Cell type-dependent difference in the distribution and frequency of excess thymidine-induced common fragile sites: T lymphocytes and skin fibroblasts

1990 ◽  
Vol 84 (6) ◽  
Author(s):  
Akira Kuwano ◽  
Ichiro Murano ◽  
Tadashi Kajii
Keyword(s):  
T Lymphocytes ◽  
Fragile Sites ◽  
Skin Fibroblasts ◽  
Cell Type ◽  
Common Fragile Sites ◽  
Excess Thymidine

The Effect of Practolol, In Vitro Generated Metabolites of Practolol and Chemical Analogues on the Rate of Growth of Human Skin Fibroblasts

1984 ◽  
Vol 12 (2) ◽  
pp. 89-97
Author(s):  
Graham R. Elliott ◽  
H.E. Amos ◽  
James W. Bridges
Keyword(s):  
Human Skin ◽  
Psoriasis Patient ◽  
Skin Fibroblasts ◽  
Human Skin Fibroblasts ◽  
Cell Type ◽  
Normal Human Skin ◽  
Rate Of Growth ◽  
Structural Analogues ◽  
Normal Human

The rate of growth of normal human skin fibroblasts was inhibited in a dose related, reversible, fashion by practolol (N-4-(2-hydroxy)-3 (1-methyl)-aminopropoxyphenylacetamine) (ID50 1.35 ± 0.14 x 10-3M), propranolol (1-(isopropylamino)-3(1-naphthyl-oxy)-2-propranolol) (ID50 0.145 ± 0.02 x 10-3M) and paracetamol (N-(4-hydroxyphenyl) acetamide) (ID50 0.85 ± 0.2 x 10-3M). Skin fibroblasts isolated from a psoriasis patient were more sensitive towards practolol (ID50 0.48 ± 0.14 x 10-3M) and propranolol (ID50 0.032 ± 0.002 x 10-3M), but less sensitive towards paracetamol (ID50 1.3 ± 0.07 x 10-3M). In vitro generated metabolites of practolol, using normal or Arochlor 1254-pretreated hamster liver preparations, and structural analogues of practolol had no effect upon the growth of either cell type.

Family study of common fragile sites

1989 ◽  
Vol 82 (2) ◽  
pp. 191-193 ◽  
Author(s):  
Yoshitsugu Sugio ◽  
Yoshikazu Kuroki
Keyword(s):  
Family Study ◽  
Fragile Sites ◽  
Common Fragile Sites

scholarly journals Increased Common Fragile Site Expression, Cell Proliferation Defects, and Apoptosis following Conditional Inactivation of Mouse Hus1 in Primary Cultured Cells

2007 ◽  
Vol 18 (3) ◽  
pp. 1044-1055 ◽  
Author(s):  
Min Zhu ◽  
Robert S. Weiss
Keyword(s):  
Cell Cycle ◽  
Cultured Cells ◽  
Chromosomal Abnormalities ◽  
Fragile Site ◽  
Loxp Site ◽  
Fragile Sites ◽  
Cell Cycle Checkpoint ◽  
Dna Breaks ◽  
Common Fragile Sites ◽  
Histone H2ax

Targeted disruption of the mouse Hus1 cell cycle checkpoint gene results in embryonic lethality and proliferative arrest in cultured cells. To investigate the essential functions of Hus1, we developed a system for the regulated inactivation of mouse Hus1 in primary fibroblasts. Inactivation of a loxP site-flanked conditional Hus1 allele by using a cre-expressing adenovirus resulted in reduced cell doubling, cell cycle alterations, and increased apoptosis. These phenotypes were associated with a significantly increased frequency of gross chromosomal abnormalities and an S-phase–specific accumulation of phosphorylated histone H2AX, an indicator of double-stranded DNA breaks. To determine whether these chromosomal abnormalities occurred randomly or at specific genomic regions, we assessed the stability of common fragile sites, chromosomal loci that are prone to breakage in cells undergoing replication stress. Hus1 was found to be essential for fragile site stability, because spontaneous chromosomal abnormalities occurred preferentially at common fragile sites upon conditional Hus1 inactivation. Although p53 levels increased after Hus1 loss, deletion of p53 failed to rescue the cell-doubling defect or increased apoptosis in conditional Hus1 knockout cells. In summary, we propose that Hus1 loss leads to chromosomal instability during DNA replication, triggering increased apoptosis and impaired proliferation through p53-independent mechanisms.

Absence of Correlations between Radiosensitivities of Human T-Lymphocytes in G 0 and Skin Fibroblasts in Log Phase

1990 ◽  
Vol 122 (3) ◽  
pp. 326 ◽  
Author(s):  
Jun-Ichi Kushiro ◽  
Nori Nakamura ◽  
Seishi Kyoizumi ◽  
Masayuki Nishiki ◽  
Kiyohiko Dohi ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Skin Fibroblasts ◽  
Human T Lymphocytes
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