Glycine transport by human diploid fibroblasts--absence of a defect in cells from patients with nonketotic hyperglycinemia.
Glycine transport in human diploid fibroblasts was shown to be by a single sodium-dependent system. Glycine transport does not appear to exhibit transstimulation or transinhibition. Transport appears to be similar to the A transport system of other mammalian cell lines, as defined by competition patterns. Normal and nonketotic hyperglycinemia (NKH) fibroblasts could not be distinguished on the basis of accumulation or initial rates. A distribution ratio of 15 to 30 was reached by both types of cells. The normal lines have slightly lower apparent Kms (1.1-1.3 mM) than the NKH lines (1.8 to 2.4 mM). The values for the Vmax of the normal cells (11.4-12.9 nmole/mg/min) and the NKH cells (7.0-16.7 nmole/mg/min) overlapped. There were no measurable differences in either the long-term incorporation into protein of leucine and glycine or the oxidation of glycine in normal and NKH fibroblasts.[1]References
- Glycine transport by human diploid fibroblasts--absence of a defect in cells from patients with nonketotic hyperglycinemia. Kelly, J.C., Otto, E.F., Hillman, R.E. Pediatr. Res. (1979) [Pubmed]
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
