Mouse Genome Informatics
hm1
    Abcc1tm1Bor/Abcc1tm1Bor
involves: 129P2/OlaHsd * FVB
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• homozygotes are viable, fertile and healthy under normal conditions, and display no differences in platelet activating factor (PAF)-induced lethality relative to wild-type mice (50% lethality at 200 g/kg) (J:44110)
• at 11-13 weeks, male homozygotes are hypersensitive to etoposide (but not vincristine) toxicity, as shown by increased mortality relative to wild-type mice

homeostasis/metabolism
• at 11-13 weeks, male homozygotes are hypersensitive to etoposide (but not vincristine) toxicity, as shown by increased mortality relative to wild-type mice
• at 11-13 weeks, male homozygotes are hypersensitive to etoposide (but not vincristine) toxicity, as shown by increased body weight loss relative to wild-type mice

immune system
• in vitro, bone marrow-derived mast cells (BMMCs) from mutant mice excrete significantly less LTC4 and accumulate more LTC4 intracellularly relative to wild-type BMMCs; no differences are noted in LTB4 excretion
• homozygotes show a significantly reduced inflammatory response to topical application arachidonic acid, as shown by reduced ear edema and decreased vascular permeability and extravasation of serum proteins relative to wild-type mice
• in contrast, homozygotes exhibit a normal inflammatory response to intradermal injection of LTC4 or topical application of phorbol ester (TPA)

hematopoietic system
• in vitro, bone marrow-derived mast cells (BMMCs) from mutant mice excrete significantly less LTC4 and accumulate more LTC4 intracellularly relative to wild-type BMMCs; no differences are noted in LTB4 excretion


Mouse Genome Informatics
cx2
    Abcc1tm1Bor/Abcc1tm1Bor
Tg(Thy1-AppDutch)#Jckr/0

FVB.Cg-Abcc1tm1Bor Tg(Thy1-AppDutch)#Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• number and severity of amyloid beta-immunoreactive vessels is increased compared to single Tg(Thy1-AppDutch)#Jckr mice indicating the development of more severe cerebral amyloid angiopathy
• amyloid beta deposits are increased in neurons of the neocortex and hippocampus

homeostasis/metabolism
• number and severity of amyloid beta-immunoreactive vessels is increased compared to single Tg(Thy1-AppDutch)#Jckr mice indicating the development of more severe cerebral amyloid angiopathy
• amyloid beta deposits are increased in neurons of the neocortex and hippocampus

Mouse Models of Human Disease
OMIM IDRef(s)
Cerebral Amyloid Angiopathy, App-Related 605714 J:178230


Mouse Genome Informatics
cx3
    Abcc1tm1Bor/Abcc1tm1Bor
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0

FVB.Cg-Abcc1tm1Bor Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• increase in microgliosis
• mutants exhibit an increase in the cortical load and size of cerebral amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

hematopoietic system
• increase in microgliosis

immune system
• increase in microgliosis

homeostasis/metabolism
• mutants exhibit an increase in the cortical load and size of cerebral amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:178230