D
D Lin
Researcher at Thomas Jefferson University
Publications - 8
Citations - 9181
D Lin is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Cell cycle & Gene expression. The author has an hindex of 7, co-authored 8 publications receiving 9009 citations.
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Journal ArticleDOI
WAF1, a potential mediator of p53 tumor suppression
Wafik S. El-Deiry,Takashi Tokino,Victor E. Velculescu,Daniel B. Levy,Ramon Parsons,Jeffrey M. Trent,D Lin,W. Edward Mercer,Kenneth W. Kinzler,Bert Vogelstein +9 more
TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
Journal ArticleDOI
Growth arrest induced by wild-type p53 protein blocks cells prior to or near the restriction point in late G1 phase.
TL;DR: It is shown that growth arrest occurs prior to or near the restriction point in late G1 phase of the cell cycle, which is more precisely localized than ever before.
Journal ArticleDOI
Growth suppression induced by wild-type p53 protein is accompanied by selective down-regulation of proliferating-cell nuclear antigen expression.
TL;DR: It is shown that inhibition of cell cycle progression into S-phase after induction of wild-type p53 protein is accompanied by selective down-regulation of proliferating-cell nuclear antigen mRNA and protein expression.
Journal Article
Mutation of the serine 15 phosphorylation site of human p53 reduces the ability of p53 to inhibit cell cycle progression.
Michele Fiscella,Ullrich Sj,Nicola Zambrano,Shields Mt,D Lin,Susan P. Lees-Miller,Carl W. Anderson,W E Mercer,E Appella +8 more
TL;DR: The inability of p53-Ala-15 to fully block cell cycle progression was not due to inadequate levels of expression or to a failure of the mutant protein to accumulate in the nucleus, and results suggest that phosphorylation of Ser-15 may affect p53 function.
Journal ArticleDOI
Constitutive expression of B-myb can bypass p53-induced Waf1/Cip1-mediated G1 arrest.
D Lin,M Fiscella,Patrick M. O'Connor,J Jackman,M Chen,L L Luo,A Sala,S Travali,E Appella,W E Mercer +9 more
TL;DR: It is shown that B- myb expression is required for cells to progress from G1 into S phase and that high levels of ectopic B-myb expression uncoupled from cell cycle regulation rescues cells from p53-induced G1 arrest even in the presence of Waf1/Cip1 transactivation and inhibition of cyclin E/Cdk2 kinase activity.