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M Rehn

Publications and source records attributed to M Rehn.

48 records · Page 3Linked to original sources

Alpha 1(XVIII), a collagen chain with frequent interruptions in the collagenous sequence, a distinct tissue distribution, and homology with type XV collagen.

We report on the isolation of mouse cDNA clones which encode a collagenous sequence designated here as the alpha 1 chain of type XVIII collagen. The overlapping clones cover 2.8 kilobases and encode an open reading frame of 928 amino acid residues comprising a putative signal peptide of 25 residues, an amino-terminal noncollagenous domain of 301 residues, and a primarily collagenous stretch of 602 residues. The clones do not cover the carboxyl-terminal end of the polypeptide, since the translation stop codon is absent. Characteristic of the deduced polypeptide is the possession of eight noncollagenous interruptions varying in length from 10 to 24 residues in the collagenous amino acid sequence. Other features include the presence of several putative sites for both N-linked glycosylation and O-linked glycosaminoglycan attachment and homology of the amino-terminal noncollagenous domain with thrombospondin. It is of particular interest that five of the eight collagenous sequences of type XVIII show homology to the previously reported type XV collagen, suggesting that the two form a distinct subgroup among the diverse family of collagens. Northern blot hybridization analysis revealed a striking tissue distribution for type XVIII collagen mRNAs, as the clones hybridized strongly with mRNAs of 4.3 and 5.3 kilobases that were present only in lung and liver of the eight mouse tissues studied.

Amino Acid Sequence↗

Primary structure of the alpha 1 chain of human type XV collagen and exon-intron organization in the 3' region of the corresponding gene.

Types XV and XVIII collagens form a new subgroup within the diverse family of collagens, both being characterized by extensive interruptions in their collagenous sequences. We isolated human alpha 1(XV) chain cDNAs that extend beyond the sequences previously derived from a 2127-nucleotide clone. The cDNAs cover 5172 nucleotides of the 5300-4400-nucleotide mRNAs and encode a polypeptide of 1388 residues, including a 25-residue signal peptide, a 530-residue NH2-terminal noncollagenous domain (NC1), a 577-residue collagenous sequence with eight interruptions of 7-45 residues, and a 256-residue COOH-terminal noncollagenous domain (NC10). A thrombospondin sequence motif found previously in certain other collagen types was identified in the NC1 domain of type XV collagen, whereas the NC10 domain was characterized by the presence of four cysteine residues. The exon-intron organization of the human gene was determined, corresponding to the extreme COOH-terminal 2/3 + 275 residues. NC10 is encoded by seven exons, six of which encode solely protein sequences and vary in size between 60 and 186 base pairs, whereas the last one corresponds to the end of the polypeptide and the 3'-untranslated sequences. The extreme 5' exon analyzed was a junction exon encoding both collagenous and noncollagenous sequences. This initial characterization is indicative of a multiexon arrangement for the alpha 1(XV) gene.

Amino Acid Sequence↗

Vaginal clear cell carcinoma in a young patient with ectopic termination of the left ureter in the vagina.

The association of clear cell adenocarcinoma of the vagina and vaginal adenosis with prenatal exposure to diethylstilbestrol (DES) is well-documented in the United States. In Europe, however, DES was never used in the therapy of threatened abortion and, therefore, clear cell adenocarcinoma and vaginal adenosis remained rare diseases. We report on the clinical and pathological features of a case of clear cell adenocarcinoma of the upper vagina in a 17-year-old German girl, who had a history of hypoplasia of the left kidney with an ectopic termination of the ureter in the upper vagina, removed surgically 2 years before. No previous report of a similar coincidence of vaginal clear cell carcinoma and a congenital disorder of the genitourinary tract exists. Congenital anomaly of the ureter interfering with the development and the differentiation of the distal Müllerian tract and its epithelium might have provided a similar histological basis for carcinogenesis in our patient to that in those provided exposed to DES.

Adenocarcinoma, Clear Cell↗

Role of inositol triphosphate isomer formation in type II pneumocyte signal transduction.

Adenosine triphosphate (ATP) is a potent agonist of surfactant secretion from type II pneumocytes. The extracellular ATP signal is transduced by both P1- and P2-purinergic pathways, which respectively initiate cyclic adenosine monophosphate formation and phosphatidyl inositol hydrolysis to inositol phosphates (Ins P). We investigated the role of inositol triphosphate (Ins P3) isomer formation in this signal transduction pathway. Primary cultures of rat type II pneumocytes were labeled with 30 microCi [3H]myoinositol/5 x 10(6) cells for 48 h. After preincubation with 10 mM LiCl for 20 min, the cells were stimulated with ATP (10(-4) M) and then were rapidly frozen with liquid N2. The Ins P3 isomers were analyzed by high performance liquid chromatography. A 4-fold increase in Ins 1,4,5 P3 occurred within 2 s after stimulation with ATP, decreased to half maximum by 60 s, and returned close to baseline values by 2 min. In contrast, Ins 1,3,4 P3 did not increase until 15 s, peaked by 60 s with a 4-fold increase, and returned to baseline values by 2 min. Intracellular calcium [( Ca2+]i), measured as Indo-1 fluorescence, also increased 3-fold within 2 s of exposure to ATP (10(-4)M) and fell to a plateau level 25% above baseline values by 10 s. We conclude that Ins 1,4,5 P3 formation and [Ca2+]i release both occur rapidly after exposure of type II pneumocytes to extracellular ATP. We speculate that these early events in type II pneumocyte signal transduction play a role in the initiation of stimulation of surfactant secretion by extracellular ATP.

Adenosine Triphosphate↗

Correlation of the EGF-receptor with cell kinetic and classical prognostic factors in breast cancer.

SPECIFIC OBJECTIVE: The Epidermal Growth Factor Receptor (EGFR) is a specific cell membrane receptor that shows homology to the product of the oncogene c-erbB2 in human breast cancer. Growth factors bound to the EGFR are able to stimulate the growth of tumor cells in an autocrine or paracrine manner. Our objective was to examine whether there is a relationship between EGFR, cell kinetic prognostic factors (ploidy, proliferation-antigen Ki67) and classical prognostic factors (hormone receptors, menopausal status, nodal status) in breast cancer. METHODS: EGFR was assayed in tumor tissue of 55 patients with breast cancer using an ELISA, the ploidy-status was evaluated by image analysis and Ki67 was determined by immune histochemistry. Estrogen- (ER) and Progesterone-Receptor (PR)-concentrations were quantified using a radioligand assay. RESULTS: There was a significant positive correlation between the EGFR and the cell kinetic prognostic factors: EGFR positive tumors were significantly-more often aneuploid and Ki67-positive. In addition there was an inverse association between EGFR- and ER-concentration, but no association between EGFR and PR. The EGFR did not correlate with the nodal and the menopausal status. CONCLUSIONS: Our study revealed associations between EGFR, ER, Ki67 and ploidy. Whether these correlations can help to predict the course of disease, providing further information in addition to the conventional factors (nodal status, steroid hormone receptors etc.) has to be investigated by several years of clinical follow up.

Breast Neoplasms↗