Annerén K G, Korenberg J R, Epstein C J
Hum Genet. 1987 May;76(1):63-5. doi: 10.1007/BF00283052.
Although the gene for the liver type (L) subunit of phosphofructokinase (PFK) is located on human chromosome 21 and PFKL subunits predominate in fibroblasts, an increase in PFK activity has not been reported in trisomy 21 fibroblasts. However, using well-matched pairs of trisomy 21 and diploid fibroblast strains, we observed an almost 1.5-fold increase in mean PFK activity of trisomic cells. In monosomy 21 fibroblasts we found an almost 0.5-fold decrease in mean PFK activity. Thus there appears to be a gene-dosage effect for the PFKL gene, as for other loci on chromosome 21. PFK activity in a cell strain deleted for the distal part of band 21q22.3 was not decreased, suggesting with other data that PFKL is located in the midportion of band 21q22.3.
尽管磷酸果糖激酶(PFK)肝脏型(L)亚基的基因位于人类21号染色体上,且PFKL亚基在成纤维细胞中占主导地位,但21三体成纤维细胞中尚未报道PFK活性增加。然而,使用配对良好的21三体和二倍体成纤维细胞系,我们观察到三体细胞的平均PFK活性几乎增加了1.5倍。在21单体成纤维细胞中,我们发现平均PFK活性几乎降低了0.5倍。因此,与21号染色体上的其他基因座一样,PFKL基因似乎存在基因剂量效应。在21q22.3带远端部分缺失的细胞系中,PFK活性并未降低,结合其他数据表明PFKL位于21q22.3带的中部。