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Biomedical subjects

M Gefter

Publications and source records attributed to M Gefter.

22 records · Page 2Linked to original sources
PubMed1966

Methylation of DNA.

The methylated bases of DNA are formed by the transfer of the methyl group from S-adenosylmethionine to a polynucleotide acceptor. This transfer is catalyzed by highly specific enzymes which recognize a limited number of available sites in the DNA. The mechanism for the recognition is presently unknown. In some instances, there is evidence that other cellular components, such as lipopolysaccharides, can influence the methylation reaction. Certain bacteriophages induce new methylases upon infection of their hosts. Phage T3 is unique in establishing an environment in which methylation of neither the phage nor the host nucleic acid can occur. By superinfecting T3-infected cells with other phages, the latter can be obtained with methyl-deficient DNA. Although a great deal is known about the enzymology of the methylation reaction, and there appears to be a strong correlation between the in vitro and in vivo reactions, studies in which DNA is either supermethylated or totally unmethylated have not yielded any insight as to what the possible function of the methylated bases may be.

Alkylation↗
PubMedDate not supplied

Role of gamma-interferon in antibody-producing responses.

Interferon preparations, especially those containing gamma-interferon (IFN-gamma), have long been known to modulate immune responses. However, because many studies used only partially purified interferons, it has been difficult to separate the immunoregulatory effects of the interferons from those of other biologically active molecules contaminating the preparations. Recently, with the cloning of the interferon genes in mouse and man, it has become possible to use these cloned interferons directly to test their effects in assays other than those involving the protection of cells from viruses. For example, cloned IFN-gamma has been shown to be a potent inducer of Ia antigen expression on macrophages. Similarly, cloned IFN-gamma has been reported to act as a macrophage activation factors, as judged by the ability of activated macrophages to kill tumour cells in vitro. We demonstrate here that cloned murine IFN-gamma can also substitute for a late-acting helper factor which acts synergistically with other helper factors in the stimulation of B-cell antibody responses in vitro.

Animals↗