes/*antagonists & inhibitors/metabolism ; Interleukin-1beta/metabolism ; Molecular Sequence Data ; Monocytes/virology ; Nod2 Signaling Adaptor Protein/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Transfection ; Viral Proteins/chemistry/genetics/*metabolism ; Virus Activation ; Virus Latency ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Structure and function of the complete internal fusion loop from Ebolavirus glycoprotein 2 (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-06-20
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Structure and function of the complete internal fusion loop from Ebolavirus glycoprotein 2 [Microbiology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-07-06
    Description: Ebolavirus (Ebov), an enveloped virus of the family Filoviridae, causes hemorrhagic fever in humans and nonhuman primates. The viral glycoprotein (GP) is solely responsible for virus–host membrane fusion, but how it does so remains elusive. Fusion occurs after virions reach an endosomal compartment where GP is proteolytically primed by cathepsins. Fusion by primed GP is governed by an internal fusion loop found in GP2, the fusion subunit. This fusion loop contains a stretch of hydrophobic residues, some of which have been shown to be critical for GP-mediated infection. Here we present liposome fusion data and NMR structures for a complete (54-residue) disulfide-bonded internal fusion loop (Ebov FL) in a membrane mimetic. The Ebov FL induced rapid fusion of liposomes of varying compositions at pH values at or below 5.5. Consistently, circular dichroism experiments indicated that the α-helical content of the Ebov FL in the presence of either lipid-mimetic micelles or small liposomes increases in samples exposed to pH ≤5.5. NMR structures in dodecylphosphocholine micelles at pH 7.0 and 5.5 revealed a conformational change from a relatively flat extended loop structure at pH 7.0 to a structure with an ∼90° bend at pH 5.5. Induction of the bend at low pH reorients and compacts the hydrophobic patch at the tip of the FL. We propose that these changes facilitate disruption of lipids at the site of virus–host cell membrane contact and, hence, initiate Ebov fusion.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Classical T Tauri stars: magnetic fields, coronae and star-disc interactions (2013)
    Oxford University Press
    Details
    Publication Date: 2013-12-27
    Description: The magnetic fields of young stars set their coronal properties and control their spin evolution via the star–disc interaction and outflows. Using 14 magnetic maps of 10 classical T Tauri stars (CTTSs) we investigate their closed X-ray emitting coronae, their open wind-bearing magnetic fields and the geometry of magnetospheric accretion flows. The magnetic fields of all the CTTSs are multipolar. Stars with simpler (more dipolar) large-scale magnetic fields have stronger fields, are slower rotators and have larger X-ray emitting coronae compared to stars with more complex large-scale magnetic fields. The field complexity controls the distribution of open and closed field regions across the stellar surface, and strongly influences the location and shapes of accretion hot spots. However, the higher order field components are of secondary importance in determining the total unsigned open magnetic flux, which depends mainly on the strength of the dipole component and the stellar surface area. Likewise, the dipole component alone provides an adequate approximation of the disc truncation radius. For some stars, the pressure of the hot coronal plasma dominates the stellar magnetic pressure and forces open the closed field inside the disc truncation radius. This is significant as accretion models generally assume that the magnetic field has a closed geometry out to the inner disc edge.
    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
  • 6
    facet.materialart.
    Unknown
    Deletion of the CSB homolog, RAD26, yields Spt- strains with proficient transcription-coupled repair (2001)
    Oxford University Press
    Details
    Publication Date: 2001-07-15
    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...