The complete amino acid sequence of human fibroblast interferon as deduced using synthetic oligodeoxyribonucleotide primers of reverse transcriptase

Houghton, Michael; Easton, M. A.; Stewart, Andrew M.; Smith, Jarrett; Doel, S. M.; Catlin, Graham; Lewis, Hilary; Patel, T.P.; Emtage, J.S.; Carey, N. H.; Porter, Andrew C.G.

doi:10.1093/nar/8.13.2885

Cited by 49 publications

(12 citation statements)

References 18 publications

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“…A cDNA clone corresponding to the mRNA encoding the major human fibroblast interferon (hIFN-,81) has been obtained and characterized (6)(7)(8). Recently, a genomic DNA segment specifying hIFN-,3l has been cloned and its sequence has been determined (9)(10)(11)(12)(13)(14) …”

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confidence: 99%

Regulated expression of human interferon beta 1 gene after transduction into cultured mouse and rabbit cells.

Canaani¹,

Berg²

1982

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

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The human interferon (31 gene has been inserted into simian virus 40 hybrid plasmid vectors carrying the bacterial phosphotransferase gene (neo), and introduced into cultured mammalian cells by DNA transfection. A majority of the transformants resistant to the antibiotic G418 were capable of synthesizing and secreting biologically active human interferon. The neo/interferon transformants contain several copies of the transfecting DNA integrated into cellular DNA sequences. In most transformants the production of human interferon and its mRNA is induced by the addition ofpoly(rI)-poly(rC); by contrast, the level of neo mRNA is not increased under the same conditions. The 5' end of the human interferon mRNA produced after induction was indistinguishable from the interferon mRNA induced in human fibroblasts. This indicates that information enabling human I31 interferon gene to be induced by poly(rI)-poly(rC) is localized to sequences within, or 5'-proximal to, the coding sequence.The induction of interferon in mammalian cells is an attractive model for studying regulation of gene expression. In contrast to hormonal stimulation, which is limited to specific cell types (1), almost all cells can be induced to produce interferons characteristic of the particular cell (2). Moreover, interferons have defined host range specificities and high specific biological activities; hence, they can be readily identified and assayed.Most fibroblast cells do not produce detectable quantities of interferon constitutively (2). But shortly after virus infection or exposure to inducers-e.g., poly(rI)-poly(rC) (2)-fibroblast interferons appear in the culture medium. Because actinomycin D blocks the induction of interferon synthesis, it has been surmised that either de novo transcription of interferon genes or stabilization of constitutively produced interferon mRNA is responsible for the inducible phenotype. Furthermore, because inhibitors of protein synthesis do not inhibit the induction of interferon mRNA (2, 3), induction is probably a primary response, much as mouse mammary tumor virus gene expression is induced by glucocorticoids (4) 5166The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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confidence: 99%

Regulated expression of human interferon beta 1 gene after transduction into cultured mouse and rabbit cells.

Canaani¹,

Berg²

1982

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

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“…Briefly we consider that the observations reported by previous investigators (25)(26)(27)(28)(29)(30) were essentially correct but that the earlier interpretations of the then available data did not fully recognize the complexities involved in the structure and expression of human IFN-/~ genes. The IFN-/~ gene family, of which only IFN-/~I has been cloned and characterized convincingly (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24), is dispersed in the human genome. We have shown earlier (12) that an IFN-/~I cDNA probe does not cross-hybridize IFN-B2 mRNA, even under rather relaxed hybridization conditions.…”

Section: Discussionmentioning

confidence: 99%

Multiple human beta interferon genes.

Sagar¹,

Sehgal²,

Slate³

et al. 1982

The Journal of Experimental Medicine

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The human a and fl interferon (IFN) gene family is even more complex than has been generally appreciated. Human interferons are classified as a (leukocyte), fl (fibroblast), and y (immune) mainly on serologic grounds (1). Several investigators (2-7) have cloned and characterized at least 8 distinct cross-hybridizing species of IFN-a cDNA and a set of up to 16 cross-hybridizing IFN-a genes and pseudogenes. These genes do not have introns (3,8), are localized to human chromosome 9 (9), and appear to correspond to mature polyadenylated mRNA of length -0.8-1.4 kilobases (kb). These are collectively referred to by us as IFN-as mRNA (I0, i I). We recently described a second heterodisperse set of translationally active IFN-a mRNA of length 1.6-3.5 kb (peak activity at 1.8 kb), designated IFN-aL, which code for interferons that are serologically of the a type, but that do not appear to cross-hybridize with as-specific DNA probes (10, 11). Several investigators have also described the molecular cloning and characterization of a single species of human IFN-fl cDNA ("/~1") (12) derived from poly(I), poly (C)-induced diploid human fibroblasts (I 3-19). Characterization of the human chromosomal DNA indicates that there exists a single gene corresponding to IFN-fll that does not have introns (20)(21)(22)(23)(24) and that can also be localized to human chromosome 9 (9). Nevertheless, earlier results of genetic experiments with somatic cell hybrids had indicated that human IFN-fl genes were located on human chromosomes 2, 5, and 9 and that the presence of any of these human chromosomes alone was sufficient for the expression of human IFN-fl in somatic cell hybrids (25-30). However, the results of these somatic cell hybrid experiments have been controversial. On the one hand, Slate and Ruddle (27, 28) obtained evidence for the involvement of chromosomes 2, 5, and 9 in IFN-fl production, while, on the other hand, Meager and his colleagues (29,30) concluded that chromosome 9 alone was involved in IFN-fl production. The latter investigators were unable to find evidence to implicate chromosomes 2 or 5, although low levels of human IFN production were observed in somatic cell hybrids lacking chromosome 9. Data presented in the present report indicate that the human IFN-fl system is quite complex and that the chromosomal localization controversy can be resolved.

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“…The nucleotide sequence analysis of about 100 bases, corresponding to the N-ternlinal region of the gene, confirmed that it coded for HuIFN-~1 of which the first 13 amino acids had been sequenced (Knight et af.~1980). The full sequence of the gene and hence of the derived protein was established independently by t\\lO other groups (Derynck et at.~1980a; Houghton et at., 1980) and published separately by the Japanese workers (Taniguchi et at., 1980a).…”

Section: Sources Of Dna For Cloning Of Ifn Genesmentioning

confidence: 99%