All Phenotypes Unc13d<tm1(KOMP)Vlcg> MGI Mouse

decreased platelet aggregation ( J:231217 )

• severely impaired aggregate formation on collagen under flow in vitro and in ferric chloride-injured mesenteric arterioles in vivo

abnormal platelet dense granule physiology ( J:231217 )

• dense granule secretion is completely abolished, as measured by ATP release upon thrombin or collagen-related peptide activation

• up to a 60% reduction in alpha-granule secretion at threshold concentrations relative to wild-type controls

impaired blood coagulation ( J:231217 )

• significantly increased occlusion time in a thrombosis model where the aorta is mechanically injured and blood flow is monitored for 30 min or until complete occlusion occurs

increased bleeding time ( J:231217 )

• profoundly prolonged tail bleeding times relative to wild-type controls

decreased susceptibility to ischemic brain injury ( J:231217 )

• significantly reduced brain infarct size and better overall neurological function (lower Bederson scores) 24 h after a 60-min transient middle cerebral artery occlusion (tMCAO) relative to wild-type controls

• significantly smaller hyperintense (bright) ischemic lesions than in wild-type controls after tMCAO, as revealed by serial MRI in living mice

• no signs of intracranial hemorrhage after GPIIb/IIIa-blockade followed by tMCAO, unlike the massive hemorrhagic transformation observed within the infarcted brain area of wild-type controls, as shown by MRI in living animals and confirmed by ex vivo examination

decreased cerebral infarct size ( J:231217 )

• brain infarct volumes are reduced to ~38% of those in wild-type controls 24 h after a 60-min tMCAO

hematopoietic system phenotype ( J:231217 )

N	• normal blood parameters and surface expression of major platelet receptors