Extension of Life-Span by Introduction of Telomerase into Normal Human Cells

Science ◽  
1998 ◽  
Vol 279 (5349) ◽  
pp. 349-352 ◽  
Author(s):  
A. G. Bodnar
Keyword(s):  
Life Span ◽  
Human Cells ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals Analysis of Genomic Integrity and p53-Dependent G1Checkpoint in Telomerase-Induced Extended-Life-Span Human Fibroblasts

1999 ◽  
Vol 19 (3) ◽  
pp. 2373-2379 ◽  
Author(s):  
Homayoun Vaziri ◽  
Jeremy A. Squire ◽  
Tej K. Pandita ◽  
Grace Bradley ◽  
Robert M. Kuba ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Life Span ◽  
P53 Protein ◽  
Human Fibroblasts ◽  
Strand Break ◽  
Human Cells ◽  
Normal Human ◽  
Normal Human Cells ◽  
Extended Life

ABSTRACT Life span determination in normal human cells may be regulated by nucleoprotein structures called telomeres, the physical ends of eukaryotic chromosomes. Telomeres have been shown to be essential for chromosome stability and function and to shorten with each cell division in normal human cells in culture and with age in vivo. Reversal of telomere shortening by the forced expression of telomerase in normal cells has been shown to elongate telomeres and extend the replicative life span (H. Vaziri and S. Benchimol, Curr. Biol. 8:279–282, 1998; A. G. Bodnar et al., Science 279:349–352, 1998). Extension of the life span as a consequence of the functional inactivation of p53 is frequently associated with loss of genomic stability. Analysis of telomerase-induced extended-life-span fibroblast (TIELF) cells by G banding and spectral karyotyping indicated that forced extension of the life span by telomerase led to the transient formation of aberrant structures, which were subsequently resolved in higher passages. However, the p53-dependent G1 checkpoint was intact as assessed by functional activation of p53 protein in response to ionizing radiation and subsequent p53-mediated induction of p21Waf1/Cip1/Sdi1. TIELF cells were not tumorigenic and had a normal DNA strand break rejoining activity and normal radiosensitivity in response to ionizing radiation.

scholarly journals Knockdown of αII spectrin in normal human cells by siRNA leads to chromosomal instability and decreased DNA interstrand cross-link repair

2009 ◽  
Vol 381 (2) ◽  
pp. 288-293 ◽  
Author(s):  
Laura W. McMahon ◽  
Pan Zhang ◽  
Deepa M. Sridharan ◽  
Joel A. Lefferts ◽  
Muriel W. Lambert
Keyword(s):  
Chromosomal Instability ◽  
Human Cells ◽  
Cross Link ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals DNA amplification is rare in normal human cells.

1990 ◽  
Vol 87 (5) ◽  
pp. 1791-1795 ◽  
Author(s):  
J. A. Wright ◽  
H. S. Smith ◽  
F. M. Watt ◽  
M. C. Hancock ◽  
D. L. Hudson ◽  
...  
Keyword(s):  
Dna Amplification ◽  
Human Cells ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals Reduction of X-ray-induced DNA damage in normal human cells treated with the PrC-210 radioprotector

Biology Open ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. bio035113 ◽  
Author(s):  
Michael Brand ◽  
Matthias Sommer ◽  
Frank Jermusek ◽  
William E. Fahl ◽  
Michael Uder
Keyword(s):  
Dna Damage ◽  
Human Cells ◽  
X Ray ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals Qualitative and quantitative difference in mutation induction between carbon- and neon-ion beams in normal human cells.

2003 ◽  
Vol 17 (4) ◽  
pp. 302-306 ◽  
Author(s):  
Masao Suzuki ◽  
Chizuru Tsuruoka ◽  
Tatsuaki Kanai ◽  
Takeshi Kato ◽  
Fumio Yatagai ◽  
...  
Keyword(s):  
Quantitative Difference ◽  
Ion Beams ◽  
Human Cells ◽  
Mutation Induction ◽  
Qualitative And Quantitative ◽  
Normal Human ◽  
Normal Human Cells ◽  
Neon Ion
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