Ellen Niederberger

Summary

Affiliation: Frankfurt am Main
Country: Germany

Publications

  1. Möser C, Möller M, Fleck S, Thomas D, Geisslinger G, Niederberger E. Inhibition of the protein kinase IKKepsilon attenuates neuropathic pain in mice. Neuropharmacology. 2018;146:198-211 pubmed publisher
    ..In summary, we conclude that IKKε modulates mechanisms of neuropathic pain by activating NF-κB. The administration of IKKε inhibitors might therefore constitute a new and promising approach for the therapy of neuropathic pain. ..
  2. Möser C, Stephan H, Altenrath K, Kynast K, Russe O, Olbrich K, et al. TANK-binding kinase 1 (TBK1) modulates inflammatory hyperalgesia by regulating MAP kinases and NF-κB dependent genes. J Neuroinflammation. 2015;12:100 pubmed publisher
    ..Inhibition of TBK1 might therefore constitute a novel effective tool for analgesic therapy. ..
  3. King T, Russe O, Möser C, Ferreirós N, Kynast K, Knothe C, et al. AMP-activated protein kinase is activated by non-steroidal anti-inflammatory drugs. Eur J Pharmacol. 2015;762:299-305 pubmed publisher
    ..AMPK might therefore contribute to their antinociceptive and anti-inflammatory properties. ..
  4. King Himmelreich T, Möser C, Wolters M, Olbrich K, Geisslinger G, Niederberger E. Age-Dependent Changes in the Inflammatory Nociceptive Behavior of Mice. Int J Mol Sci. 2015;16:27508-19 pubmed publisher
    ..In conclusion, our results reveal a reduced nociceptive response in aged mice, which might be at least partially mediated by an augmented inflammation-induced increase in the hormonal inhibitory system involving cortisol. ..
  5. Niederberger E, Geisslinger G. Proteomics in neuropathic pain research. Anesthesiology. 2008;108:314-23 pubmed publisher
    ..This might allow a better understanding of the pathophysiologic signaling pathways in this impairment, facilitate the discovery of specific biomarkers, and thus promote the development of novel pain therapies. ..
  6. Niederberger E, King T, Russe O, Geisslinger G. Activation of AMPK and its Impact on Exercise Capacity. Sports Med. 2015;45:1497-509 pubmed publisher
    ..In this review, we intend to shed light on currently published AMPK-activating drugs, their working mechanisms, and their impact on body fitness. ..
  7. Niederberger E, Geisslinger G. The IKK-NF-kappaB pathway: a source for novel molecular drug targets in pain therapy?. FASEB J. 2008;22:3432-42 pubmed publisher
    ..Therefore, a modulation of specific participants in the NF-kappaB signal transduction might exert a useful approach for the development of new painkillers. ..
  8. request reprint
    Niederberger E, Moser C, Kynast K, Geisslinger G. The non-canonical I?B kinases IKK? and TBK1 as potential targets for the development of novel therapeutic drugs. Curr Mol Med. 2013;13:1089-97 pubmed
    ..In this review, we summarize the roles of IKK? and TBK1 in different diseases and outline therapeutic options for modulation of these kinases. ..
  9. King Himmelreich T, Schramm S, Wolters M, Schmetzer J, Möser C, Knothe C, et al. The impact of endurance exercise on global and AMPK gene-specific DNA methylation. Biochem Biophys Res Commun. 2016;474:284-290 pubmed publisher
    ..Taken together, these results suggest that exercise influences AMPK?2 gene methylation in human blood and eminently in the skeletal muscle of mice and therefore might repress AMPK?2 gene expression. ..

More Information

Publications12

  1. King Himmelreich T, Möser C, Wolters M, Schmetzer J, Schreiber Y, Ferreirós N, et al. AMPK contributes to aerobic exercise-induced antinociception downstream of endocannabinoids. Neuropharmacology. 2017;124:134-142 pubmed publisher
    ..In conclusion, our data suggest that AMPK is an intermediate effector in endocannabinoid-mediated exercise-induced antinociception. This article is part of the Special Issue entitled "A New Dawn in Cannabinoid Neurobiology". ..
  2. request reprint
    Niederberger E, Schmidtko A, Gao W, Kühlein H, Ehnert C, Geisslinger G. Impaired acute and inflammatory nociception in mice lacking the p50 subunit of NF-kappaB. Eur J Pharmacol. 2007;559:55-60 pubmed
    ..The participation to persistent pain might rely on activation of NF-kappaB by inflammatory stimuli while the contribution to acute pain responses might be related to constitutive NF-kappaB activity in neurons of the nociceptive system. ..
  3. request reprint
    Niederberger E, Ehnert C, Gao W, Coste O, Schmidtko A, Popp L, et al. The impact of CREB and its phosphorylation at Ser142 on inflammatory nociception. Biochem Biophys Res Commun. 2007;362:75-80 pubmed
    ..Thus, our data confirm that CREB is essential for spinal nociceptive processing. However, prevention of phosphorylation only at serine 142 is not sufficient to modulate the nociceptive response. ..