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M Canton

Publications and source records attributed to M Canton.

6 recordsLinked to original sources
PubMed1995

Nature of respiratory stimulation in hyperthyroidism: the redox behaviour of cytochrome c.

Hyperthyroid mitochondria show an increased Km and Vmax in the high affinity phase of cytochrome oxidase kinetics. During inhibitor titrations, cytochrome c shows a different redox behaviour in hyperthyroid with respect to protonophore-treated euthyroid mitochondria. The observations are discussed in terms of a different regulation of electron input and output into the respiratory chain during slip and leak types of uncoupling. In hyperthyroid mitochondria during inhibitor titrations, the pattern of the relationship between uncoupler-induced extra-respiration and membrane potential is highly non-linear. The complex nature of the respiratory stimulation in hyperthyroid mitochondria is discussed.

Animals↗
PubMed1988

Retinoid-binding proteins in retinoblastoma tumors.

A combination of Western blot, Northern blot, and radiolabeled ligand-binding techniques was used to investigate retinoid-binding proteins in retinoblastoma (RB) cells from fresh tumors and from 19 RB tumor lines cultured in vitro. Using rabbit anti-bovine cellular retinal-binding protein (CRA1BP) antibodies, no CRA1BP could be detected. As determined by [3H]retinol binding, cellular retinol-binding protein was sometimes not detectable but averaged 2.3 +/- 2.7 means +/- SD, n = 7) pmol [3H]retinol bound/mg protein, similar to adult retina cytosol. Using [3H]retinoic acid as ligand, cellular retinoic acid-binding protein was not detectable in some lines and averaged 1.0 +/- 1.2 (means +/- SD, n = 7) pmol [3H]retinoic acid bound/mg protein, well below the adult retina cytosol level of 94.4 +/- 16.3 (means +/- SD, n = 4) pmol [3H]retinoic acid bound/mg. Using rabbit antibovine interstitial retinol-binding protein (IRBP) antibodies, IRBP of the same molecular mass as human IRBP (135,000) was detected in the medium from all cultured RB cells and averaged 75.9 +/- 19.2 pmol/10(8) cells (bovine IRBP immunochemical equivalents). Cytosol levels were less than 1% of the medium. Using a human IRBP complementary DNA probe, levels of IRBP RNA transcripts in 19 RB cell lines were comparable to adult retina. The Y-79 RB cell line was different from the others; the amount of IRBP in the medium was only about 1% of the RB cell lines. Levels of cellular retinol-binding protein were comparable with the other lines, but cellular retinoic acid-binding protein was 9 times more abundant. IRBP RNA transcripts in Y-79 cells were below the limits of detectability but appeared at low levels after induction of differentiation of Y-79 by 10(-6) M retinoic acid. Although this cell line has been in culture longer than the others, it may also have been initiated at an earlier stage of retinal development.

Carrier Proteins↗
PubMed1988

Infrequent genomic rearrangement and normal expression of the putative RB1 gene in retinoblastoma tumors.

Retinoblastoma (RB) tumors develop when both alleles of a gene (RB1) are mutated and unable to function normally. Recently, Friend et al. [S. H. Friend, R. Bernards, S. Rogelj, R. A. Weinberg, J. M. Rapaport, D. M. Albert, and T. P. Dryja, Nature (London) 32:643-646, 1986] reported the cloning of a gene, 4.7R, with some properties expected for the RB1 gene, namely, a high frequency (30%) of genomic rearrangements in tumors and absence of message in all RB tumors examined. To extend the characterization of this gene, we used 4.7R probes to search for genomic rearrangements of DNA and to study the expression of the 4.7R gene in RB tumors, osteosarcoma (OS) tumors arising in RB patients, and other normal and malignant tissues. In 34 previously unreported RB and OS tumors arising in RB patients, we observed only four (12%) with genomic abnormalities. Transcripts of 4.7R were present in 12 of 17 RB tumors, 2 of 2 OS tumors, and all non-RB tumors and normal tissues tested. We were unable to confirm the high frequency of truncated messages of 4.7R in RB tumors reported by Lee et al. (W. H. Lee, R. Bookstein, F. Hong, L. J. Young, J. Y. Shaw, and E. Y. Lee, Science 235:1394-1399, 1987) and Fung et al. (Y. K. Fung, A. L. Murphree, A. Tang, J. Qian, S. H. Hinrichs, and W. F. Benedict, Science 236:1657-1661, 1987) but did confirm the presence of a truncated transcript in the RB cell line Y79. Of the RB and RB-related OS tumors which appeared normal on Southern blots, 2 of 26 or 12% had abnormal transcripts, giving a combined frequency of 22% abnormalities in the 4.7R gene detectable by Southern and Northern (RNA) blot analyses.

Gene Expression Regulation↗
PubMedDate not supplied

Tumour induction by the retinoblastoma mutation is independent of N-myc expression.

Retinoblastoma (RB) tumours form in the eyes of young children when homozygosity for a mutation at the Rb-1 locus develops in a somatic retinal cell. A similar shift to homozygosity for the RB mutation has been observed in osteogenic sarcoma (OS) tumours that commonly arise as second tumours in children who survive RB. This observation suggests that the Rb-1 locus controls the expression of genes with oncogenic potential; a possible target is the oncogene N-myc, which is sometimes amplified and over-expressed in the neuroectodermal tumours neuroblastoma and RB. However, N-myc is developmentally regulated in normal murine embryogenesis, and an alternative possibility is that the expression of the gene in tumour cells reflects their embryonic origin and is unrelated to the RB mutation. We have therefore examined N-myc expression in various fetal, adult and tumour tissues, and report here that the gene is expressed in fetal but not in adult brain and retina and in near-diploid RB tumour samples at levels similar to those observed in normal fetal retina. Only RB tumours with genomic amplification of the N-myc gene exhibited increased levels of expression; and no N-myc transcripts were detected in osteogenic sarcomas initiated by mutations at the Rb-1 locus. We therefore conclude that the expression of N-myc in RB tumours probably reflects the origin of the tumour from an embryonic tissue normally expressing the gene and is not directly associated with the mutation at the RB locus.

Animals↗