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Department of Hematology  School of Medical Sciences  Tarbiat Modares University May.28.2008 Najmaldin  saki
 
[object Object],Introduction: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
Materials and methods : ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],All antibodies from BD Pharmingen , Stockholm , Sweden
Results Hoxa9/b3/b4 null mice display a marked reduction in spleen size and cellularity
 
Hoxa9/b3/b4 and hoxa9 null CFU-S progenitors generate small spleen colonies
Lin- , Sca+ , c-Kit+ , CD 150+ (LSKCD150) Lin- , Sca+ , c-Kit+ , Cd34- , (LSKCD34-) Hoxa9/b3/b4 null mice exhibit an increase in the frequency of immunophenotypic HSCs
Loss of hoxb3 and hoxb4 does not exacerbate the repopulating defect observed in hoxa9¯’¯HSCs The key question emerging from this study is why the deficiency of hoxa9 alone results in such dramatic reduction in repopulating capacity and is not significantly compromised by the additional deletions (hoxb3/b4) ?
 

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Hoxa9hoxb3hoxb4

  • 1. Department of Hematology School of Medical Sciences Tarbiat Modares University May.28.2008 Najmaldin saki
  • 3.
  • 4.
  • 5.
  • 6. Results Hoxa9/b3/b4 null mice display a marked reduction in spleen size and cellularity
  • 8. Hoxa9/b3/b4 and hoxa9 null CFU-S progenitors generate small spleen colonies
  • 9. Lin- , Sca+ , c-Kit+ , CD 150+ (LSKCD150) Lin- , Sca+ , c-Kit+ , Cd34- , (LSKCD34-) Hoxa9/b3/b4 null mice exhibit an increase in the frequency of immunophenotypic HSCs
  • 10. Loss of hoxb3 and hoxb4 does not exacerbate the repopulating defect observed in hoxa9¯’¯HSCs The key question emerging from this study is why the deficiency of hoxa9 alone results in such dramatic reduction in repopulating capacity and is not significantly compromised by the additional deletions (hoxb3/b4) ?
  • 11.  

Hinweis der Redaktion

  1. Hoxa9/hoxb3/hoxb4 compound null mice display severe hematopoietic defects