Search PubMed⌕ Search

Biomedical subjects

A M Harvey

Publications and source records attributed to A M Harvey.

At least 19 recordsLinked to original sources
PubMed1993

A Century of Biomedical Science at Johns Hopkins: an interview with Dr. A. McGehee Harvey about this historic publication. Interview by Victor R. Hrehorovich and Kelly White.

Research achievements at the Johns Hopkins School of Medicine over the past century are too numerous to document in anything but a catalog. But a group of Hopkins physicians and researchers compiled a representative sample of papers documenting the intellectual history of the institution, reproducing them in a two-volume text. A discussion with one of the editors, A. McGehee Harvey, M.D., offers some insight into the process of selecting papers to be included in this historic publication.

Baltimore↗
PubMed1984

Cecil James Watson.

Explore the source record for details and available documents.

History, 20th Century↗
PubMed1983

P22 antirepressor protein prevents in vivo recA-dependent proteolysis of P22 repressor.

A method was developed to demonstrate recA-dependent P22-repressor breakdown in vivo by SDS-polyacrylamide electrophoresis of unfractionated extracts of phage-infected, lysogenic Salmonella typhimurium strains TA1530 rec+ and TA1530 recA1-. The antirepressor of P22 is not cleaved by recA protein. Under conditions of unregulated ant-overproduction (Harvey et al. 1981) antirepressor protects c2-repressor in vivo against proteolytic cleavage by recA protein.

Bacterial Proteins↗
PubMed1981

Kinetics of c2-repressor synthesis in a regulatory defective P22 mutant.

Phage P22 defective in gene 24 and harbouring the Oc mutation k5 in OR exhibits a strongly increased c2-repressor synthesis after infection of non-lysogenic S. typhimurium. The repressor synthesis depends strictly on an intact c1 gene. The kinetics of its synthesis, as monitored by polyacrylamide gel electrophoresis, is the same as with P22 c+, namely a turn off 8-10 min after infection. - After infection of P22-lysogenic bacteria with either P22 24- k5 or P22 24- k5 c1, much lower amounts of repressor are synthesized but again with the same kinetics. These results suggest a cro-like function acting at PRE and PRM of P22. The possible reason for the c2 overproduction is discussed.

Genes, Viral↗
PubMed1981

Kinetics of P22 early gene expression suggests a cro-like regulatory function.

Analysis of phage-specified protein synthesis after phage infection of UV-irradiated cells shows a turn-off of early gene expression, a regulatory event that is independent of the known P22 regulatory functions. This supports the suggestion of a cro lambda-like function in P22. We have identified the products of genes 18 and int as contributing to the complex 40,000 dalton band in our SDS-polyacrylamide gels. Both gene products appear to be subject to regulation by the cro-like function of P22. Proteins of 33,000, 29,000, 27,000, 25,000, and 24,000 MW, specified by as yet unidentified P22 genes of the early leftward operon, are regulated by the same function. Our data suggest that the cro-like function is expressed from the early rightward operon.

Electrophoresis, Polyacrylamide Gel↗
PubMed1981

Repression of ant synthesis early in the lytic cycle of phage P22.

Using SDS-polyacrylamide gel electrophoresis to study the early expression of P22 genes we show that early expression of the ant-gene (imm I region) is turned off after 6-8 min, independent of the 'late' acting mnt-repressor. A semi-clear mutant called cir5 is defective for this early ant turn-off. The mutation cir5 maps in the imm I region of P22 between genes mnt and ant. P22 cir5 mutants are defective for a repressor which acts in trans to regulate early ant synthesis. There appears to be no absolute requirement of the cir5 allele for the establishment of lysogeny. The overproduction of ant in the P22 cir5 mutant leads to a marked increase in abortive infections, killing the infected cells. The cir5-phenotype can be suppressed by an ant- mutation.

Gene Expression Regulation↗