Gene for a major cell surface glycoprotein of mouse macrophages and other phagocytic cells is on chromosome 2.

Colombatti, Alfonso; Hughes, Edward N.; Taylor, Benjamin A.; August, J. Thomas

doi:10.1073/pnas.79.6.1926

Cited by 51 publications

(13 citation statements)

References 36 publications

(27 reference statements)

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“…By comparison, the frequency of cells bearing Ly-24, the major surface glycoprotein of phagocytic cells (20,21), and the density of Ly-24 antigens per cell was greatly increased in lpr as compared with normal SJL mice (Table I and Fig. 2).…”

Section: Lymphoproliferation In Mice Homozygous For Lprmentioning

confidence: 99%

“…The frequency of cells bearing markers not previously examined in lpr mice was also determined. These include Lyb-2 (24), the B cell-specific antigen; Ly-17 (18), the granulocyte-specific marker; "8C5" (R. L. Coffman, H. C. Morse III, unpublished observations), the myelomonocytic determinant; Mac-1 (19), and an antigen expressed by the great majority of hematopoietic cells of all lineages, Ly-24 (20,21). The frequencies of Lyb-2 + and Ly-17 + cells in both lpr/ lpr and normal tissues corresponded closely to the frequencies of B cells defined by expression of sIg, ThB or Ia ( Table I), emphasizing that the only B cell determinant greatly altered in expression on lpr cells is Ly-5(B220).…”

Section: Lymphoproliferation In Mice Homozygous For Lprmentioning

confidence: 99%

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Abnormalities induced by the mutant gene, lpr. Patterns of disease and expression of murine leukemia viruses in SJL/J mice homozygous and heterozygous for lpr.

Morse¹,

Roths²,

Davidson³

et al. 1985

The Journal of Experimental Medicine

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The lpr locus was defined by an autosomai recessive mutation initially observed in strain MRL (1). Whereas nonmutant mice of this strain develop late-onset autoimmune disease characterized by chronic glomerulonephritis, MRL-lpr/lpr mice experience severe ear!y-onset subacute glomerulonephritis, arteritis, and arthritis associated with massive lymphadenopathy and splenomegaly (1-3). The lymph nodes and spleens of lpr homozygotes are expanded by an abnormal population of cells that coexpress cell surface determinants usually restricted to T cells (Thy-1, Ly-1) or B cells [Ly-5(B220)] (4-9), and are deficient in their ability to produce interleukin 2 (IL-2) 1 (9-12). These aberrant cells were clearly shown not to be B cells, in that they had no rearrangements of Ig heavy chain genes (6). MRL-lpr/+ resemble MRL-+/+ mice in terms of disease patterns, longevity, and phenotypic and functional characteristics of their lymphocytes, indicating that the mutation is fully recessive in this strain.To determine if this mutation would produce similar abnormalities when present on other genetic backgrounds, lpr was backcrossed onto strains NZB/BINJ, SJL/J, C3H/HeJ, AKR/J, C57BL/6J, and BALB/cJ. Ongoing phenotypic, functional, and histopathologic studies of mice (from these strains) homozygous for lpr have shown that, although aberrant T cells were detected in the lymphoid tissues of mice from all strains (6, 9, and H. C. Morse III, W. F. Davidson, and J. B. Roths, unpublished observations), lpr/lpr mice differed considerably among strains in the degree of lymphadenopathy they exhibited, as well as in their longevity and rates of development, and severity of the autoimmune disease they incurred (5, 9-13, and J. B. Roths and E. D. Murphy, unpublished observations).During the course of these studies, it was noted that the survival of SJL-lpr/+ mice was shortened in comparison to SJL-+/+ mice, suggesting that, in this strain, lpr had an effect in the heterozygous state. To evaluate this possibility,

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Section: Lymphoproliferation In Mice Homozygous For Lprmentioning

confidence: 99%

Section: Lymphoproliferation In Mice Homozygous For Lprmentioning

confidence: 99%

Abnormalities induced by the mutant gene, lpr. Patterns of disease and expression of murine leukemia viruses in SJL/J mice homozygous and heterozygous for lpr.

