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Biomedical subjects

M Whitford

Publications and source records attributed to M Whitford.

6 recordsLinked to original sources
PubMed1992

A structural polypeptide of the baculovirus Autographa californica nuclear polyhedrosis virus contains O-linked N-acetylglucosamine.

A structural glycopeptide, gp41, derived from the occluded virus of the baculovirus Autographa californica nuclear polyhedrosis virus was characterized. The peptide specifically bound wheat germ agglutinin but was not recognized by a panel of seven other lectins. Reactivity with wheat germ agglutinin was eliminated by treatment of gp41 with beta-N-acetylglucosaminidase, indicating that N-acetylglucosamine (GlcNAc) was present as terminal residues. gp41 was efficiently galactosylated by galactosyltransferase only in the presence of Nonidet P-40, suggesting that GlcNAc residues are not exposed on the surface of the virion. Metabolic labelling of gp41 with [3H]GlcNAc occurred in the presence of tunicamycin. The carbohydrate was released by alkaline borohydride treatment and comigrated with N-acetylglucosaminitol in descending paper chromatography. The data indicate that gp41 contains single residues of GlcNAc O glycosidically linked to the polypeptide chain. Evidence suggesting that gp41 is located in the region between the envelope membrane and the capsid (defined here as the tegument) of the occluded virus is also presented.

Acetylglucosamine↗
PubMed1992

Nucleotide sequence and transcriptional analysis of a gene encoding gp41, a structural glycoprotein of the baculovirus Autographa californica nuclear polyhedrosis virus.

We have identified and sequenced a region of the Autographa californica nuclear polyhedrosis virus (AcMNPV) genome encoding the major polyhedron-derived virus structural glycoprotein gp41. The open reading frame is located entirely within the AcMNPV SstII-M fragment. The protein sequence does not have hydrophobic regions characteristic of integral membrane proteins and contains a putative O-linked GlcNAc glycosylation site. gp41 is expressed as a late gene, with transcripts starting within two consensus late transcription start sites (TAAG) located immediately upstream of the first methionine codon. A major transcription termination signal is bypassed, possibly generating a bicistronic message. Finally, the nucleotide and protein sequences of AcMNPV and Bombyx mori nuclear polyhedrosis virus are highly conserved.

Amino Acid Sequence↗
PubMed1989

Identification and sequence analysis of a gene encoding gp67, an abundant envelope glycoprotein of the baculovirus Autographa californica nuclear polyhedrosis virus.

Monoclonal antibodies with specificity for the abundant envelope surface glycoprotein (gp67) of Autographa californica nuclear polyhedrosis virus (AcMNPV) were used to screen a lambda gt11 expression library of AcMNPV DNA fragments. The gp67 gene was mapped to the left end of the EcoRI H fragment in a right-to-left orientation on the consensus map of AcMNPV. A 2.1-kilobase transcript which hybridized to the region was first detected in cell extracts at 2 h postinfection; it peaked in abundance at 18 h postinfection and thereafter was present at lower levels. The nucleotide sequence of the region was determined, and a 1,590-nucleotide open reading frame flanked by an AT-rich sequence was identified that could encode a polypeptide with 529 amino acid residues (molecular mass of 60,167 daltons). Computer analysis indicated that the peptide possesses two hydrophobic regions near the N and C termini as well as six potential N-linked glycosylation sites. We suggest that following cleavage of a signal peptide, the polypeptide undergoes further processing and becomes anchored at its C terminus in the virus envelope. The final seven amino acid residues at the C terminus contain basic amino acids and may have a role in virion assembly.

Amino Acid Sequence↗
PubMed1980

Clinical and pharmacokinetic factors affecting response to phenelzine.

Sixty patients, 30 with depressive neurosis, 15 with anxiety neurosis and 15 with phobic anxiety states, were treated with the monoamine oxidase inhibitor, phenelzine, in two different dosage schedules for four weeks. All patients received an initial dose of 15 mg daily, increasing to 30 mg daily between the third and seventh day, but subsequently, using double-blind procedure, one group tooke the commonly prescribed dose of 45 mg daily and the other took 90 mg daily. Acetylator status was independently determined before the start of treatment. Each diagnostic group showed a similar response to treatment, but patients taking the higher dose improved significantly more than those taking normal dosage, and the rate of improvement, measured by weekly self-ratings, was also more rapid with higher dosage. Acetylator status did not affect clinical response. The results suggest that dosage is more important in determining clinical response to phenelzine in neurotic disorder than specific diagnosis or acetylator status.

Anxiety Disorders↗