- altered response to myocardial infarction / MGI
- abnormal leukocyte adhesion / MGI
- abnormal cellular extravasation / MGI
- decreased mast cell number / MGI
- decreased susceptibility to type III hypersensitivity reaction / MGI
- abnormal Kupffer cell morphology / MGI
- impaired hematopoiesis / MGI
- abnormal neutrophil physiology / MGI
- granulomatous inflammation / MGI
- increased susceptibility to parasitic infection / MGI
- immune system phenotype / MGI
- increased susceptibility to fungal infection / MGI
C.129S4(B6)-Ccr1tm1Gao/Biat
Status | Available to order |
EMMA ID | EM:11132 |
International strain name | C.129S4(B6)-Ccr1tm1Gao/Biat |
Alternative name | 1-C |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Ccr1tm1Gao |
Gene/Transgene symbol | Ccr1 |
Information from provider
Provider | Bruno Luckow |
Provider affiliation | Nephrologisches Zentrum, Arbeitsgruppe Klinische Biochemie, Klinikum der Universitaet Muenchen, Medizinische Klinik und Poliklinik IV |
Additional owner | Original Ccr1 allele was provided by Phil Murphy without any restrictions. |
Genetic information | The chemokine receptor Ccr1 has been inactivated by homologous recombination, initially backcrossed for 6 generations to the C57BL/6J and then for 14 generations to the BALB/c genetic background. |
Phenotypic information | Homozygous:Homozygous animals appear healthy and fertile and show unchallenged no obvious phenotype. Upregulated in many infectious and inflammatory diseases. Important role in leukocyte chemotaxis and innate immunity.Heterozygous:Unknown, but most likely wildtype phenotype. |
Breeding history | Currently maintained on the background of BALB/cAnNCrl, N14+F4 |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | not known |
Information from EMMA
Archiving centre | University of Veterinary Medicine, Vienna, Austria |
Animals used for archiving | homozygous BALB/c |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- decreased mast cell number / MGI
- altered response to myocardial infarction / MGI
- impaired hematopoiesis / MGI
- lung inflammation / MGI
- decreased airway responsiveness / MGI
- decreased susceptibility to viral infection / MGI
- decreased susceptibility to bacterial infection / MGI
- abnormal macrophage physiology / MGI
- abnormal neutrophil physiology / MGI
- granulomatous inflammation / MGI
- glomerulonephritis / MGI
- increased urine protein level / MGI
- abnormal leukocyte adhesion / MGI
- increased length of allograft survival / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- increased susceptibility to parasitic infection / MGI
- glomerulosclerosis / MGI
- abnormal renal glomerulus morphology / MGI
- immune system phenotype / MGI
- increased susceptibility to fungal infection / MGI
- increased blood urea nitrogen level / MGI
- decreased susceptibility to type III hypersensitivity reaction / MGI
- increased susceptibility to type IV hypersensitivity reaction / MGI
- decreased CD4-positive, alpha beta T cell number / MGI
- decreased CD8-positive, alpha-beta T cell number / MGI
- abnormal Kupffer cell morphology / MGI
- increased IgG2a level / MGI
- increased tumor necrosis factor secretion / MGI
- decreased tumor necrosis factor secretion / MGI
- increased interferon-gamma secretion / MGI
- decreased circulating interferon-gamma level / MGI
- decreased interleukin-10 secretion / MGI
- increased interleukin-12 secretion / MGI
- decreased interleukin-13 secretion / MGI
- impaired neutrophil recruitment / MGI
- abnormal chemokine secretion / MGI
- cecum inflammation / MGI
- decreased susceptibility to bacterial infection induced morbidity/mortality / MGI
- abnormal cellular extravasation / MGI
- abnormal circulating chemokine level / MGI
- increased macrophage nitric oxide production / MGI
- glomerular crescent / MGI
Literature references
- Impaired host defense, hematopoiesis, granulomatous inflammation and type 1-type 2 cytokine balance in mice lacking CC chemokine receptor 1.;Gao J L, Wynn T A, Chang Y, Lee E J, Broxmeyer H E, Cooper S, Tiffany H L, Westphal H, Kwon-Chung J, Murphy P M, ;1997;The Journal of experimental medicine;185;1959-68; 9166425
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