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  1. Article ; Online: LKB1 regulates germinal center formation and termination.

    Waters, Lynnea R / Walsh, Nicole C / Teitell, Michael A

    Cell cycle (Georgetown, Tex.)

    2015  Volume 14, Issue 14, Page(s) 2183–2184

    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Germinal Center/metabolism ; Mice ; Mice, Knockout ; Protein-Serine-Threonine Kinases/deficiency ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Transcription Factors/metabolism
    Chemical Substances Crtc2 protein, mouse ; Transcription Factors ; Stk11 protein, mouse (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2015-06-01
    Publishing country United States
    Document type Editorial
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2015.1056610
    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)
    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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  2. Article ; Online: Initial B Cell Activation Induces Metabolic Reprogramming and Mitochondrial Remodeling.

    Waters, Lynnea R / Ahsan, Fasih M / Wolf, Dane M / Shirihai, Orian / Teitell, Michael A

    iScience

    2018  Volume 5, Page(s) 99–109

    Abstract: B lymphocytes provide adaptive immunity by generating antigen-specific antibodies and supporting the activation of T cells. Little is known about how global metabolism supports naive B cell activation to enable an effective immune response. By coupling ... ...

    Abstract B lymphocytes provide adaptive immunity by generating antigen-specific antibodies and supporting the activation of T cells. Little is known about how global metabolism supports naive B cell activation to enable an effective immune response. By coupling RNA sequencing (RNA-seq) data with glucose isotopomer tracing, we show that stimulated B cells increase programs for oxidative phosphorylation (OXPHOS), the tricarboxylic acid (TCA) cycle, and nucleotide biosynthesis, but not glycolysis. Isotopomer tracing uncovered increases in TCA cycle intermediates with almost no contribution from glucose. Instead, glucose mainly supported the biosynthesis of ribonucleotides. Glucose restriction did not affect B cell functions, yet the inhibition of OXPHOS or glutamine restriction markedly impaired B cell growth and differentiation. Increased OXPHOS prompted studies of mitochondrial dynamics, which revealed extensive mitochondria remodeling during activation. Our results show how B cell metabolism adapts with stimulation and reveals unexpected details for carbon utilization and mitochondrial dynamics at the start of a humoral immune response.
    Language English
    Publishing date 2018-07-10
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2018.07.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Initial B Cell Activation Induces Metabolic Reprogramming and Mitochondrial Remodeling

    Lynnea R. Waters / Fasih M. Ahsan / Dane M. Wolf / Orian Shirihai / Michael A. Teitell

    iScience, Vol 5, Iss , Pp 99-

    2018  Volume 109

    Abstract: Summary: B lymphocytes provide adaptive immunity by generating antigen-specific antibodies and supporting the activation of T cells. Little is known about how global metabolism supports naive B cell activation to enable an effective immune response. By ... ...

    Abstract Summary: B lymphocytes provide adaptive immunity by generating antigen-specific antibodies and supporting the activation of T cells. Little is known about how global metabolism supports naive B cell activation to enable an effective immune response. By coupling RNA sequencing (RNA-seq) data with glucose isotopomer tracing, we show that stimulated B cells increase programs for oxidative phosphorylation (OXPHOS), the tricarboxylic acid (TCA) cycle, and nucleotide biosynthesis, but not glycolysis. Isotopomer tracing uncovered increases in TCA cycle intermediates with almost no contribution from glucose. Instead, glucose mainly supported the biosynthesis of ribonucleotides. Glucose restriction did not affect B cell functions, yet the inhibition of OXPHOS or glutamine restriction markedly impaired B cell growth and differentiation. Increased OXPHOS prompted studies of mitochondrial dynamics, which revealed extensive mitochondria remodeling during activation. Our results show how B cell metabolism adapts with stimulation and reveals unexpected details for carbon utilization and mitochondrial dynamics at the start of a humoral immune response. : Immunology; Immune Response; Components of the Immune System; Metabolomics Subject Areas: Immunology, Immune Response, Components of the Immune System, Metabolomics
    Keywords Science ; Q
    Subject code 570
    Language English
    Publishing date 2018-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Ampk regulates IgD expression but not energy stress with B cell activation

    Lynnea R. Waters / Fasih M. Ahsan / Johanna ten Hoeve / Jason S. Hong / Diane N. H. Kim / Aspram Minasyan / Daniel Braas / Thomas G. Graeber / Thomas A. Zangle / Michael A. Teitell

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Volume 14

    Abstract: Abstract Ampk is an energy gatekeeper that responds to decreases in ATP by inhibiting energy-consuming anabolic processes and promoting energy-generating catabolic processes. Recently, we showed that Lkb1, an understudied kinase in B lymphocytes and a ... ...

    Abstract Abstract Ampk is an energy gatekeeper that responds to decreases in ATP by inhibiting energy-consuming anabolic processes and promoting energy-generating catabolic processes. Recently, we showed that Lkb1, an understudied kinase in B lymphocytes and a major upstream kinase for Ampk, had critical and unexpected roles in activating naïve B cells and in germinal center formation. Therefore, we examined whether Lkb1 activities during B cell activation depend on Ampk and report surprising Ampk activation with in vitro B cell stimulation in the absence of energy stress, coupled to rapid biomass accumulation. Despite Ampk activation and a controlling role for Lkb1 in B cell activation, Ampk knockout did not significantly affect B cell activation, differentiation, nutrient dynamics, gene expression, or humoral immune responses. Instead, Ampk loss specifically repressed the transcriptional expression of IgD and its regulator, Zfp318. Results also reveal that early activation of Ampk by phenformin treatment impairs germinal center formation but does not significantly alter antibody responses. Combined, the data show an unexpectedly specific role for Ampk in the regulation of IgD expression during B cell activation.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2019-06-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Ampk regulates IgD expression but not energy stress with B cell activation.

