Nucleotide sequence of the cDNA from the mouse leukocyte adhesion protein CD18

Wilson, Raymond W.; O’Brien, William E.; Beaudet, Arthur L.

doi:10.1093/nar/17.13.5397

Cited by 37 publications

(11 citation statements)

References 3 publications

(2 reference statements)

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“…Two alleles were identified, differing by eight silent substitutions (C57T, A87G, T138C, C261T, T312C, T429C, G489A and A525G). The region immediately preceding the ATG start codon is roughly similar to that in other species, containing the sequence AG (n) AC, where n = 5 in the mouse (Wilson et al, 1989), n = 4 in the sheep (present study) and the bovine (Shuster et al, 1992), and n = 3 in the human (Kishimoto et al, 1987), which pleads for a regulatory role of this motif. The mature OvCD18 contains a 22-aa putative leader peptide, an extracellular domain of 679 residues (23 -701), a single hydrophobic transmembrane region of 23 residues (702 -724) and a short cytoplasmic tail of 46 residues (Fig.…”

Section: Characterisation Of Ovcd18-encoding Cdna and Deduced Aa Sequsupporting

confidence: 61%

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Molecular cloning and characterisation of the CD18 partner in ovine (Ovis aries) β2-integrins

Zecchinon

Fett

Baise

et al. 2004

Gene

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Section: Characterisation Of Ovcd18-encoding Cdna and Deduced Aa Sequsupporting

confidence: 61%

“…Overall, the general organization of ovine, human (Weitzman et al, 1991), murine (Wilson et al, 1989) and bovine (Shuster et al, 1992) CD18 proteins is quite similar (Fig. 2).…”

Section: Comparison Among Speciesmentioning

confidence: 89%

Molecular cloning and characterisation of the CD18 partner in ovine (Ovis aries) β2-integrins

Zecchinon

Fett

Baise

et al. 2004

Gene

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“…Previously, a construct for homologous recombination in the CD18 gene was prepared by screening a murine genomic DNA library using the mouse cDNA clone p17.4 as a probe for CD18 gene (37). A single clone containing exons 1-3 was isolated and a construct for homologous recombination was prepared as published earlier (38).…”

Section: Nature Of the Targeting Mutationmentioning

confidence: 99%

Identification of Susceptibility Loci for Skin Disease in a Murine Psoriasis Model

Keß

Lindqvist

Peters

et al. 2006

The Journal of Immunology

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Psoriasis is a frequently occurring inflammatory skin disease characterized by thickened erythematous skin that is covered with silvery scales. It is a complex genetic disease with both heritable and environmental factors contributing to onset and severity. The CD18 hypomorphic PL/J mouse reveals reduced expression of the common chain of β2 integrins (CD11/CD18) and spontaneously develops a skin disease that closely resembles human psoriasis. In contrast, CD18 hypomorphic C57BL/6J mice do not demonstrate this phenotype. In this study, we have performed a genome-wide scan to identify loci involved in psoriasiform dermatitis under the condition of low CD18 expression. Backcross analysis of a segregating cross between susceptible CD18 hypomorphic PL/J mice and the resistant CD18 hypomorphic C57BL/6J strain was performed. A genome-wide linkage analysis of 94 phenotypically extreme mice of the backcross was undertaken. Thereafter, a complementary analysis of the regions of interest from the genome-wide screen was done using higher marker density and further mice. We found two loci on chromosome 10 that were significantly linked to the disease and interacted in an additive fashion in its development. In addition, a locus on chromosome 6 that promoted earlier onset of the disease was identified in the most severely affected mice. For the first time, we have identified genetic regions associated with psoriasis in a mouse model resembling human psoriasis. The identification of gene regions associated with psoriasis in this mouse model might contribute to the understanding of genetic causes of psoriasis in patients and pathological mechanisms involved in development of disease.

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“…These experiments are now also done with the alpha-subunit cDNA [58]. Furthermore, we use the mouse CD18 beta-chain cDNA which was recently cloned [59]. The latter experiments should yield transfectants expressing the mouse intraspecies dimer, which should be functional, and the metastatic capacity of which can be tested in syngeneic rather than immune-deprived mice.…”

Section: Invasiveness Of Revertants and Transfectantsmentioning

confidence: 99%

Adhesion molecules in lymphoma metastasis

Roos

1991

Cancer Metast Rev

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Recently, many surface proteins of lymphoid cells that mediate adhesion to other cells and extracellular matrix have been identified. Several of these cellular adhesion molecules (CAM) are also expressed by metastatic lymphoma cells and may mediate adhesion to tissue components during the metastatic process. Correlations observed between expression of certain CAM, like MEL-14 and CD44, and particular patterns of spread, support this notion, but conclusive evidence is scarce. We have used T-cell hybridomas to study the mechanisms of wide-spread lymphoid metastasis. The results obtained with this model are reviewed here. The advantages are that a large number of genetically similar cell lines can be generated, which can be grouped in large panels of highly invasive and non-invasive cells. Invasiveness of these cells in hepatocyte and fibroblast monolayers correlates with experimental metastasis. Lymphoid CAM that are potentially involved in metastasis are reviewed. Several of these CAM are not, or not consistently, expressed by the invasive T-cell hybridomas, indicating that they are not indispensable. Notably, some of the CAM involved in the onset of an immune response or in migration into inflamed tissues, like ICAM-1 and VLA-4, and the 'homing receptors' MEL-14 and LPAM-1 do not seem to be involved. CAM that are consistently expressed by the T-cell hybrids include LFA-1, the beta-1 integrin subunit CD29, CD31 (PECAM-1) and CD44 ('Hermes homing receptor'). We have generated considerable evidence that LFA-1 is required for efficient metastasis of T-cell hybrids, based on the behavior of LFA-1-deficient mutants and revertants. High levels of LFA-1 are required. The relevant counterstructure is probably ICAM-2 rather than ICAM-1. Preliminary results suggest that also a beta-1 integrin, possibly VLA-5, plays a role. Finally, we summarize evidence indicating that CD31 and CD44 are primary candidates for involvement in metastatic spread of T-cell hybridomas.

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Nucleotide sequence of the cDNA from the mouse leukocyte adhesion protein CD18

Cited by 37 publications

References 3 publications

Molecular cloning and characterisation of the CD18 partner in ovine (Ovis aries) β2-integrins

Molecular cloning and characterisation of the CD18 partner in ovine (Ovis aries) β2-integrins

Identification of Susceptibility Loci for Skin Disease in a Murine Psoriasis Model

Adhesion molecules in lymphoma metastasis

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