Phenotypes Associated with This Genotype

Genotype
MGI:3037334

• Allelic Composition: Zfp36^tm1Pjb/Zfp36^tm1Pjb
• Genetic Background: B6.Cg-Zfp36^tm1Pjb

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

immune system

blood vessel inflammation ( J:214114 )

• increase in pro-inflammatory and atherosclerosis marker gene expression in aortas indicating vascular inflammation

increased granulocyte number ( J:214114 )

• slight enhancement in the blood

increased neutrophil cell number ( J:214114 )

• slight enhancement in the blood

decreased lymphocyte cell number ( J:214114 )

• decrease in lymphocyte cell numbers

increased monocyte cell number ( J:214114 )

• slight enhancement in the blood

abnormal macrophage physiology ( J:88443 )

• in macrophages from double homozygotes lipopolysaccharide-induced expression of TNF- alpha is significantly increased

arthritis ( J:88443 )

• homozygotes develop severe arthritis

• finger joints from double homozygotes display inflammatory pannus and bony erosions

skeleton

arthritis ( J:88443 )

• homozygotes develop severe arthritis

• finger joints from double homozygotes display inflammatory pannus and bony erosions

hematopoietic system

increased granulocyte number ( J:214114 )

• slight enhancement in the blood

increased neutrophil cell number ( J:214114 )

• slight enhancement in the blood

thrombocytosis ( J:214114 )

• slight enhancement in the blood

decreased lymphocyte cell number ( J:214114 )

• decrease in lymphocyte cell numbers

increased monocyte cell number ( J:214114 )

• slight enhancement in the blood

abnormal macrophage physiology ( J:88443 )

• in macrophages from double homozygotes lipopolysaccharide-induced expression of TNF- alpha is significantly increased

cardiovascular system

decreased systemic arterial blood pressure ( J:214114 )

• reduction in blood pressure

abnormal vasodilation ( J:214114 )

• aortas are less responsive to acetylcholine-induced relaxation mice however show similar relaxation responses to the NOS inhibitor L-NAME and to the NO-donor sodium nitroprusside

blood vessel inflammation ( J:214114 )

• increase in pro-inflammatory and atherosclerosis marker gene expression in aortas indicating vascular inflammation

cellular

increased cellular sensitivity to oxidative stress ( J:214114 )

• mice show higher reactive oxygen and nitrogen species (RONS) formation in the presence of NADPH in cardiac membrane fractions, indicating enhanced burden of oxidative stress

oxidative stress ( J:214114 )

• mice show higher reactive oxygen and nitrogen species (RONS) formation under PDBu-stimulated conditions in whole blood, indicating enhanced burden of oxidative stress

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:214114 )

N • mice show normal blood cholesterol, triglyceride and glucose levels

abnormal nitric oxide homeostasis ( J:214114 )

• marker analysis indicates reduced NO bioavailability

muscle

abnormal vasodilation ( J:214114 )

• aortas are less responsive to acetylcholine-induced relaxation mice however show similar relaxation responses to the NOS inhibitor L-NAME and to the NO-donor sodium nitroprusside

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
rheumatoid arthritis		DOID:7148	OMIM:180300	J:214114