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
    Mg2+ regulates cytotoxic functions of NK and CD8 T cells in chronic EBV infection through NKG2D (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-13
    Description: The magnesium transporter 1 (MAGT1) is a critical regulator of basal intracellular free magnesium (Mg(2+)) concentrations. Individuals with genetic deficiencies in MAGT1 have high levels of Epstein-Barr virus (EBV) and a predisposition to lymphoma. We show that decreased intracellular free Mg(2+) causes defective expression of the natural killer activating receptor NKG2D in natural killer (NK) and CD8(+) T cells and impairs cytolytic responses against EBV. Notably, magnesium supplementation in MAGT1-deficient patients restores intracellular free Mg(2+) and NKG2D while concurrently reducing EBV-infected cells in vivo, demonstrating a link between NKG2D cytolytic activity and EBV antiviral immunity in humans. Moreover, these findings reveal a specific molecular function of free basal intracellular Mg(2+) in eukaryotic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894782/" 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/PMC3894782/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaigne-Delalande, Benjamin -- Li, Feng-Yen -- O'Connor, Geraldine M -- Lukacs, Marshall J -- Jiang, Ping -- Zheng, Lixin -- Shatzer, Amber -- Biancalana, Matthew -- Pittaluga, Stefania -- Matthews, Helen F -- Jancel, Timothy J -- Bleesing, Jack J -- Marsh, Rebecca A -- Kuijpers, Taco W -- Nichols, Kim E -- Lucas, Carrie L -- Nagpal, Sunil -- Mehmet, Huseyin -- Su, Helen C -- Cohen, Jeffrey I -- Uzel, Gulbu -- Lenardo, Michael J -- T32 GM007618/GM/NIGMS NIH HHS/ -- ZIA AI001187-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 12;341(6142):186-91. doi: 10.1126/science.1240094.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Development of the Immune System Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23846901" target="_blank"〉PubMed〈/a〉
    Keywords: CD8-Positive T-Lymphocytes/*immunology ; Cation Transport Proteins/genetics/metabolism ; *Cytotoxicity, Immunologic ; Epstein-Barr Virus Infections/*immunology ; Humans ; Killer Cells, Natural/*immunology ; Magnesium/*immunology ; Magnesium Deficiency/*immunology ; NK Cell Lectin-Like Receptor Subfamily K/genetics/*metabolism ; X-Linked Combined Immunodeficiency Diseases/immunology
    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
  • 2
    facet.materialart.
    Unknown
    Second messenger role for Mg2+ revealed by human T-cell immunodeficiency (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-07-29
    Description: The magnesium ion, Mg(2+), is essential for all life as a cofactor for ATP, polyphosphates such as DNA and RNA, and metabolic enzymes, but whether it plays a part in intracellular signalling (as Ca(2+) does) is unknown. Here we identify mutations in the magnesium transporter gene, MAGT1, in a novel X-linked human immunodeficiency characterized by CD4 lymphopenia, severe chronic viral infections, and defective T-lymphocyte activation. We demonstrate that a rapid transient Mg(2+) influx is induced by antigen receptor stimulation in normal T cells and by growth factor stimulation in non-lymphoid cells. MAGT1 deficiency abrogates the Mg(2+) influx, leading to impaired responses to antigen receptor engagement, including defective activation of phospholipase Cgamma1 and a markedly impaired Ca(2+) influx in T cells but not B cells. These observations reveal a role for Mg(2+) as an intracellular second messenger coupling cell-surface receptor activation to intracellular effectors and identify MAGT1 as a possible target for novel therapeutics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159560/" 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/PMC3159560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Feng-Yen -- Chaigne-Delalande, Benjamin -- Kanellopoulou, Chrysi -- Davis, Jeremiah C -- Matthews, Helen F -- Douek, Daniel C -- Cohen, Jeffrey I -- Uzel, Gulbu -- Su, Helen C -- Lenardo, Michael J -- ZIA AI000769-14/Intramural NIH HHS/ -- ZIA AI000769-15/Intramural NIH HHS/ -- England -- Nature. 2011 Jul 27;475(7357):471-6. doi: 10.1038/nature10246.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21796205" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/immunology ; Cation Transport Proteins/genetics ; Female ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Magnesium/*immunology ; Male ; Phospholipase C gamma/genetics/metabolism ; Second Messenger Systems/*immunology ; T-Lymphocytes/*immunology ; T-Lymphocytopenia, Idiopathic CD4-Positive/genetics/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    CD95 triggers Orai1-mediated localized Ca2+ entry, regulates recruitment of protein kinase C (PKC) {beta}2, and prevents death-inducing signaling complex formation [Physiology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-11-23
    Description: The death receptor CD95 plays a pivotal role in immune surveillance and immune tolerance. Binding of CD95L to CD95 leads to recruitment of the adaptor protein Fas-associated death domain protein (FADD), which in turn aggregates caspase-8 and caspase-10. Efficient formation of the CD95/FADD/caspase complex, known as the death-inducing signaling complex (DISC), culminates in the induction of apoptosis. We show that cells exposed to CD95L undergo a reorganization of the plasma membrane in which the Ca2+ release-activated Ca2+ channel Orai1 and the endoplasmic reticulum-resident activator stromal interaction molecule 1 colocalize with CD95 into a micrometer-sized cluster in which the channel elicits a polarized entry of calcium. Orai1 knockdown and expression of a dominant negative construct (Orai1E106A) reveal that on CD95 engagement, the Orai1-driven localized Ca2+ influx is fundamental to recruiting the Ca2+-dependent protein kinase C (PKC) β2 to the DISC. PKCβ2 in turn transiently holds the complex in an inactive status, preventing caspase activation and transmission of the apoptotic signal. This study identifies a biological role of Ca2+ and the Orai1 channel that drives a transient negative feedback loop, introducing a lag phase in the early steps of the CD95 signal. We suggest that these localized events provide a time of decision to prevent accidental cell death.
    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
    CD95 engagement mediates actin-independent and -dependent apoptotic signals (2009)
    Springer Nature
    Details
    Publication Date: 2009-08-14
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
    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...