Assignment of aMus musculus gene for triosephosphate isomerase to chromosome 6 and for Glyoxalase-I to chromosome 17 using somatic cell hybrids

1978 ◽  
Vol 4 (2) ◽  
pp. 241-252 ◽  
Author(s):  
John D. Minna ◽  
Gail A. P. Bruns ◽  
Andrew H. Krinsky ◽  
Peter A. Lalley ◽  
Uta Francke ◽  
...  
Keyword(s):  
Somatic Cell ◽  
Triosephosphate Isomerase ◽  
Chromosome 17 ◽  
Glyoxalase I ◽  
Chromosome 6 ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids

Regional submapping of human chromosome 6 by the use of human-mouse somatic cell hybrids

1978 ◽  
Vol 22 (1-6) ◽  
pp. 412-414 ◽  
Author(s):  
K.-H. Grzeschik ◽  
A. Mayerová ◽  
K. Bender ◽  
R. Johannsmann
Keyword(s):  
Human Chromosome ◽  
Somatic Cell ◽  
Chromosome 6 ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids ◽  
Human Chromosome 6 ◽  
Mouse Somatic Cell

Assignment of the human acid ?-glucosidase gene (?GLU) to chromosome 17 using somatic cell hybrids

1979 ◽  
Vol 42 (3) ◽  
pp. 273-281 ◽  
Author(s):  
ELLEN SOLOMON ◽  
DALLAS SWALLOW ◽  
SUZANNE BURGESS ◽  
LORRAINE EVANS
Keyword(s):  
Somatic Cell ◽  
Chromosome 17 ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids ◽  
Human Acid

scholarly journals Assignment of the myeloperoxidase geneMPO to human chromosome 17 using somatic cell hybrids and flow-sorted chromosomes

1988 ◽  
Vol 33 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Jun Kudoh ◽  
Shinsei Minoshima ◽  
Kazuya Hashinaka ◽  
Chika Nishio ◽  
Michiyuki Yamada ◽  
...  
Keyword(s):  
Human Chromosome ◽  
Somatic Cell ◽  
Chromosome 17 ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids ◽  
Human Chromosome 17

Identification of chromosomes implicated in suppression of apoptosis in somatic cell hybrids

1994 ◽  
Vol 72 (11-12) ◽  
pp. 655-662 ◽  
Author(s):  
Marsha D. Speevak ◽  
Mario Chevrette
Keyword(s):  
Somatic Cell ◽  
Polymerase Chain Reaction Amplification ◽  
Growth Arrest ◽  
Chromosome 17 ◽  
Human Chromosomes ◽  
Somatic Cell Hybrids ◽  
Apoptosis Pathway ◽  
Whole Cell ◽  
Cell Hybrids ◽  
Diploid Cells

In vitro exposure of tumorigenic cell lines to the chemotherapeutic agent PALA (N-(phosphonoacetyl)-L-aspartate) usually results in cell death (shown here to be apoptosis), followed by clonal growth of rare survivors. On the other hand, normal diploid cells respond to PALA by arresting in G1 and G2 of the cell cycle. It was previously suggested that growth control mechanisms might exist to prevent cells from entering S phase under toxic conditions and that genes involved in such mechanisms were mutated or deleted in tumor cells. Interestingly, the tumor suppressor gene p53, a putative G1 control gene, was shown to mediate PALA-induced growth arrest. However, growth arrest occurs in cells that lack wild-type p53, suggesting that other genes are involved as well. To identify these genes, we have generated whole cell hybrids between mouse melanoma and normal human fibroblast cells. At early passage, a whole cell hybrid (BHF12) responds to PALA with growth arrest, while at later passage, the same hybrid undergoes apoptosis. To determine which human chromosomes are required for the PALA-induced growth arrest phenotype, we isolated subclones of the hybrid and tested them for their PALA response. FISH (fluorescence in situ hybridization) and PCR (polymerase chain reaction) amplification have been used to identify the human chromosome content of BHF12 and its subclones. Several human chromosomes, in addition to chromosome 17 (the location of p53), are consistently associated with the growth arrest phenotype. These findings provide evidence that one or more genes in addition to p53 may be involved in the suppression of a drug-induced apoptosis pathway and may lie on one or more of these chromosomes.Key words: apoptosis, growth arrest, N-(phosphonoacetyl)-L-aspartate, somatic cell hybrids.

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