Lobelia Samavati

Summary

Affiliation: Wayne State University
Country: USA

Publications

  1. ncbi Regulation of mitochondrial oxidative phosphorylation through cell signaling
    Maik Huttemann
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Biochim Biophys Acta 1773:1701-20. 2007
  2. ncbi The multiple functions of cytochrome c and their regulation in life and death decisions of the mammalian cell: From respiration to apoptosis
    Maik Huttemann
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mitochondrion 11:369-81. 2011
  3. ncbi Tumor necrosis factor alpha inhibits oxidative phosphorylation through tyrosine phosphorylation at subunit I of cytochrome c oxidase
    Lobelia Samavati
    Department of Medicine, Division of Pulmonary Critical Care and Sleep Medicine, Wayne State University School of Medicine, 3990 John R, Detroit, MI 48201, USA
    J Biol Chem 283:21134-44. 2008
  4. ncbi STAT3 tyrosine phosphorylation is critical for interleukin 1 beta and interleukin-6 production in response to lipopolysaccharide and live bacteria
    Lobelia Samavati
    Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mol Immunol 46:1867-77. 2009
  5. ncbi TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages
    Christian P Bauerfeld
    Department of Pediatrics, St John Hospital and Medical Center, Detroit, MI 48236, USA
    J Immunol 188:2847-57. 2012
  6. ncbi Isolation of regulatory-competent, phosphorylated cytochrome C oxidase
    Icksoo Lee
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan, USA
    Methods Enzymol 457:193-210. 2009
  7. ncbi Regulation of mitochondrial respiration and apoptosis through cell signaling: cytochrome c oxidase and cytochrome c in ischemia/reperfusion injury and inflammation
    Maik Huttemann
    Wayne State University School of Medicine, Detroit, MI 48201, USA
    Biochim Biophys Acta 1817:598-609. 2012
  8. ncbi Dysregulation of p38 and MKP-1 in response to NOD1/TLR4 stimulation in sarcoid bronchoalveolar cells
    Ruchi Rastogi
    Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, Michigan, USA
    Am J Respir Crit Care Med 183:500-10. 2011
  9. ncbi Mitochondrial K(ATP) channel openers activate the ERK kinase by an oxidant-dependent mechanism
    Lobelia Samavati
    Department of Medicine, University of Iowa College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa 52242, USA
    Am J Physiol Cell Physiol 283:C273-81. 2002

Collaborators

Detail Information

Publications9

  1. ncbi Regulation of mitochondrial oxidative phosphorylation through cell signaling
    Maik Huttemann
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Biochim Biophys Acta 1773:1701-20. 2007
    ....
  2. ncbi The multiple functions of cytochrome c and their regulation in life and death decisions of the mammalian cell: From respiration to apoptosis
    Maik Huttemann
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mitochondrion 11:369-81. 2011
    ..Cytc regulation in respiration and cell death is discussed in a human disease context including neurodegenerative and cardiovascular diseases, cancer, and sepsis...
  3. ncbi Tumor necrosis factor alpha inhibits oxidative phosphorylation through tyrosine phosphorylation at subunit I of cytochrome c oxidase
    Lobelia Samavati
    Department of Medicine, Division of Pulmonary Critical Care and Sleep Medicine, Wayne State University School of Medicine, 3990 John R, Detroit, MI 48201, USA
    J Biol Chem 283:21134-44. 2008
    ..35 cells. We postulate that an important contributor in TNFalpha-mediated pathologies, such as sepsis, is energy paucity, which parallels the poor tissue oxygen extraction and utilization found in such patients...
  4. ncbi STAT3 tyrosine phosphorylation is critical for interleukin 1 beta and interleukin-6 production in response to lipopolysaccharide and live bacteria
    Lobelia Samavati
    Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mol Immunol 46:1867-77. 2009
    ..This inhibition did not affect caspase-1 activation. These results highlight the complex role of STAT3 in cytokine production and the key role of STAT3 tyrosine phosphorylation in IL-1beta and IL-6 production in response to inflammation...
  5. ncbi TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages
    Christian P Bauerfeld
    Department of Pediatrics, St John Hospital and Medical Center, Detroit, MI 48236, USA
    J Immunol 188:2847-57. 2012
    ..Importantly, using a genetic approach, we show that the AKT1 isoform is pivotal in regulating mitochondrial biogenesis in response to TLR4 agonist...
  6. ncbi Isolation of regulatory-competent, phosphorylated cytochrome C oxidase
    Icksoo Lee
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan, USA
    Methods Enzymol 457:193-210. 2009
    ..This phosphorylation site is located close to the ATP and ADP binding site, which adjusts CcO activity to cellular energy demand, and we propose that phosphorylation of tyrosine 11 enables allosteric regulation...
  7. ncbi Regulation of mitochondrial respiration and apoptosis through cell signaling: cytochrome c oxidase and cytochrome c in ischemia/reperfusion injury and inflammation
    Maik Huttemann
    Wayne State University School of Medicine, Detroit, MI 48201, USA
    Biochim Biophys Acta 1817:598-609. 2012
    ..Although operating at opposite poles of the ETC activity spectrum, both conditions can lead to cell death through energy deprivation or ROS-triggered apoptosis...
  8. ncbi Dysregulation of p38 and MKP-1 in response to NOD1/TLR4 stimulation in sarcoid bronchoalveolar cells
    Ruchi Rastogi
    Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, Michigan, USA
    Am J Respir Crit Care Med 183:500-10. 2011
    ..Recognition of microbial moieties through Toll-like or Nod-like receptors evokes sequential activation of mitogen-activated protein kinases (MAPKs), which plays a role in Th1-immune response...
  9. ncbi Mitochondrial K(ATP) channel openers activate the ERK kinase by an oxidant-dependent mechanism
    Lobelia Samavati
    Department of Medicine, University of Iowa College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa 52242, USA
    Am J Physiol Cell Physiol 283:C273-81. 2002
    ..We conclude that mitochondrial K(ATP) channel openers trigger ERK activation via mitochondria-derived ROS...