Regional mapping of the gene coding for enolase-2 on human chromosome 12

1982 ◽  
Vol 53 (1) ◽  
pp. 245-254
Author(s):  
M.L. Law ◽  
F.T. Kao

Enolase-2 (ENO2), previously termed 14-3-2 protein, is an isozyme of enolase that is enriched in neuronal tissue. The gene coding for ENO2 was previously assigned to human chromosome 12. The present study presents data for a regional mapping of gene ENO2 using cell hybrids containing various deletions of human chromosome 12. These deletions were produced by treatment with chromosome-breaking agents. Cytogenetic analysis has allowed assignment of ENO2 to the short arm of chromosome 12, in the region of pter-p1205. This assignment is consistent with the segregation pattern of the 93 hybrid clones analysed. The segregation pattern has also established the linear order of 6 genes on chromosome 12:pter-TPI-GAPD-LDHB-ENO2-centromere-SHMT-PEPB-qter. Estimation of the relative distances between the 6 genes on chromosome 12 has been made by a statistical mapping analysis of the segregation data of the hybrid clones. A set of deletion hybrids containing various combinations of these 6 markers has been established for a rapid regional mapping of genes in one of these regions on chromosome 12.

1984 ◽  
Vol 68 (4) ◽  
pp. 351-352 ◽  
Author(s):  
J. J. M. van Dongen ◽  
I. L. M. Tettero ◽  
A. H. M. Geurts van Kessel ◽  
M. A. Versnel ◽  
H. Hooijkaas ◽  
...  

Diabetes ◽  
1995 ◽  
Vol 44 (12) ◽  
pp. 1408-1413 ◽  
Author(s):  
S. Menzel ◽  
K. Yamagata ◽  
J. B. Trabb ◽  
J. Nerup ◽  
M. A. Permutt ◽  
...  

1993 ◽  
Vol 90 (5) ◽  
Author(s):  
M.W. Berchtold ◽  
M. Koller ◽  
R. Egli ◽  
J.A. Rhyner ◽  
H. Hameister ◽  
...  

2003 ◽  
Vol 108 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Erich B. Jaeger ◽  
Marina A. Chekmareva ◽  
Thelma R. Tennant ◽  
Hue H. Luu ◽  
Jonathan A. Hickson ◽  
...  

2003 ◽  
Vol 102 (1-4) ◽  
pp. 139-144 ◽  
Author(s):  
C.R. Farber ◽  
N.E. Raney ◽  
V.D. Rilington ◽  
P.J. Venta ◽  
C.W. Ernst

1992 ◽  
Vol 60 (3-4) ◽  
pp. 194-196 ◽  
Author(s):  
J.G. Wauters ◽  
P.J. Bossuyt ◽  
J. Davidson ◽  
J. Hendrickx ◽  
M.W. Kilimann ◽  
...  

2002 ◽  
pp. 30-31
Author(s):  
David Adamah ◽  
Paul J. Gokhale ◽  
James Walsh ◽  
Peter W. Andrews

1989 ◽  
Vol 82 (3) ◽  
pp. 234-238 ◽  
Author(s):  
Adelina A. Davies ◽  
Stephen E. Moss ◽  
Mark R. Crompton ◽  
Tania A. Jones ◽  
Nigel K. Spurr ◽  
...  

1977 ◽  
Vol 24 (1) ◽  
pp. 255-263
Author(s):  
J. Jonasson ◽  
H. Harris

Diploid human fibroblasts and lymphocytes were fused with the cells of a malignant mouse melanoma and a range of hybrid clones selected for study. The ability of these clones to produce progressive tumours was assayed in nude mice. Although human chromosomes were preferentially eliminated in all the hybrid clones, the human diploid cells were as effective as mouse diploid cells in suppressing the malignancy of the mouse melanoma cells. The suppression produced by fibroblasts was again more profound than that produced by lymphocytes. Malignancy was also found to be suppressed in a hybrid clone in which a single X was the only human chromosome present; and this clone continued to give a very low take incidence even after the human X had been eliminated by back selection. Hybrids were made between the melanoma cells and diploid human fibroblasts that had been given 100 J kg-1 of gamma radiation before cell fusion. These hybrids contained no recognizable human chromosomes, but their ability to produce progressive tumours was greatly reduced compared to that of the melanoma parent cells. The take incidences given by the crosses between the melanoma cells and the irradiated human fibroblasts were, however, substantially higher than those given by the crosses between the melanoma cells and unirradiated fibroblasts. These findings suggest that the suppression of malignancy involves the activity of some extra-chromosomal element and that this element is radio-sensitive.


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