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Biomedical subjects

N Van Cong

Publications and source records attributed to N Van Cong.

At least 37 records · Page 2Linked to original sources
PubMed1980

Investigations on the chromosomal localizations of the human and chimpanzee interferon genes: possible role of chromosomes 9 and 13.

Analysis of a great number of independent hamster-human and mouse-chimpanzee somatic cell hybrid clones confirms the role of chromosome 9 as carrying one or more primate beta interferon genes. The presence of chromosome 13 in producing hybrids and its absence in all non producing clones must be kept in mind for future studies. The strong negative regulation of interferon production in the parental hamster cells also affects the human gene product. The UV irradiation target for these regulatory genes is significantly greater than the structural genes responsible for interferon production.

Animals↗
PubMed1980

[Assignment of the creatine kinase BB gene to chromosome 14 by man-rodent cell hybridization (author's transl)].

The value of man-rodent hybrids for detecting creatine kinase BB (CKBB) was greatly increased by the use of an agar technique, in extended incubation (20 hours) with a concentrated solution of creatine as substrate (8 mg/ml instead of 1 mg/ml as usual). The selection of a man-rodent hybrid without discordant between chr. 14 and nucleoside phosphorylase (NP) (a marker of this chromosome) contributed efficiently to the detection of the positive correlation between CKBB and chr. 14/NP. Among 22 independent hybrids, the following were observed : 8 NP + CKBB+, 3 NP + CKBB(+), 11 NP-CKBB- and 6 chr. 14 + CKBB+, 2 chr. 14 + CKBB(+), 11 chr. 14 CKBB-, 2 chr. 14/CKBB+ and 1 chr. 14/CKBB(+). The presence of the chromosome was noted + or - according to its presence in more or less than 30% of the cells. These results show that the gene for CKBB is located on chr. 14 and that the presence of this single chr. 14 is sufficient for the expression of human CKBB in man-rodent hybrids. Discordant results reported by others (Povey et al., 1979) may be due to the weakness of the human CKBB detection in man-rodent hybrids or to the bad conservation of this enzyme.

Animals↗
PubMed1979

[Localization of the gene for phosphoglycolate phosphatase (PGP) on the chromosome 16 by interspecific hybridization (author's transl)].

Eight primary man-mouse (C11D/TK-) hybrids, twenty three primary and seven secondary man-hamster (CH/HGPRT-) were analyzed for human phosphoglycolate phosphatase (PGP) and for human chromosomes. The following results were obtained: 1. A positive correlation is observed between the chromosome 16 and PGP. 15 hybrids are chr.16+PGP+, 14 hybrids are chr.16-PGP- and 4 hybrids are chr.16-PGP+. 2. The percentage of dissociation between PGP and the chr.16 is low (12%) in comparison with the high percentage of dissociation between PGP and the other autosomes (between 37% and 65%). 3. Excepted the chromosome 16, the other autosomes are observed in hybrids PGP-. These different results indicate the localization of the gene for human PGP on the chromosome 16. The dissociation results chr.16-PGP+ are explained by the breakage of the chr.16 in the hybrids.

Animals↗
PubMed1978

[Assignment of alpha-Fuc to1p in man and the chimpanzee and to chromosome 4 in the African green monkey].

Analysis of cellular hybrids confirms the assignment of alpha-L-fucosidase (alpha-FUC) to 1p in man. Discordant results are in favour of the following gene order: 1pter (ENO-1, alpha-FUC,AK2) PGM1 centromere Pep-C but give no information on the relative positions of ENO-1,alpha-FUC, and AK2. The assignments of alpha-FUC to chromosome 1 in the chimpanzee and to chromosome 4 in the African green monkey are demonstrated (chromosome nomenclature by Finaz et al, 1976). These results confirm the homology of chromosome 4 of the African green monkey and 1p of man and the chimpanzee.

Animals↗
PubMed1976

[Permissivity of mouse-man hybrid cell clones to three enteroviruses: poliovirus II, coxsackie B3 and echovirus 11. Role of human chromosome F. 19 (author's transl)].

