Complementation of mutations in the LDL pathway of receptor-mediated endocytosis by cocultivation of LDL receptor-defective hamster cell mutants.
We have previously isolated Chinese hamster ovary (CHO) cell mutants that do not express low density lipoprotein (LDL) receptors. When one mutant clone was cocultivated with other receptor-defective clones, it was induced to express receptors that could mediate normal endocytosis. These LDL receptor-defective clones defined two classes of mutations: cbc (complemented by cocultivation) and icc (inducer cells in cocultivation). The induction and short-term (18 hr) stability of LDL receptors in cbc cells did not require protein synthesis by icc cells. Receptor activity could not be induced by DMSO, 5-azacytidine, phosphatidylcholine liposomes, dibutyryl cAMP, compactin, soybean trypsin inhibitor, low temperature (30 degrees C), or conditioned medium, but could be induced by cocultivation with parental CHO cells and normal and LDL receptor-negative human fibroblasts. Complementation by cocultivation only occurred when the cbc and inducing cells were in close proximity, suggesting that an unstable diffusible factor or intimate cell-to-cell association was required for complementation.[1]References
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