Morse¹,

Roths²,

Davidson³

et al. 1985

The Journal of Experimental Medicine

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“…GP80 (also referred to as pgp-1) was identified by a mAb raised against mouse fibroblasts Trowbridge et al, 1982). The antigen has been characterized biochemically and genetically 1982;Colombatti et al,, 1982). GP80 is present in high copy number, about 106/ce11.…”

mentioning

confidence: 99%

Analysis of lateral redistribution of a plasma membrane glycoprotein- monoclonal antibody complex [corrected] [published erratum appears in J Cell Biol 1988 Apr;106(4):following 1403]

Ishihara

Holifield

Jacobson

1988

The Journal of Cell Biology

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Abstract. The lateral redistribution of a major murine glycoprotein, GP80, was studied on locomoting fibroblasts, using rhodamine-conjugated mAbs and ultralow light level digitized fluorescence microscopy. Confirming an earlier study (Jacobson, K., D. O'Dell, B. Holifield, T. L. Murphy, and J. T. August. 1984. J. Cell Biol. 99:1613-1623, the distribution of GP80 was coupled with cell locomotion; motile cells exhibited a gradated distribution of the GP80-mAb complex over the cell surface, increasing from the front to the rear, whereas stationary cells exhibited a nearly uniform GP80 distribution. By monitoring locomoting single cells, we found the gradated fluorescence distribution to be maintained as an approximate steady state. Newly extended leading edges were almost devoid of the fluorescence labeling. This was strikingly demonstrated in prechilled cells in which the extension of fluorescence-free leading edges caused a pronounced boundary between fluorescent and nonfluorescent zones. Subsequently this boundary eroded gradually in a manner consistent with diffusional relaxation. Evidence indicated that the GP80 redistribution was primarily caused by the lateral motion of GP80 in the plasma membrane and not via intracellular membrane traffic. Two cell locomotion models which, in principle, could account for the GP80 redistribution were tested: the retrograde lipid flow (RLF) model (Bretscher, M. S., 1984. Science (Wash. DC).224:681-686) and an alternative hypothesis, the retraction-induced spreading (RIS) model. The predictions of these models were simulated by computer and compared with experiment to assess which model was more appropriate. Whereas both models predicted steady-state gradients similar to the experimental result, only the RIS model predicted the lack of retrograde movement of the fluorescent boundary.

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“…CD44 is a large, highly conserved, and complex gene containing 19 exons located on human chromosome 11 [2] and mouse chromosome 2 [3]. The predominant CD44 transcript (exons 1–5 and 16–20) produces the standard or haemopoietic form of CD44 (CD44s or CD44h) [4].…”

Section: Introductionmentioning

confidence: 99%

CD44 Expression in Oro-Pharyngeal Carcinoma Tissues and Cell Lines

et al. 2012

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Expression of CD44, a transmembrane hyaluronan-binding glycoprotein, is variably considered to have prognostic significance for different cancers, including oral squamous cell carcinoma. Although unclear at present, tissue-specific expression of particular isoforms of CD44 might underlie the different outcomes in currently available studies. We mined public transcriptomics databases for gene expression data on CD44, and analyzed normal, immortalized and tumour-derived human cell lines for splice variants of CD44 at both the transcript and protein levels. Bioinformatics readouts, from a total of more than 15,000 analyses, implied an increased CD44 expression in head and neck cancer, including increased expression levels relative to many normal and tumor tissue types. Also, meta-analysis of over 260 cell lines and over 4,000 tissue specimens of diverse origins indicated lower CD44 expression levels in cell lines compared to tissue. With minor exceptions, reverse transcribed polymerase chain reaction identified expression of the four main isoforms of CD44 in normal oral keratinocytes, transformed lines termed DT and HaCaT, and a series of paired primary and metastasis-derived cell lines from oral or pharyngeal carcinomas termed HN4/HN12, HN22/HN8 and HN30/HN31. Immunocytochemistry, Western blotting and flow cytometric assessments all confirmed the isoform expression pattern at the protein level. Overall, bioinformatic processing of large numbers of global gene expression analyses demonstrated elevated CD44 expression in head and neck cancer relative to other cancer types, and that the application of standard cell culture protocols might decrease CD44 expression. Additionally, the results show that the many variant CD44 exons are not fundamentally deregulated in a diverse range of cultured normal and transformed keratinocyte lines.

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Gene for a major cell surface glycoprotein of mouse macrophages and other phagocytic cells is on chromosome 2.

Cited by 51 publications

References 36 publications

Abnormalities induced by the mutant gene, lpr. Patterns of disease and expression of murine leukemia viruses in SJL/J mice homozygous and heterozygous for lpr.

Abnormalities induced by the mutant gene, lpr. Patterns of disease and expression of murine leukemia viruses in SJL/J mice homozygous and heterozygous for lpr.

Analysis of lateral redistribution of a plasma membrane glycoprotein- monoclonal antibody complex [corrected] [published erratum appears in J Cell Biol 1988 Apr;106(4):following 1403]

CD44 Expression in Oro-Pharyngeal Carcinoma Tissues and Cell Lines

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