G6PT Inhibition Model Using HL-60 Cells and Induction of ROS Production through PKC/NOX2 Activation: Clinical Condition for Elucidation of Glycogen Storage Disease Type Ib

Author:

Satoh Daisuke1,Ohte Mariko2,Maeda Tohru13,Nakamura Katsunori12,Matsunaga Tamihide12

Affiliation:

1. Department of Clinical Pharmacy, Graduate School of Pharmaceutical Sciences, Nagoya City University

2. Educational Research Center for Clinical Pharmacy, Faculty of Pharmaceutical Science, Nagoya City University

3. College of Pharmacy, Kinjo Gakuin University

Publisher

Pharmaceutical Society of Japan

Subject

Pharmaceutical Science,Pharmacology,General Medicine

Reference29 articles.

1. 1) Chou JY, Matern D, Mansfield BC, Chen YT. Type I glycogen storage disease: disorder of the glucose-6-phosphate complex. Curr. Mol. Med., 2, 121–143 (2002).

2. 2) Hiraiwa H, Pan CJ, Lin B, Moses SW, Chou JY. Inactivation of the glucose 6-phosphate transporter causes glycogen storage disease type Ib. J. Biol. Chem., 274, 5532–5536 (1999).

3. 3) Gerin I, Veiga-da-Cunha M, Noël G, Van Schaftingen E. Structure of the gene mutated in glycogen storage disease type Ib. Gene, 227, 189–195 (1999).

4. 4) Chou JY, Jun HS, Mansfield BC. Neutropenia in type Ib glycogen storage disease. Curr. Opin. Hematol., 17, 36–42 (2010).

5. 5) Kure S, Suzuki Y, Matsubara Y, Sakamoto O, Shintaku H, Isshiki G, Hoshida C, Izumi I, Sakura N, Narisawa K. Molecular analysis of glycogen storage disease type Ib; Identification of a prevalent mutation among Japanese patients and assignment of a putative glucose-6-phosphate translocase gene to chromosome 11. Biochem. Biophys. Res. Commun., 248, 426–431 (1998).

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