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N Stewart

Publications and source records attributed to N Stewart.

At least 37 records · Page 2Linked to original sources
PubMed1995

Evidence for a second cell cycle block at G2/M by p53.

Wild type p53 can induce cell cycle arrest at specific points in the cell cycle, in particular G1/S, an ability lost by most p53 mutants. We have previously reported that p53 mutant genes can rescue REF52 cells from ras-induced growth arrest and that over expression of wild type p53 inhibits cell growth in these cells. In this paper we examined whether p53 can also induce cell cycle arrest at the G2/M boundary of the cell cycle. To accomplish this we used the REF52 cell line and the temperature sensitive p53val135 mutant allele. Cells were enriched in the late G1 and early S phases before the temperature shift. REF52 cells expressing mutant-p53val135 alone with an activated H-ras gene arrest primarily at the G1/S and G2/M parts of the cell cycle at the restrictive temperature, as determined by flow cytometry analysis. These results suggest that the anti-proliferative activity of p53 may be involved in regulation of the cell cycle at the G2/M restriction point as well as transit through G1/S and initiation of DNA synthesis.

Animals↗
PubMed1994

Induction of genomic instability in SV40 transformed human cells: sufficiency of the N-terminal 147 amino acids of large T antigen and role of pRB and p53.

Genomic instability is an early event in the transformation of human cells by SV40 and may contribute, as a mutagenic process, to the generation of the rare cells which survive crisis and yield immortal populations. We have previously reported that expression of large T antigen is responsible for induction of chromosome aberrations and aneuploidy. In the present study we have demonstrated that the amino terminal 147 amino acids of the protein are as proficient as full length T antigen for this destabilization of the cell genome. Analysis of mutants within this region indicated that T antigens defective for binding to pRB or lacking the first 127 amino acids are significantly reduced in their ability to induce aneuploidy and/or aberrations, whereas a cytoplasmic T antigen is less severely impaired. In addition, we have shown that binding of T antigen to p53 is dispensable for genome destabilization but may be required for continued proliferation of genetically aberrant cells.

Amino Acids↗
PubMed1993

Are adolescent suicide attempters noncompliant with outpatient care?

The outpatient clinic attendance patterns of 115 consecutively referred 10- to 18-year-old suicide attempters and of 110 nonattempters were compared. The two groups did not differ in number of appointments scheduled or missed, but attempters kept significantly fewer appointments than did nonattempters. Seventy-seven percent of each group dropped out of treatment, but attempters dropped out significantly faster. Attendance and dropout were unrelated to age, reason for referral, or previous attempts. Girls missed more appointments than did boys, and Hispanic patients kept a smaller percentage of scheduled appointments than did other ethnic groups. We conclude that adolescent attempters are not more likely to drop out of treatment but keep fewer appointments and remain in care more briefly than do other outpatients. Recommendations for triage and brief case management are made.

Adolescent↗
PubMed1991

Expression of SV40 large T antigen, but not small t antigen, is required for the induction of chromosomal aberrations in transformed human cells.

Expression of the Simian virus 40 (SV40) early region in human cells results in the induction of chromosomal aberrations and polyploidy, and in transformation. To understand how genetic damage occurs and what role it plays in transformation, human diploid fibroblasts and embryonic kidney cells were transfected with plasmids encoding wild type or mutant forms of the viral early region, and the neo gene. Clones selected for G418 resistance and expressing viral genes were initially analyzed within 20 cell divisions. Our results demonstrate that expression of the SV40 large T antigen is sufficient for the induction of chromosomal damage and ploidy changes, and that small t does not contribute to these processes. Mutant plasmids lacking the SV40 origin of DNA replication were as proficient as wild type plasmids, indicating that viral DNA replication is not required for cytogenetic damage. We have also shown that chromosome aberrations, but not necessarily polyploidy, increase in frequency and complexity upon subculturing of the clones regardless of whether such populations arrest at crisis or yield immortal lines. Our results are compatible with the hypothesis that large T antigen destabilizes the cellular genome, and that specific mutations arising from this process may contribute to cell immortalization.

Antibodies, Monoclonal↗
PubMed1988

Bargaining point.

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Economics, Nursing↗
PubMed1987

Benchmark of NHS.

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Health Expenditures↗