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L T May

Publications and source records attributed to L T May.

58 records · Page 4Linked to original sources
PubMed1983

Isolation of novel human genomic DNA clones related to human interferon-beta 1 cDNA.

Southern blot-hybridization analyses of human DNA (from Namalwa lymphoblastoid cells) digested with the restriction endonuclease EcoRI were carried out under optimal conditions with two human fibroblast interferon (IFN-beta 1) cDNA probes, pD19 and pD24, which contain IFN-beta 1 inserts 0.8 and 0.7 kilobase (kb) long, respectively. The analyses revealed the presence of several hybridizable DNA fragments, including two of lengths 6.8 and 5.5 kb, in addition to the classical IFN-beta 1 genomic DNA fragment of length approximately equal to 2.0 kb. We have screened a human DNA library in lambda bacteriophage Charon 4A by using a 32P-labeled IFN-beta 1 insert cDNA (pD24) and thereby isolated six strongly positive human genomic DNA clones. One of these (lambda B37) represents the classical human IFN-beta 1 gene; another (lambda B37) contains a 6.8-kb EcoRI DNA fragment(s) which cross-hybridizes with the IFN-beta 1 cDNA insert probes pD19 and pD24; and the remaining four (which are identical to each other and are exemplified by lambda B4) contain two EcoRI DNA fragments approximately 5.5 and 9 kb long which also cross-hybridize the IFN-beta 1 cDNA probes. A mRNA 0.9 kb long derived from the classical IFN-beta1 gene is expressed in poly(I) . poly(C)-induced human diploid fibroblasts (FS-4 strain). Induced FS-4 cells also contain polyadenylylated RNA 1.8, 3, 5, and approximately equal to 8 kb long derived from the lambda B3 gene, all of which appear to code for biologically active human IFN-beta as tested by using the Xenopus laevis oocyte translation assay. These data strongly indicate that lambda B3 represents a novel functional IFN-beta gene. A 12-kb polyadenylylated RNA, derived from lambda B4, is expressed constitutively at a low level in FS-4 cells, but the amount of this RNA increases 5-7 hr after exposure of the cells to poly(I) . poly(C).

Base Sequence↗
PubMed1982

Unusually long mRNA species coding for human alpha and beta interferons.

Each of the several intronless interferon (IFN) alpha S genes is embedded in 4- to 5-kilobase (kb) DNA homology units which are arranged more or less in tandem in the human genome. In addition to the expected 0.8- to 1.4-kb-long IFN-alpha S mRNA species, we have detected polyadenylylated RNA molecules approximately 2-2.7, 3.5-4.5, and 7-8 kb long derived from IFN-alpha S genes in the cytoplasm of Sendai virus-induced bromodeoxyuridine-treated human lymphoblastoid (Namalwa) cells. These transcripts were detected by electrophoresis of cytoplasmic polyadenylylated RNA through agarose-CH3HgOH gels followed by blothybridization using an IFN-alpha 1 (a prototype alpha S) cDNA probe and also by translation of the eluted RNA into biologically active IFN in the Xenopus oocyte assay. At least some of these long translationally active RNA molecules appear to represent functional mRNA species because they can be detected in polysomes. In addition, the oocyte translation assay has revealed the presence of unusually long (2-8 kb) IFN-beta mRNA species both in Sendai virus-induced Namalwa cells and in poly(I) . poly(C)-induced diploid human fibroblasts (FS-4). The detection of very long IFN-alpha 1-related mRNA species suggests that some of the DNA sequence features observed in the flanking homology units may affect the transcription of the IFN-alpha S genes. Our hybridization analyses also indicate that the 1.8-kb human IFN-alpha L mRNA(s) shows no detectable cross-hybridization with an IFN-alpha 1 cDNA probe. Thus, this mRNA is derived from a gene(s) that is distinct from the IFN-alpha S set.

Cell Line↗
PubMed1978

Limited effect of erythrocyte and plasma infusions in adenosine deaminase deficiency.

A 10-month-old child with a profound deficiency of adenosine deaminase and severe combined immunodeficiency was treated for a period of 17 months with red cell and plasma transfusions containing normal amounts of the deficient enzyme. Following each transfusion, the plasma adenosine, red cell and lymphocyte ATP, urinary adenine, and urinary deoxyadenosine decreased transiently. During this period, the absolute blood lymphocyte count rose and a limited increased in the response of the lymphocytes to PHA-P was observed. Delayed hypersensitivity skin tests remained negative during the transfusion periods. A quantitative elevation of serum immunoglobulins occurred, but specific antibody formation was not elicited. In contrast to a previous report of successful therapy of ADA deficiency with red cell and plasma infusions, this patient responded poorly to enzyme replacement therapy. The difference may be related to a more profound enzyme deficiency in our patient.

Adenine↗