All Phenotypes Pecam1<tm1Mak> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Pecam1^tm1Mak/Pecam1^tm1Mak	B6.129P2-Pecam1^tm1Mak	MGI:3622544
hm2	Pecam1^tm1Mak/Pecam1^tm1Mak	D1.129P2-Pecam1^tm1Mak	MGI:3622538
hm3	Pecam1^tm1Mak/Pecam1^tm1Mak	involves: 129P2/OlaHsd * C57BL/6	MGI:4950707
ht4	Pecam1^tm1Mak/Pecam1⁺	D1.129P2-Pecam1^tm1Mak	MGI:3622539
cx5	Pecam1^tm1Mak/Pecam1^tm1Mak Pitgp^C57BL/6/Pitgp^C57BL/6	involves: 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:3845116

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

cardiovascular system

kidney vascular congestion ( J:95226 )

• in knockouts, LPS treatment induces glomerular and peri-tubular capillary vascular congestion as well as occasional peritubular endothelial cell karyorexis and karyolysis, compared to induction of mild congestion in wild-type

glomerular capillary congestion ( J:95226 )

• after LPS treatment

liver vascular congestion ( J:95226 )

• after LPS treatment, livers from knockouts show vascular congestion

pulmonary vascular congestion ( J:95226 )

• after LPS treatment, lungs from knockouts show vascular congestion

spleen vascular congestion ( J:95226 )

• after LPS treatment, spleens from knockouts show vascular congestion of the red pulp

increased vascular permeability ( J:95226 )

• in response to LPS stimulation, one day later, a pronounced increased in organ/tissue specific permeability is observed in nulls compared to wild-type, particularly in the lung, liver, and kidney

hematopoietic system

spleen vascular congestion ( J:95226 )

• after LPS treatment, spleens from knockouts show vascular congestion of the red pulp

homeostasis/metabolism

pulmonary edema ( J:95226 )

• one day after LPS administration, lungs from knockouts show edema compared to treated wild-type lungs

immune system

spleen vascular congestion ( J:95226 )

• after LPS treatment, spleens from knockouts show vascular congestion of the red pulp

abnormal cytokine secretion ( J:95226 )

• after LPS treatment over a 24-hour period, cytokine levels in the serum of null mice are elevated

liver inflammation ( J:95226 )

• sinusoidal and portal inflammation is observed in knockouts following LPS treatment

liver/biliary system

liver vascular congestion ( J:95226 )

• after LPS treatment, livers from knockouts show vascular congestion

liver inflammation ( J:95226 )

• sinusoidal and portal inflammation is observed in knockouts following LPS treatment

renal/urinary system

kidney vascular congestion ( J:95226 )

glomerular capillary congestion ( J:95226 )

• after LPS treatment

respiratory system

pulmonary vascular congestion ( J:95226 )

• after LPS treatment, lungs from knockouts show vascular congestion

pulmonary edema ( J:95226 )

• one day after LPS administration, lungs from knockouts show edema compared to treated wild-type lungs

Allelic Composition	Pecam1^tm1Mak/Pecam1^tm1Mak
Genetic Background	D1.129P2-Pecam1^tm1Mak

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pecam1^tm1Mak mutation (1 available); any Pecam1 mutation (227 available)

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

immune system

abnormal leukocyte physiology ( J:106275 )

• larger numbers of cells from the spleen and lymph nodes of arthritic null animals migrate into the joints of arthritic mice than cells from wild-type mice

increased interferon-gamma secretion ( J:106275 )

• lymph node cells taken on day 14 from immunized mice produce significantly larger amounts of IFNG in response to stimulation by denatured CII or concanavalin A; cells obtained from mice on day 28 also produce greater amounts of IFNG in response to CII, but not concanavalin A

joint inflammation ( J:106275 )

• 6 weeks after initial CII immunization, joints of nulls showed more severe inflammation than wild-type

increased susceptibility to induced arthritis ( J:106275 )

• mice have an earlier arthritis onset after CII immunization and a higher incidence (55.3% by day 33 versus 25.7% by day42 in wild-type) than wild-type

skeleton

joint inflammation ( J:106275 )

• 6 weeks after initial CII immunization, joints of nulls showed more severe inflammation than wild-type

increased susceptibility to induced arthritis ( J:106275 )

• mice have an earlier arthritis onset after CII immunization and a higher incidence (55.3% by day 33 versus 25.7% by day42 in wild-type) than wild-type

hematopoietic system

abnormal leukocyte physiology ( J:106275 )

• larger numbers of cells from the spleen and lymph nodes of arthritic null animals migrate into the joints of arthritic mice than cells from wild-type mice

Allelic Composition	Pecam1^tm1Mak/Pecam1^tm1Mak
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pecam1^tm1Mak mutation (1 available); any Pecam1 mutation (227 available)

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

respiratory system

decreased lung endothelial cell migration ( J:110561 )

• neonatal mutant lungs show a significant reduction in wound-induced endothelial cell (EC) migration relative to wild-type lungs

• however, no significant differences in lung EC content, proliferation or survival are observed

abnormal lung morphology ( J:110561 )

• although appropriately inflated, mutant lungs display a very disorganized architecture at P1

impaired lung alveolus development ( J:110561 )

• at P7, secondary septation appears to be retarded relative to wild type mice

• postnatal mutant lungs display evidence of arrested/delayed alveolarization

• by 8 weeks of age (adult), differences in alveolarization are smaller but still present

• at P1, P7 and at 8 weeks (adult), mean alveolar areas are significantly increased while radial alveolar counts are significantly reduced, indicating impaired alveolarization

• however, no significant differences in alveolar cell apoptosis are observed by TUNEL staining

abnormal pulmonary alveolar sac morphology ( J:110561 )

• at P1, mutant primary alveolar sacs are larger than wild-type

increased pulmonary alveolus wall thickness ( J:110561 )

• at P1, mutant alveolar walls are thicker than wild-type

cellular

decreased lung endothelial cell migration ( J:110561 )

• neonatal mutant lungs show a significant reduction in wound-induced endothelial cell (EC) migration relative to wild-type lungs

• however, no significant differences in lung EC content, proliferation or survival are observed

Allelic Composition	Pecam1^tm1Mak/Pecam1⁺
Genetic Background	D1.129P2-Pecam1^tm1Mak

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pecam1^tm1Mak mutation (1 available); any Pecam1 mutation (227 available)

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

immune system

increased susceptibility to induced arthritis ( J:106275 )

• susceptibility to induced arthritis MP:0003724heterozygotes display an intermediate incidence of arthritis compared to nulls and wild-type mice

skeleton

increased susceptibility to induced arthritis ( J:106275 )

• susceptibility to induced arthritis MP:0003724heterozygotes display an intermediate incidence of arthritis compared to nulls and wild-type mice

Allelic Composition	Pecam1^tm1Mak/Pecam1^tm1Mak Pitgp^C57BL/6/Pitgp^C57BL/6
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pecam1^tm1Mak mutation (1 available); any Pecam1 mutation (227 available)
Pitgp^C57BL/6 mutation (0 available); any Pitgp mutation (0 available)

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

digestive/alimentary system

peritoneal inflammation ( J:144817 )

• restoration of inflammatory response

• normal transendothelial migration of leukocytes after thioglycollate-induced peritonitis

immune system

peritoneal inflammation ( J:144817 )

• restoration of inflammatory response

• normal transendothelial migration of leukocytes after thioglycollate-induced peritonitis

Contributing Projects: 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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