The permissivity of human cells to enteroviruses is linked to the presence of specific cell receptors. Owing to the chance elimination of human chromosomes, the man-mouse hybrid cells may be permissive or not depending on the genome responsible for synthesis of the receptors, and whether it has been conserved or not. By comparison of the cytopathogenic effects and virus production after inoculation of the viruses Polio II, Echo 11 and Coxsachie B3 to various hybrid strains, we observed an identity of the spectrum of permissivity to these three viruses. The enzyme study revealed a very high correlation between this permissivity and expression by the clones of the human glucose phosphate isomerase enzyme, of which the structural gene was localised on chromosome F 19. These results suggest the presence on this chromosome of a gene or syntenic genes, governing the synthesis of specific cell receptors to the viruses studied.

Binding Sites↗
PubMed1975

Chromosomal localization of human genes governing the interferon-induced antiviral state.

Interferon sensitivity of different normal and aneusomic human cells and of different mouse-human hybrids cells has been compared. G21 trisomic cells are more sensitive than diploid cells; whereas, on the contrary, triploid cells are normal in their human interferon sensitivity. Among other aneusomic cell lines tested, E16 trisomic cells are significantly less sensitive. These data are in favor of the hypotheses that the G21 chromosome carries genetic information for structural proteins involved in the receptor system for interferon, that there is a regulatory mechanism governing the antiviral state, and that the E16 chromosome is a possible candidate for carrying information for such a depressive regulatory mechanism. None of the chromosome abnormalities studies are involved with interferon synthesis.

Cell Line↗
PubMed1975

A study of hexosaminadases in interspecific hybrids and in GM2 gangliosidosis with a discussion on their genetic control.

1. Hexosaminidases were studied by electrophoresis with different human fibroblast extracts. We found in the same conditions of detection and culture three bands from the cathode to the anode, namely Hex B, Hex A, Hex C for the normal fibroblast, Hex B for the two different Tay-Sachs and Hex C for the two unrelated Sandhoff patients. 2. The analysis of man-rodent hybrids (hamster and mouse with normal and Sandhoff human fibroblasts) indicates a probable synteny between MPI, Hex C, "Hex A fast", and "Hex A-like". "Hex A fast" is probably a man-hamster hybrid enzyme, "Hex A-like" a man-mouse enzyme. Our data agree with the model of Ropers and Schwantes (Hex C = (alphaalpha)n; Hex A = (alphabeta)n; Hex B = (betabeta)n). Probably Hex A-fast = (alphabeta')n with hamster Hex B' = (beta'beta')n; and Hex A-like = (alphabeta1)n with mouse Hex B1 = (beta1beta1)n; and probably n = 2 according to the tetrameric structure model of Tallman et al. (1974). 3. As an explanation of the results given by Poenaru et al. (anti Hex A reacts with Hex A and Hex B but not with Hex C) we propose the existence of a compound antigen (alphabeta) for Hex A. Anti Hex A specific = anti (alphabeta); anti Hex A non-specific = anti Hex B = anti B, anti alpha being absent or negligible. 4. In our opinion, the Tay-Sachs mutation opposes the alphaB association while the alphaalpha association is possible at a low rate or unstable; it is thus possible to observe Hex C in certain conditions, e.g. in foetal brain. 5. We present a discussion about the genetic control of hexosaminidases, GM2 gangliosidosis, and the possible localization of the different mutations in the variants.

Animals↗
PubMed1975

[Gene localization in the chimpanzee (Pan troglodytes). Comparison with the factor mapping of man (Homo sapiens)].

Ten independant cellular hybrids were obtained from Chimpanzee (Pan troglodytes) fibroblasts and the murine cell line C11D. The comparison of electrophoretic and cytogenetic studies showed that 9 markers with known localizations in Man could also be localized on the homologous chromosomes of the Chimpanzee: pyrophosphate hydratase (PPH), phosphoglucomutase-1 (PGM1), and peptidase-C (Pep-C) on the No. 1; malate dehydrogenase MDH(NAD) on the No. 2; lactico dehydrogenase-A (LDH-A) on the No. 11; lactico dehydrogenase-B (LDH-B) on the No. 12; thymidine kinase (TK) on the No. 17; superoxide dismutase-1 (SOD-1) on the No. 21; glucose-6-phosphate dehydrogenase (G6PD) on the X. The localization of mannose phosphate isomerase (MPI) on the No. 7 could be excluded. One discrepancy between Chimpanzee and Man was noted: the localization of superoxide dismutase-2 (SOD-2) on the 6 is excluded.

Animals↗