Evidence for linkage between HLA antigens and receptors for complement components C3b and C3d in human-mouse hybrids

Curry, Russell A.; Dierich, Manfred P.; Pellegrino, Michele; Hoch, James A.

doi:10.1007/bf01576975

Cited by 19 publications

(12 citation statements)

References 21 publications

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“…The trichloroacetic acid was extracted with HCl-acidified ether, and cAMP was measured by the isotope dilution method of Brown (12). Protein on the plates was solubilized with 0.5 M NaOH and aliquots of solubilized protein were assessed by the method of Lowry et aL (13 [20][21][22][23][24][25][26][27][28][29][30] metaphase spreads were examined for identification of human chromosomes. Human chromosome classification followed the scheme recommended by the Paris Conference (15).…”

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confidence: 99%

See 1 more Smart Citation

Chromosomal assignment of the gene for the human beta 2-adrenergic receptor.

Sheppard¹,

Wehner²,

McSwigan³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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Chinese hamster fibroblasts (CHW) fail to physiologically respond to the (-adrenergic agonist isoproterenol with an increase in cellular cAMP. This unresponsiveness is due to a lack of (3-adrenergic receptors as indicated by an absence of specific binding of '25I-labeled hydroxybenzylpindolol (125I-HYP) to CHW plasma membranes. Preparation of somatic cell hybrids between CHW and human peripheral blood leukocytes led to the selection of a panel of 15 human-Chinese hamster cell hybrid clones, some of which had P2-adrenergic receptors (specifically bound '25I-HYP) and responded to isoproterenol (accumulated cAMP). Biochemical analysis of independent cloned cell hybrids indicated that (32-adrenergic receptor density and the intensity of the associated physiological response were closely correlated (r = 0.98). Both of these parameters were concordant in all cell hybrids with the presence ofhuman chromosome 5. All other human chromosomes could be ruled out. These results suggest that the structural gene for the fi2-adrenergic receptor is found on human chromosome 5. (6,7). In an effort to examine pharmacogenetic aspects of ,3-adrenergic receptors, human-Chinese hamster cell hybrids were examined and it was observed that some of the hamster-human hybrid clones possessed 83-adrenergic receptors, were also sensitive to /3-adrenergic agonists, and exhibited characteristics ofthe ,B2 subtype. The random and preferential loss of human chromosomes from these hybrids allowed us to identify the human chromosome upon which the human P32-adrenergic gene was located. By examining the expression of specific human isozyme markers as an indication of specific human chromosomes, we demonstrate here that the structural gene for the human 82-adrenergic receptor is located on human chromosome 5. MATERIALS AND METHODSParental Cells and Hybrids. The Chinese hamster lines used were CHW-1102 (hypoxanthine phosphoribosyltransferase deficient) maintained on Dulbecco's modified Eagle's medium with 10% fetal calf serum. Fresh human leukocytes used for fusion were prepared as described (8).Human and Chinese hamster cells were fused, cloned, and maintained on hypoxanthine/aminopterin/thymidine (HAT) selection medium in Dulbecco's modified Eagle's medium with 10% fetal calf serum (8, 9). A total of 15 hybrids were examined for ,&adrenergic receptors and response. They were designated CDC as previously noted (8). ,B-Adrenergic Receptors. 3-Adrenergic receptors were measured in the hamster-human hybrids with the f3-adrenergic antagonist "2I-labeled hydroxybenzylpindolol ('25I-HYP) according to the methods of Sporn and Molinoff (10). Cells were washed twice with phosphate-buffered saline containing Ca2+ and Mg2' and scraped in phosphate-buffered saline. The preparation was swollen in 10 mM Tris HCl, pH 7.3, at 4°C for 20 min and homogenized with seven strokes ofa Teflon-glass Polyscience model RZR10 homogenizer at setting 10. The homogenate was centrifuged for 5 min at 900 X g and the supernatant was centrifuged for 20 min at 11,500 X g. ...

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“…These include receptors for viruses (21,22), diphtheria toxin (23), interferon (24), histocompatibility antigens (25), and complement (26). Nevertheless, only one other hormone receptor has been previously mapped to a human chromosome.…”

mentioning

confidence: 99%

Chromosomal assignment of the gene for the human beta 2-adrenergic receptor.

Sheppard¹,

Wehner²,

McSwigan³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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“…Subsequent biochemical and molecular characterization of the variants suggested that a highly homologous repeating unit was duplicated or deleted (reviewed in references 1 and 2) . Further, these investigations pointed out that the structural gene for CRI was not linked to HLA (10), as had been initially proposed (11,12), and also led to the discovery of a new linkage group at 1g32 of complement regulatory and receptor proteins (13,14) .…”

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confidence: 99%

The C3b/C4b receptor is recognized by the Knops, McCoy, Swain-langley, and York blood group antisera.

Nickells

Moulds

Brown

et al. 1991

The Journal of Experimental Medicine

109

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SummaryErythrocytes (E) lacking high incidence blood group antigens were screened by an antiglobulin test with a monoclonal antibody to human complement receptor type 1 (CR1 ; C3b/C4b receptor; CD35) . Some examples of E lacking Knops, McCoy, Swain-Langley, and York antigens, a serologically related group, were not agglutinated . Moreover, E of the null phenotype for these same antigens were nonreactive. To further explore this relationship, E expressing these antigens were surface labeled, solubilized, and incubated with the corresponding blood group-specific antisera. CR1 was immunoprecipitated, indicating that the epitopes recognized by each of these antisera are expressed on CR1 .

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“…I was fascinated by somatic cell hybrids between human and mouse cells; so I set up the tissue culture system for their production. These hybrids allowed us to map several human lymphocyte receptors with HLA genes (8,28,51) as well as to study alkaline phosphatase from human tumor cell lines in such hybrids (89). We also ventured into studies of other mammalian genes of interest (1,2).…”

Section: Identifying Signal Transduction Proteins In Sporulationmentioning

confidence: 99%

A Life inBacillus subtilisSignal Transduction

Hoch

2017

Annu. Rev. Microbiol.

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This is a tale of how technology drove the discovery of the molecular basis for signal transduction in the initiation of sporulation in Bacillus subtilis and in bacterial two-component systems. It progresses from genetics to cloning and sequencing to biochemistry to structural biology to an understanding of how proteins evolve interaction specificity and to identification of interaction surfaces by statistical physics. This is about how the people in my laboratory accomplished this feat; without them little would have been done.

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Evidence for linkage between HLA antigens and receptors for complement components C3b and C3d in human-mouse hybrids

Cited by 19 publications

References 21 publications

Chromosomal assignment of the gene for the human beta 2-adrenergic receptor.

Chromosomal assignment of the gene for the human beta 2-adrenergic receptor.

The C3b/C4b receptor is recognized by the Knops, McCoy, Swain-langley, and York blood group antisera.

A Life inBacillus subtilisSignal Transduction

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