    Waters, Lynnea R / Ahsan, Fasih M / Ten Hoeve, Johanna / Hong, Jason S / Kim, Diane N H / Minasyan, Aspram / Braas, Daniel / Graeber, Thomas G / Zangle, Thomas A / Teitell, Michael A

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 8176

    Abstract: Ampk is an energy gatekeeper that responds to decreases in ATP by inhibiting energy-consuming anabolic processes and promoting energy-generating catabolic processes. Recently, we showed that Lkb1, an understudied kinase in B lymphocytes and a major ... ...

    Abstract Ampk is an energy gatekeeper that responds to decreases in ATP by inhibiting energy-consuming anabolic processes and promoting energy-generating catabolic processes. Recently, we showed that Lkb1, an understudied kinase in B lymphocytes and a major upstream kinase for Ampk, had critical and unexpected roles in activating naïve B cells and in germinal center formation. Therefore, we examined whether Lkb1 activities during B cell activation depend on Ampk and report surprising Ampk activation with in vitro B cell stimulation in the absence of energy stress, coupled to rapid biomass accumulation. Despite Ampk activation and a controlling role for Lkb1 in B cell activation, Ampk knockout did not significantly affect B cell activation, differentiation, nutrient dynamics, gene expression, or humoral immune responses. Instead, Ampk loss specifically repressed the transcriptional expression of IgD and its regulator, Zfp318. Results also reveal that early activation of Ampk by phenformin treatment impairs germinal center formation but does not significantly alter antibody responses. Combined, the data show an unexpectedly specific role for Ampk in the regulation of IgD expression during B cell activation.
    MeSH term(s) AMP-Activated Protein Kinase Kinases ; AMP-Activated Protein Kinases ; Adenosine Triphosphate/metabolism ; Anabolic Agents/pharmacology ; Animals ; B-Lymphocytes/drug effects ; B-Lymphocytes/metabolism ; Cyclic AMP Receptor Protein/drug effects ; Cyclic AMP Receptor Protein/genetics ; DNA-Binding Proteins/genetics ; Energy Metabolism/drug effects ; Energy Metabolism/genetics ; Gene Expression Regulation/drug effects ; Germinal Center/drug effects ; HeLa Cells ; Humans ; Immunoglobulin D/genetics ; Metabolomics ; Phenformin/pharmacology ; Protein Kinases/genetics ; Protein Serine-Threonine Kinases/genetics
    Chemical Substances Anabolic Agents ; Cyclic AMP Receptor Protein ; DNA-Binding Proteins ; Immunoglobulin D ; Zfp318 protein, mouse ; Adenosine Triphosphate (8L70Q75FXE) ; Phenformin (DD5K7529CE) ; Protein Kinases (EC 2.7.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Stk11 protein, mouse (EC 2.7.11.1) ; AMP-Activated Protein Kinase Kinases (EC 2.7.11.3) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2019-06-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-43985-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: LKB1 inhibition of NF-κB in B cells prevents T follicular helper cell differentiation and germinal center formation.

    Walsh, Nicole C / Waters, Lynnea R / Fowler, Jessica A / Lin, Mark / Cunningham, Cameron R / Brooks, David G / Rehg, Jerold E / Morse, Herbert C / Teitell, Michael A

    EMBO reports

    2015  Volume 16, Issue 6, Page(s) 753–768

    Abstract: T-cell-dependent antigenic stimulation drives the differentiation of B cells into antibody-secreting plasma cells and memory B cells, but how B cells regulate this process is unclear. We show that LKB1 expression in B cells maintains B-cell quiescence ... ...

    Abstract T-cell-dependent antigenic stimulation drives the differentiation of B cells into antibody-secreting plasma cells and memory B cells, but how B cells regulate this process is unclear. We show that LKB1 expression in B cells maintains B-cell quiescence and prevents the premature formation of germinal centers (GCs). Lkb1-deficient B cells (BKO) undergo spontaneous B-cell activation and secretion of multiple inflammatory cytokines, which leads to splenomegaly caused by an unexpected expansion of T cells. Within this cytokine response, increased IL-6 production results from heightened activation of NF-κB, which is suppressed by active LKB1. Secreted IL-6 drives T-cell activation and IL-21 production, promoting T follicular helper (TFH ) cell differentiation and expansion to support a ~100-fold increase in steady-state GC B cells. Blockade of IL-6 secretion by BKO B cells inhibits IL-21 expression, a known inducer of TFH -cell differentiation and expansion. Together, these data reveal cell intrinsic and surprising cell extrinsic roles for LKB1 in B cells that control TFH -cell differentiation and GC formation, and place LKB1 as a central regulator of T-cell-dependent humoral immunity.
    MeSH term(s) Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cell Differentiation ; Germinal Center/physiology ; Interleukin-6/immunology ; Interleukin-6/metabolism ; Interleukins/immunology ; Lymphocyte Activation ; Mice ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/genetics ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/physiology
    Chemical Substances Interleukin-6 ; Interleukins ; NF-kappa B ; Stk11 protein, mouse (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; interleukin-21 (MKM3CA6LT1)
    Language English
    Publishing date 2015-04-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201439505
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5433: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MG 41: Show issues

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