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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gpld1em2Smoc
endonuclease-mediated mutation 2, Shanghai Model Organisms Center
MGI:7289957
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gpld1em2Smoc/Gpld1em2Smoc C57BL/6JSmoc-Gpld1em2Smoc/Smoc MGI:8375451


Genotype
MGI:8375451
hm1
Allelic
Composition
Gpld1em2Smoc/Gpld1em2Smoc
Genetic
Background
C57BL/6JSmoc-Gpld1em2Smoc/Smoc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gpld1em2Smoc mutation (0 available); any Gpld1 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice show an increase in the cross-sectional area of cardiomyocytes at 12 months of age
• intramyocardial AAV9-GPLD1 administration restores cross-sectional areas to wild-type values
• mice show an increase in heart weight to body weight (HW/BW) and heart weight to tibia length (HW/TL) ratios at 12 months of age
• intramyocardial AAV9-GPLD1 administration restores these ratios to wild-type values
• mice exhibit an exaggerated cardiac hypertrophy phenotype with markedly increased protein levels of hypertrophic markers (NPPA/ANF and MYH7/beta-MHC) in cardiac tissues at 12 months of age
• intramyocardial AAV9-GPLD1 administration reduces the protein levels of hypertrophic markers and reverses this pathology
• 12-month-old mice show an increase in LV size
• 12-month-old mice show an increase in LV wall thickness
• mice exhibit an increased collagen volume in cardiac tissues at 12 months of age
• intramyocardial AAV9-GPLD1 administration reduces collagen volume to near wild-type baseline levels
• mice show an age-dependent decline in LV function, as determined by 3-D LV radial strain maps and global longitudinal strain curves; a reduction in ejection fraction (EF) and fractional shortening (FS) is noted at 12 months of age
• intramyocardial injection-mediated delivery of AAV9-GPLD1 significantly improves cardiac function, as evidenced by echocardiographic assessments
• 12-month-old mice show LV diastolic dysfunction with a significant reduction in the mitral valve E/A ratio (early to late diastolic transmitral flow velocity)
• intramyocardial AAV9-GPLD1 administration significantly improves diastolic function by normalizing the E/A ratio

growth/size/body
• mice show an increase in heart weight to body weight (HW/BW) and heart weight to tibia length (HW/TL) ratios at 12 months of age
• intramyocardial AAV9-GPLD1 administration restores these ratios to wild-type values
• mice exhibit an exaggerated cardiac hypertrophy phenotype with markedly increased protein levels of hypertrophic markers (NPPA/ANF and MYH7/beta-MHC) in cardiac tissues at 12 months of age
• intramyocardial AAV9-GPLD1 administration reduces the protein levels of hypertrophic markers and reverses this pathology

muscle
• mice show an increase in the cross-sectional area of cardiomyocytes at 12 months of age
• intramyocardial AAV9-GPLD1 administration restores cross-sectional areas to wild-type values
• mice show an age-dependent decline in LV function, as determined by 3-D LV radial strain maps and global longitudinal strain curves; a reduction in ejection fraction (EF) and fractional shortening (FS) is noted at 12 months of age
• intramyocardial injection-mediated delivery of AAV9-GPLD1 significantly improves cardiac function, as evidenced by echocardiographic assessments
• 12-month-old mice show LV diastolic dysfunction with a significant reduction in the mitral valve E/A ratio (early to late diastolic transmitral flow velocity)
• intramyocardial AAV9-GPLD1 administration significantly improves diastolic function by normalizing the E/A ratio





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
07/08/2026
MGI 6.24
The Jackson Laboratory