{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:10:07Z","timestamp":1791047407235,"version":"4.1.0"},"reference-count":59,"publisher":"American Society of Hematology","issue":"6","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,3,15]]},"abstract":"<jats:p>Mutations in the gene of the hepatic glucose-6-phosphate transporter cause glycogen storage disease type 1b. In this disease, the altered glucose homeostasis and liver functions are accompanied by an impairment of neutrophils\/monocytes. However, neither the existence of a microsomal glucose-6-phosphate transport, nor the connection between its defect and cell dysfunction has been demonstrated in neutrophils\/monocytes. In this study we have characterized the microsomal glucose-6-phosphate transport of human neutrophils and differentiated HL-60 cells. The transport of glucose-6-phosphate was sensitive to the chlorogenic acid derivative S3483,N-ethylmaleimide, and 4,4\u2032-diisothiocyanostilbene-2,2\u2032-disulfonic acid, known inhibitors of the hepatic microsomal glucose-6-phosphate transporter. A glucose-6-phosphate uptake was also present in microsomes from undifferentiated HL-60 and Jurkat cells, but it was insensitive to S3483. The treatment with S3484 of intact human neutrophils and differentiated HL-60 cells mimicked some leukocyte defects of glycogen storage disease type 1b patients (ie, the drug inhibited phorbol myristate acetate\u2013induced superoxide anion production and reduced the size of endoplasmic reticulum Ca2+ stores). Importantly, the treatment with S3484 also resulted in apoptosis of human neutrophils and differentiated HL-60 cells, while undifferentiated HL-60 and Jurkat cells were unaffected by the drug. The proapoptotic effect of S3483 was prevented by the inhibition of nicotinamide adenine dinucleotide phosphate oxidase or by antioxidant treatment. These results suggest that microsomal glucose-6-phosphate transport has a role in the antioxidant protection of neutrophils, and that the genetic defect of the transporter leads to the impairment of cellular functions and apoptosis.<\/jats:p>","DOI":"10.1182\/blood-2002-08-2576","type":"journal-article","created":{"date-parts":[[2003,2,27]],"date-time":"2003-02-27T18:28:53Z","timestamp":1046370533000},"page":"2381-2387","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":61,"title":["Inhibition of microsomal glucose-6-phosphate transport in human neutrophils results in apoptosis: a potential explanation for neutrophil dysfunction in glycogen storage disease type 1b"],"prefix":"10.1182","volume":"101","author":[{"given":"Rosanna","family":"Leuzzi","sequence":"first","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ga\u0301bor","family":"Ba\u0301nhegyi","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tama\u0301s","family":"Kardon","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paola","family":"Marcolongo","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Piero-Leopoldo","family":"Capecchi","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Joerg","family":"Burger","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelo","family":"Benedetti","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosella","family":"Fulceri","sequence":"additional","affiliation":[{"name":"From the Dipartimento di Fisiopatologia e Medicina Sperimentale and Istituto di Semeiotica Medica, Universita\u0300 di Siena, Siena, Italy; Semmelweis Egyetem Orvosi Vegytani, Molekula\u0301ris Biolo\u0301giai e\u0301s Patobioke\u0301miai Inte\u0301zete, Budapest, Hungary; and Aventis Pharma Deutschland, Metabolic Diseases, Frankfurt, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2019111822022251900_B1","doi-asserted-by":"crossref","first-page":"91","DOI":"10.1016\/S0083-6729(08)60269-1","article-title":"The role of hepatic glucose-6-phosphatase in the regulation of carbohydrate metabolism.","volume":"17","author":"Ashmore","year":"1959","journal-title":"Vitam Horm."},{"key":"2019111822022251900_B2","doi-asserted-by":"crossref","first-page":"513","DOI":"10.1042\/bj3620513","article-title":"The glucose-6-phosphatase system.","volume":"362","author":"van Schaftingen","year":"2002","journal-title":"Biochem J."},{"key":"2019111822022251900_B3","doi-asserted-by":"crossref","first-page":"10396","DOI":"10.1016\/S0021-9258(19)70478-5","article-title":"Evidence for the participation of independent translocases for phosphate and glucose-6-phosphate in the microsomal glucose-6-phosphatase system.","volume":"255","author":"Arion","year":"1980","journal-title":"J Biol Chem."},{"key":"2019111822022251900_B4","doi-asserted-by":"crossref","first-page":"580","DOI":"10.1126\/science.8211187","article-title":"Mutations in the glucose-6-phosphatase gene that cause glycogen storage disease type 1a.","volume":"262","author":"Lei","year":"1993","journal-title":"Science."},{"key":"2019111822022251900_B5","doi-asserted-by":"crossref","first-page":"235","DOI":"10.1016\/S0014-5793(97)01463-4","article-title":"Sequence of a putative glucose-6-phosphate translocase, mutated in glycogen storage disease type 1b.","volume":"419","author":"Gerin","year":"1997","journal-title":"FEBS Lett."},{"key":"2019111822022251900_B6","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1016\/S0021-9258(18)38504-1","article-title":"Glucose-6-phosphatase of the liver in glycogen storage disease.","volume":"199","author":"Cori","year":"1952","journal-title":"J Biol Chem."},{"key":"2019111822022251900_B7","first-page":"935","article-title":"Glycogen storage diseases","volume-title":"The metabolic basis of inherited disease. 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