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T Martinsson

Publications and source records attributed to T Martinsson.

137 records · Page 8Linked to original sources
PubMedDate not supplied

Amplification and enhanced expression of the c-myc oncogene in mouse SEWA tumour cells.

SEWA tumour cells are derived from an osteosarcoma induced in an A.SW mouse by infection with polyoma virus. Cytogenetic analyses have revealed three different characteristic chromosomal abnormalities diagnostic for the presence of amplified genes: 'double minutes' (DMs), homogeneously staining chromosomal regions (HSRs) and C-bandless chromosomes (CMs; for review see ref. 2). DMs may undergo fluctuation in number depending on the conditions in which the cells grow. Their number usually increases after injection of cells into a mouse and often is reduced to undetectable levels when the cells are explanted back into tissue culture; when the cells are re-introduced into the mouse, they again acquire multiple DMs. We show here that cells of SEWA lines carrying DMs, HSRs or CMs contain amplified copies of the proto-oncogene c-myc and enhanced levels of c-myc messenger RNA and c-myc protein. DMs or CMs are the sites of c-myc amplification in two different SEWA lines.

Animals↗
PubMedDate not supplied

Detailed mapping of the phosphomannomutase 2 (PMM2) gene and mutation detection enable improved analysis for Scandinavian CDG type I families.

The gene for carbohydrate-deficient glycoprotein syndrome type I (CDG1) has previously been localised by us close to marker D16S406 in chromosome region 16p13.2-3. We also presented data indicating a strong founder mutation associated with a specific haplotype in CDG I patients from western Scandinavia. The phosphomannomutase 2 (PMM2) gene was recently put forward as a likely CDG1 candidate gene. We have now shown that the specific haplotype is associated with the PMM2 mutation 357C > A. Using data from radiation hybrid panel we have refined the position of the PMM2 gene to very close to marker D16S3020 in the interval between D16S406 and AFM282ze1 on the distal side and D16S3087 on the proximal side. Due to the severity of the disease many families request prenatal diagnostic services for CDG I. In the meantime, until the mutation spectrum is fully examined, we propose the combined use of mutation analysis and linkage analysis with polymorphic markers as diagnostic tools for Scandinavian CDG I families requesting prenatal diagnosis. Using this strategy we have to date successfully performed 15 prenatal diagnoses for CDG I.

Base Sequence↗
PubMedDate not supplied

Psoriasis susceptibility locus in chromosome region 3q21 identified in patients from southwest Sweden.

We have performed a pair-wise linkage study in the search for psoriasis susceptibility regions. A preliminary scan was performed on 20 families. In this set we obtained indications of linkage on chromosome 3q21. This region was further investigated using material from a total of 104 families (set 1B) resulting in a non-parametric linkage (NPL) of 1.77. The material was stratified in families whose parental origin is in southwest Sweden (set 1C). A maximum NPL value of 2.77 was obtained in this group. A transmission disequilibrium test (TDT) was performed on the stratified material (set 1C) and a significant P value of 0.005 was obtained, at marker D3S1269. The locus was confirmed with TDT in replicate material consisting of 148 families in which a single member was affected (P value 0.0007) at marker D3S1551. Thus, we have observed a significant P value using TDT in the vicinity of markers D3S1269/D3S1551, suggesting a novel psoriasis susceptibility region.

Chromosome Mapping↗
PubMedDate not supplied

Characterization of multidrug resistance in SEWA mouse tumor cells: increased glutathione transferase activity and reversal of resistance with verapamil.

The glutathione transferase (EC 2.5.1.18) activity of multidrug-resistant and drug-sensitive SEWA mouse tumor cells was determined. Increase in activity was found in all multidrug-resistant sublines. Electrophoretic separation of cytosolic proteins and immunodetection, using antisera against Class Alpha, Class Mu and Class Pi glutathione transferase, revealed a two-fold increase of the Class Pi transferase in the resistant cells. The role of glutathione transferase of Class Pi in the multidrug resistance and its distinction from the over-produced 21,000 dalton protein p21 is discussed. Reversal of the resistance, using the calcium antagonist verapamil, and different sensitivity to verapamil between different sublines are also reported.

Animals↗
PubMedDate not supplied

Pleiotropic drug resistance, protein overexpression, and cytogenetic signs of gene amplification in mouse tumor cells.

We have isolated pleiotropic drug resistant mouse tumor cell lines with resistance-associated double minute chromosomes (DM) or homogeneously staining regions (HSR). In resistant cells, two-dimensional protein electrophoresis revealed elevated levels of a 21,000 dalton protein. Two resistant lines, with cytogenetically unstable (DM) and stable (HSR) gene amplification, were grown in the absence of drug for several weeks. The resistance and the protein overexpression was correlated to the presence of either HSR or DM. This suggests that the 21,000 dalton protein is a gene amplification product, and its importance for the resistance is discussed.

Animals↗
PubMedDate not supplied

"Specific" binding of [3H]-[Sar9,Met(O2)11]-substance P to tissue culture plates is found when substance P is used to define non-specific binding.

Following incubation at 4 degrees C, [3H]-[Sar9,Met(O2)11]-substance P bound to tissue culture plates in a manner displaceable by substance P (SP). The IC50 for SP was about 100 nM. Although the total binding to the wells could be reduced by increasing the assay bovine serum albumin concentration, by the presence of divalent ions and by gelatin-precoating of the wells, the remaining binding could be inhibited by about 70% by SP, and would thus appear as "specific" binding in assays. The non-peptide antagonist (+/-)CP-96345 also inhibited the binding to the wells at high concentrations (IC50 about 2 mcM), whereas physalaemin did not. Physalaemin is thus a better agent to define non-specific binding. The consequences of the "specific" binding to the culture wells observed with SP to define non-specific binding are demonstrated in two cell systems: in cultured human umbilical vein endothelial cells, an apparent receptor density of about 100,000/cell is shown to be due mainly to binding to the wells, rather than the cells. In UC11MG cells, which express 40,000-60,000 NK-1 recognition sites/cell, the use of SP to define binding gives artifactually high KD and Bmax values, and an artifactually low potency (and Hill slope) of (+/-)CP-96345 when compared with data obtained using physalaemin to define the non-specific binding.

Astrocytoma↗
PubMedDate not supplied

Novel mutations in the APC gene and clinical features in Swedish patients with polyposis coli.

The adenomatous polyposis coli (APC) gene was investigated in Swedish patients with familial adenomatous polyposis (FAP). A combination of analyses including single stranded conformation polymorphism (SSCP), heteroduplex (HD), protein truncation test (PTT) and direct sequencing was used to enable optimal mutation detection. Three novel mutations in the gene were identified, i.e. nt2644C- > T (giving an Arg876Stop mutation), nt4025del173 (leading to premature truncation of the protein at codon 1337) and nt3526insG (giving truncation at codon 1178). In addition, one previously described mutation, i.e. the 5-bp-deletion nt3942del5(AAAGA) in codon 1309 (giving a premature termination of the protein at codon 1314) was detected. All four mutations were located in the 5'-half of exon 15. The two latter mutations were associated with the CHRPE (congenital hypertrophy of retina pigment epithelium) phenotype (CHRPE was not examined in the other two cases). The patients with mutations in codon 1309 and 1336 had a more severe FAP phenotype.

Adenomatous Polyposis Coli↗