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Heterokaryon studies suggest that senescent and quiescent human diploid fibroblasts (HDF) contain a common inhibitor of entry into S phase. DNA synthesis can be induced in senescent and quiescent HDF by fusing them with cells containing DNA viral oncogenes such as SV40 T antigen, adenovirus E1A, or human papillomavirus E7. Both senescent and quiescent HDF contained the unphosphorylated form (p110Rb) of the retinoblastoma protein, a putative inhibitor of proliferation. After serum stimulation, senescent HDF did not phosphorylate p110Rb and did not enter S phase, whereas quiescent HDF phosphorylated p110Rb and entered S phase. These findings, combined with the observations that T antigen, E1A, and E7 form complexes with, and presumably inactivate, unphosphorylated p110Rb, suggest that failure to phosphorylate p110Rb may be an immediate cause of failure to enter S phase in senescent HDF.
G H Stein, and
M Beeson, and
L Gordon
July 1991,
Oncogene,
G H Stein, and
M Beeson, and
L Gordon
August 1993,
The Journal of biological chemistry,
G H Stein, and
M Beeson, and
L Gordon
July 1993,
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G H Stein, and
M Beeson, and
L Gordon
January 1989,
Experimental gerontology,
G H Stein, and
M Beeson, and
L Gordon
October 1993,
Oncogene,
G H Stein, and
M Beeson, and
L Gordon
January 1992,
Cancer surveys,
G H Stein, and
M Beeson, and
L Gordon
November 1990,
The New England journal of medicine,
G H Stein, and
M Beeson, and
L Gordon
April 1995,
Human pathology,
G H Stein, and
M Beeson, and
L Gordon
January 1993,
The Journal of biological chemistry,
G H Stein, and
M Beeson, and
L Gordon
November 1994,
British journal of cancer,
