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Biomedical subjects

K Willecke

Publications and source records attributed to K Willecke.

178 records · Page 10Linked to original sources
PubMed1974

C4-dicarboxylate transport in Bacillus subtilis studied with 3-fluoro-L-erythro-malate as a substrate.

Bacillus subtilis cells grown in yeast extract medium accumulated 3-fluoro-l-erythro-[1,2-(14)C(2)]malate more than 30-fold from the surrounding medium. No metabolic products derived from 3-fluoro-l-erythro-malate could be detected in these cells. l-Malate competitively inhibited transport of 3-fluoro-l-erythro-malate. This malate analogue was itself a competitive inhibitor of l-malate uptake. Cells that had been grown in yeast extract supplemented with 5 mM l-malate showed a 10-fold increased affinity towards 3-fluoro-l-erythro-malate relative to cells grown in yeast extract medium with no added malate. Our results suggest that two transport systems for l-malate can be induced in B. subtilis. The first of these systems seems to effect uptake of C(4)-dicarboxylates (l-malate, succinate, and fumarate) in yeast extract medium. The second transport system (or possibly a modification of the first transport system) seems to be induced by addition of l-malate to this medium and is also functioning in malate minimal medium.

Autoradiography↗
PubMed1971

Induction of citrate transport in Bacillus subtilis during the absence of phospholipid synthesis.

Citrate transport can be induced in a glycerol-requiring mutant of Bacillus subtilis even after deprival of glycerol. Under these conditions de novo phospholipid synthesis is stopped although ribonucleic acid, deoxyribonucleic acid, and protein syntheses continue. It is concluded that the inducibility of bacterial transport systems must not necessarily require de novo phospholipid synthesis.

Acetates↗
PubMedDate not supplied

Two homologous protein components of hepatic gap junctions.

Gap junctions consist of closely packed pairs of transmembrane channels, the connexons, through which materials of low relative molecular mass diffuse from the cell to neighbouring cells. In liver, connexons consist of six protein subunits which, until now, were believed to be identical. However, besides the major polypeptide of relative molecular mass (Mr) 28,000 (and see refs 4 and 6), a component of Mr 21,000 (21K) has been repeatedly observed in liver. The amino-terminal sequence (18 residues) of this less abundant protein shows that it is related to, but distinct from, the Mr 28K protein. Immuno-staining and immuno-precipitation show both proteins to be in the same gap junctional plaques. Thus, it seems that hepatic gap junction channels (and by extension possibly others) are composed of two (or more) homologous proteins.

Amino Acid Sequence↗
PubMedDate not supplied

Altered expression of proto-oncogenes in human lymphoid cells immortalized by transfection with extrachromosomal DNA of mouse L cells.

Human lymphocytes were induced to proliferate continuously in vitro by transfection with extrachromosomal DNA from mouse L929 cytoplasts. The immortalized cells contain 2- to 5-fold increased mRNA levels of only 3 (c-Ha-ras-1, c-Ki-ras, c-myc) out of 18 proto-oncogenes tested compared to quiescent lymphocytes. Furthermore, the immortalized cells contain decreased amounts of c-fos mRNA, 2- to 20-fold decreased amounts of lck and c-fgr mRNA and 10-fold increased levels of JD15 mRNA compared to primary lymphocytes. The immortalised cells do not harbor amplified copies or any major rearrangement of these genes. No additional copy of these genes transferred from the mouse genome could be detected in the immortalized human cell lines. Thus, the changes in the level of these proto-oncogene transcripts in the lymphoid cells are likely to be induced by the immortalizing DNA from L929 cytoplasts and appear to be associated with continuous proliferation of these cells. Since the immortalized cell lines do not form colonies in soft agar medium and do not induce tumors in nude mice, we suggest that the altered expression of these proto-oncogenes may be due to the transition from quiescent to continuous proliferation in vitro ("immortalization"), but does not correlate with a tumorigenic phenotype of the cells.

Cell Line, Transformed↗
PubMedDate not supplied

Adenovirus type 5 persisting in human lymphocytes is unlikely to be involved in immortalization of lymphoid cells by fusion with cytoplasts or by transfection with DNA of mouse L cells.

Human peripheral blood lymphocytes were induced to proliferate indefinitely in vitro by fusion with cytoplasts from mouse L 929 cells or, alternatively, by transfection with DNA isolated from L929 cytoplasts. Since adenoviruses epidemically infect human lymphocytes, the newly established cell lines were assayed for the presence of adenoviral DNA sequences. In 8 of 10 lymphoid cell lines of both B and T cell origin, adenovirus type 5 (serogroup C) DNA sequences were detected. The cells harbor approximately 40 to 70 genome copies per cell. Adenovirus type 5 transcripts of the E1A and E1B early regions that are responsible for the transforming capacity of adenoviruses could not be detected in the lymphoid cell lines. Therefore we conclude that the adenovirus genome persisting in immortalized lymphoid cells is not involved in the maintenance of indefinite proliferation induced by fusion with L929 cytoplasts or by DNA transfection.

Adenovirus Early Proteins↗
PubMedDate not supplied

[Activation of ras and myc proto-oncogenes in human breast carcinoma and neuroblastoma].

DNA from human breast carcinoma (SK-BR-3) and neuroblastoma (LA-N-1) cell lines are capable of inducing foci of transformed NIH 3T3 cells after DNA-mediated gene transfer. The blot hybridization analysis of DNA from primary and secondary NIH 3T3 transformants identified additional sequences homologous to the c-Ha-ras 1 oncogene, and revealed amplification of nucleotide sequences homologous to the v-myc oncogene. Restriction fragments of the amplified myc-related sequences correspond to c-myc (SK-BR-3) and N-myc (LA-N-1) loci of the human genome. The results show that active Ha-ras oncogenes can coexist with altered myc oncogenes in breast carcinomas and neuroblastomas. This suggests that a multi-step mechanism involves both ras and myc genes and their cooperation in the development of these tumors.

Animals↗