Structure of the entire human muscle phosphofructokinase-encoding gene: a two-promoter system

Yamasaki, Tomoyuki; Nakajima, Hitoshi; Kôno, Norio; Hotta, Kikuko; Yamada, Kazuya; Imai, Enyu; Kuwajinia, Masamichi; Noguchi, T.; Tanaka, Takehiko; Tarui, Seiichiro

doi:10.1016/0378-1119(91)90262-a

Cited by 46 publications

(32 citation statements)

References 20 publications

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“…The human aminopeptidase N gene uses two separate promoters to control transcription in myeloid and intestinal epithelial cells (30). Such alternative use of tissue-specific promoters has also been found in the carbonic anhydrase I gene (31), the human Ick gene (32), and the phosphofructokinase gene (33). The human gene coding for insulin-like growth factor II contains four promoters that are subject to tissue-specific and development-dependent regulation (34).…”

Section: Discussionmentioning

confidence: 99%

Six mRNAs with different 5' ends are encoded by a single gamma-glutamyltransferase gene in mouse.

Rajagopalan

Wan

Habib

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Section: Discussionmentioning

confidence: 99%

Six mRNAs with different 5' ends are encoded by a single gamma-glutamyltransferase gene in mouse.

Rajagopalan

Wan

Habib

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…The coding sequence of the exons for the rabbit PFK-M gene [16] and the full-length mRNA sequence for human PFK-M [17] have also been reported. Recently observed features of the human PFK-M gene are the occurrence of alternative RNA splicing [18,191 and the existence of tissue-specific alternative promoters [20]. Molecukdr cloning of mouse and human PFK-L cDNA have also been reported [21, 221 and, very recently, the whole structure of the human and mouse PFK-L genes were reported [23,241.…”

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confidence: 99%

Rat‐liver‐type phosphofructokinase mRNA

Hotta

Nakajima

Yamasaki

et al. 1991

European Journal of Biochemistry

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We have cloned a full-length cDNA for rat-liver-type phosphofructokinase. The similarities of the rat livertype phosphofructokinase mRNA to the human and mouse counterparts were 94% and 99% in their amino acid sequences and 88% and 94% in the nucleotide sequences of their coding regions, respectively. Rat liver-type phosphofructokinase mRNA was expressed in all tissues examined, but its level was regulated tissue-specifically. The nutritional and hormonal regulations of the mRNA in the liver were examined in comparison with those of two other key glycolytic enzymes, glucokinase and L-type pyruvate kinase. The level of liver-type phosphofructokinase mRNA was essentially unchanged by starvation (72 h) or diabetes. The mRNA level also did not change significantly on refeeding starved rats on a high carbohydrate diet, or treating diabetic ones with insulin. These results suggested that rat liver-type phosphofructokinase mRNA in the liver was not under control of diet or insulin, in contrast to glucokinase and L-type pyruvate kinase.Phosphofructokinase (PFK) is a key regulatory enzyme in the glycolytic pathway catalyzing the phosphorylation of fructose 6-phosphate to fructose 1,6-bisphosphate [l]. The activity of PFK is under the regulation by various allosteric effectors [2, 31. Three distinct subunits of PFK have been described [4], that is, in human tissue, the liver type (L), muscle type (M) and platelet type (P) IS]. In rats, the platelet type is also called the C-type. The isozymes of PFK show different kinetic properties, such as in their inhibition by ATP and affinity for fructose 6-phosphate. Liver-type PFK is less sensitive to activation by ADP, AMP or CAMP [3]. These three subunits are expressed in various amounts in different tissues. In rat liver, 75% of the total PFK activity is due to the L type, 21% to the M type and 4% to the P type [6].Liver-type PFK plays an important role in hepatic glycolysis. In addition to the regulation at substrate levels, some hormones such as insulin and glucagon are considered to regulate PFK-L by affecting its protein level. The catalytic activity and immunoreactivity of PFK-L in the liver were demonstrated to decrease in starved rats and diabetic rats, and to be restored to the normal level or even more increased in these animals by refeeding and insulin treatment, respectively [7, 81. The decrease in the level of PFK-L protein in starved rats and diabetic rats has been reported to be the result of its Male Sprague-Dawley rats (170-190 g) were made diabetic by intravenous injection of streptozotocin (50 mg/kg body mass, Sigma Chemical Co., St. Louis, MO) after starvation for 20 h as described [25]. Plasma glucose was assayed 2 days after the treatment by the glucose oxidase method 1261. Rats with blood glucose levels of over 37 mM were used for experiments. They were given a high carbohydrate diet ad libitum (81Y0 dextrin, 10% casein and 2% fat) for 36 h, and then were treated with bovine intermediate acting insulin

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“…Therefore, for amplification of these genes by HGQ-PCR, the sequence of the sense primer has been designed to differ by one nucleotide from the PFKL-CH21 gene in exon 8, whereas the antisense primer differs by one nucleotide from the PFKM-CH1 gene in exon 9 ( Fig. 1; Levanon et al 1989;Sharma et al 1990;Yamasaki et al 1991;Elson et al 1990). Two PCR products of 185 bp and 345 bp were generated by the PFKL-CH21 and the PFKM-CH1 genes, respectively (Fig.…”

Section: Resultsmentioning

confidence: 99%

Rapid detection of trisomy 21 by homologous gene quantitative PCR (HGQ-PCR)

et al. 1997

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Down's syndrome results from the production of three copies of chromosome 21 within a cell. We have devised a method termed the homologous gene quantitative polymerase chain reaction (HGQ-PCR), which uses one pair of primers and which can directly identify the additional copy of chromosome 21 by simultaneously amplifying two highly homologous genes of the human liver-type phosphofructokinase located on chromosome 21 (PFKL-CH21) and the human muscle-type phosphofructokinase located on chromosome 1 (PFKM-CH1) for self-detecting determination. On analysis of 34 cases of Down's syndrome, including two cases of unbalanced translocation 46, XY, der (14; 21) (q10; q10), + 21, and 100 normal individuals, the relative ratio of the PFKM-CH1/PFKL-CH21 product was 1.33 +/- 0.323 (mean +/- SD) and 0.40 +/- 0.16 (mean +/- SD) for disomy DNA and trisomy DNA, respectively. The difference between these two groups was highly significant (P < 0.001). These results indicate that this quantitative method is practical and may be used for the prenatal diagnosis of Down's syndrome caused by trisomy 21.

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Structure of the entire human muscle phosphofructokinase-encoding gene: a two-promoter system

Cited by 46 publications

References 20 publications

Six mRNAs with different 5' ends are encoded by a single gamma-glutamyltransferase gene in mouse.

Six mRNAs with different 5' ends are encoded by a single gamma-glutamyltransferase gene in mouse.

Rat‐liver‐type phosphofructokinase mRNA

Rapid detection of trisomy 21 by homologous gene quantitative PCR (HGQ-PCR)

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