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P.A. Oldenborg

Department of Integrative Medical Biology

Section for Histology and Cell Biology

Umeå University

SE-901 87 Umeå

Sweden

[email]@histocel.umu.se

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Department of Integrative Medical Biology, Section for Histology and Cell Biology, Umeå University, SE-901 87 Umeå, Sweden. 2004
  • Department of Histology and Cell Biology, Umeå University, Sweden. 1998 - 2002
  • Division of Infectious Diseases, Department of Internal Medicine and Department of Molecular Microbiology and Pathogenesis, Washington University School of Medicine, St. Louis, USA. 2001

References

  1. Role of CD47 in erythroid cells and in autoimmunity. Oldenborg, P.A. Leuk. Lymphoma (2004) [Pubmed]
  2. Lethal autoimmune hemolytic anemia in CD47-deficient nonobese diabetic (NOD) mice. Oldenborg, P.A., Gresham, H.D., Chen, Y., Izui, S., Lindberg, F.P. Blood (2002) [Pubmed]
  3. CD47-signal regulatory protein alpha (SIRPalpha) regulates Fcgamma and complement receptor-mediated phagocytosis. Oldenborg, P.A., Gresham, H.D., Lindberg, F.P. J. Exp. Med. (2001) [Pubmed]
  4. Different effects of glucose on extracellular and intracellular respiratory burst response in normal human neutrophils activated with the soluble agonist fMet-Leu-Phe. Oldenborg, P.A., Sundqvist, I.M., Sehlin, J. Diabet. Med. (2000) [Pubmed]
  5. Hyperglycemia in vitro attenuates insulin-stimulated chemokinesis in normal human neutrophils. Role of protein kinase C activation. Oldenborg, P.A., Sehlin, J. J. Leukoc. Biol. (1999) [Pubmed]
  6. Effects of insulin on N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe)-stimulated production of reactive oxygen metabolites from normal human neutrophils. Oldenborg, P.A. Inflamm. Res. (1999) [Pubmed]
  7. The glucose concentration modulates N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe)-stimulated chemokinesis in normal human neutrophils. Oldenborg, P.A., Sehlin, J. Biosci. Rep. (1999) [Pubmed]
  8. Insulin-stimulated chemokinesis in normal human neutrophils is dependent on D-glucose concentration and sensitive to inhibitors of tyrosine kinase and phosphatidylinositol 3-kinase. Oldenborg, P.A., Sehlin, J. J. Leukoc. Biol. (1998) [Pubmed]
 
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