Mouse Genome Informatics
cx
    Hbatm1(HBA)Tow/Hbatm1(HBA)Tow
Hbbtm2(HBG1,HBB*)Tow/Hbbtm2(HBG1,HBB*)Tow

Not Specified
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
hematopoietic system
• abundant hemosiderin deposits
• pooling of sinusoidal erythrocytes and vasoocclusion of splenic vessels
• slightly thalassemic
• many rigid elongated cells are seen in blood smears
• erythroid progenitors are present in the hepatic sinusoids
• massive expansion of the red pulp
• complete loss of lymphoid follicular structure

liver/biliary system
• pronounced congestion of intrahepatic vessels and aggregates of sickled red blood cells
• abundant hemosiderin deposits
• pronounced congestion of intrahepatic vessels
• abundant hemosiderin deposits in the Kupffer cells

renal/urinary system
• engorgement and occlusion of renal blood vessels
• occlusion is most obvious at the corticomedullary junctions where dilated capillaries are easily detected
• occlusion is most obvious at the corticomedullary junctions where dilated capillaries are easily detected

cardiovascular system
• engorgement and occlusion of renal blood vessels
• occlusion is most obvious at the corticomedullary junctions where dilated capillaries are easily detected
• abundant hemosiderin deposits
• pronounced congestion of intrahepatic vessels
• pooling of sinusoidal erythrocytes and vasoocclusion of splenic vessels

homeostasis/metabolism
• abundant hemosiderin deposits in the Kupffer cells

immune system
• abundant hemosiderin deposits
• pooling of sinusoidal erythrocytes and vasoocclusion of splenic vessels
• massive expansion of the red pulp
• complete loss of lymphoid follicular structure

Mouse Models of Human Disease
OMIM IDRef(s)
Sickle Cell Anemia 603903 J:134980