Nancy J Wandersee

Summary

Affiliation: Blood Research Institute
Country: USA

Publications

  1. ncbi Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis
    Nancy J Wandersee
    Blood Research Institute, The Blood Center of Southeastern Wisconsin, 8727 Watertown Plank Rd, Milwaukee, WI 53226, USA
    Blood 103:710-6. 2004
  2. ncbi Ca2+-CaM activation of AMP deaminase contributes to adenine nucleotide dysregulation and phosphatidylserine externalization in human sickle erythrocytes
    Richard L Sabina
    Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA
    Br J Haematol 144:434-45. 2009
  3. ncbi Erythrocyte adhesion is modified by alterations in cellular tonicity and volume
    Nancy J Wandersee
    Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA
    Br J Haematol 131:366-77. 2005
  4. ncbi Vascular dysfunction in a murine model of severe hemolysis
    Anne C Frei
    Blood Research Institute, Blood Center of Wisconsin, Milwaukee, Wisconsin, USA
    Blood 112:398-405. 2008
  5. ncbi Transient receptor potential vanilloid 1 mediates pain in mice with severe sickle cell disease
    Cheryl A Hillery
    Department of Pediatrics and Children s Research Institute, Division of Hematology Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
    Blood 118:3376-83. 2011
  6. ncbi Mutations in the murine erythroid alpha-spectrin gene alter spectrin mRNA and protein levels and spectrin incorporation into the red blood cell membrane skeleton
    Nancy J Wandersee
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Blood 101:325-30. 2003

Collaborators

Detail Information

Publications6

  1. ncbi Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis
    Nancy J Wandersee
    Blood Research Institute, The Blood Center of Southeastern Wisconsin, 8727 Watertown Plank Rd, Milwaukee, WI 53226, USA
    Blood 103:710-6. 2004
    ..005). While the mechanism of infarction in these mice is unknown, we speculate that changes in RBC adhesive characteristics contribute to this pathology...
  2. ncbi Ca2+-CaM activation of AMP deaminase contributes to adenine nucleotide dysregulation and phosphatidylserine externalization in human sickle erythrocytes
    Richard L Sabina
    Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA
    Br J Haematol 144:434-45. 2009
    ....
  3. ncbi Erythrocyte adhesion is modified by alterations in cellular tonicity and volume
    Nancy J Wandersee
    Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA
    Br J Haematol 131:366-77. 2005
    ..In summary, these findings demonstrate that changes in hydration can significantly impact adhesion, causing normal erythrocytes to display adhesive properties similar to those of sickle cells and vice versa...
  4. ncbi Vascular dysfunction in a murine model of severe hemolysis
    Anne C Frei
    Blood Research Institute, Blood Center of Wisconsin, Milwaukee, Wisconsin, USA
    Blood 112:398-405. 2008
    ..Together, these data indicate that sph/sph mice with severe HS have increased plasma hemoglobin and NO scavenging capacity, likely contributing to aberrant vasoregulation and initiating oxidative damage...
  5. ncbi Transient receptor potential vanilloid 1 mediates pain in mice with severe sickle cell disease
    Cheryl A Hillery
    Department of Pediatrics and Children s Research Institute, Division of Hematology Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
    Blood 118:3376-83. 2011
    ..Therefore, TRPV1-targeted compounds that lack thermoregulatory side effects may provide relief from pain in patients with SCD...
  6. ncbi Mutations in the murine erythroid alpha-spectrin gene alter spectrin mRNA and protein levels and spectrin incorporation into the red blood cell membrane skeleton
    Nancy J Wandersee
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Blood 101:325-30. 2003
    ..The sph(J) deletion is near the 4.1/actin-binding region at the junctional complex providing new evidence that this 13-amino acid segment at the COOH-terminus of alpha-spectrin is crucial to the stability of the junctional complex...