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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Solute carrier family 37

glucose-6-phosphate translocase, G6PT, glucose-6-phosphate transporter, GSD Ib, G6PT1
This gene regulates glucose-6-phosphate transport from the cytoplasm to the lumen of the endoplasmic reticulum, in order to maintain glucose homeostasis. It also plays a role in ATP-mediated calcium sequestration in the lumen of the endoplasmic reticulum. Mutations in this gene have been associated with various forms of glycogen storage disease. Alternative splicing in this gene results in multiple transcript variants.[provided by RefSeq, Aug 2009] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, Insulin, AGE
Papers on glucose-6-phosphate translocase
Safety and Efficacy of Chronic Extended Release Cornstarch Therapy for Glycogen Storage Disease Type I.
Weinstein et al., Gainesville, United States. In Jimd Rep, Sep 2015
RESULTS: Of the 106 subjects (93 GSD Ia/13 GSD Ib), efficacy was demonstrated in 82 patients (88%) with GSD Ia and 10 patients (77%) with GSD Ib.
Identification of glucose-6-phosphate transporter as a key regulator functioning at the autophagy initiation step.
Jung et al., Seoul, South Korea. In Febs Lett, Aug 2015
By performing gain-of-function screening, we identified G6PT as an autophagy activator.
Type I glycogen storage diseases: disorders of the glucose-6-phosphatase/glucose-6-phosphate transporter complexes.
Mansfield et al., Bethesda, United States. In J Inherit Metab Dis, May 2015
Disorders of the glucose-6-phosphatase (G6Pase)/glucose-6-phosphate transporter (G6PT) complexes consist of three subtypes: glycogen storage disease type Ia (GSD-Ia), deficient in the liver/kidney/intestine-restricted G6Pase-α (or G6PC); GSD-Ib, deficient in a ubiquitously expressed G6PT (or SLC37A4); and G6Pase-β deficiency or severe congenital neutropenia syndrome type 4 (SCN4), deficient in the ubiquitously expressed G6Pase-β (or G6PC3).
High Incidence of Serologic Markers of Inflammatory Bowel Disease in Asymptomatic Patients with Glycogen Storage Disease Type Ia.
Weinstein et al., Gainesville, United States. In Jimd Rep, 2014
The development of IBD seems to be associated with the defect of neutrophil function in GSD Ib.
Regression of hepatocellular adenomas with strict dietary therapy in patients with glycogen storage disease type I.
Weinstein et al., Gainesville, United States. In Jimd Rep, 2014
The charts of 163 patients with GSD Ia and 42 patients with GSD Ib were reviewed, and HCAs were documented in 47 subjects (43 Ia/4 Ib).
Diagnosis and management of glycogen storage disease type I: a practice guideline of the American College of Medical Genetics and Genomics.
American College of Medical Genetics and Genomics et al., In Genet Med, 2014
It is caused by deficient activity of the glucose 6-phosphatase enzyme (GSD Ia) or a deficiency in the microsomal transport proteins for glucose 6-phosphate (GSD Ib), resulting in excessive accumulation of glycogen and fat in the liver, kidney, and intestinal mucosa.
Neutrophil energetics and oxygen sensing.
Whyte et al., Sheffield, United Kingdom. In Blood, 2014
In this issue of Blood, Jun et al, through the study of neutrophils deficient in the glucose-6-phosphate transporter, describe a novel role for the peroxisome proliferator-activated receptor-γ (PPARG) pathway in the regulation of key neutrophil functions and link this to concomitant hypoxia-inducible factor (HIF) 1α stabilization.
Pregnancy in women with glycogen storage disease Ia and Ib.
Weinstein et al., Gainesville, United States. In J Perinat Neonatal Nurs, 2014
Prior to the introduction of granulocyte colony-stimulating factor (G-CSF), infections caused significant mortality in GSD Ib.
Establishment and directed differentiation of induced pluripotent stem cells from glycogen storage disease type Ib patient.
Matsunaga et al., Nagoya, Japan. In Genes Cells, 2013
Glycogen storage disease type Ib (GSDIb) is caused by a deficiency in the glucose-6-phosphate transporter (G6PT), which leads to neutrophil dysfunction.
The SLC37 family of sugar-phosphate/phosphate exchangers.
Mansfield et al., Bethesda, United States. In Curr Top Membr, 2013
SLC37A4, better known as the G6P transporter (G6PT), has been extensively characterized, functionally and structurally, and is the best characterized family member.
Glycogen storage disease type 1b: an early onset severe phenotype associated with a novel mutation (IVS4) in the glucose 6-phosphate translocase (SLC37A4) gene in a Turkish patient.
Açoğlu et al., In Genet Couns, 2013
GSD-Ib is caused by a deficiency in the glucose-6-phosphate transporter (G6PT) caused by a mutation in the SLC37A4 gene coding for G6PT.
The SLC37 family of phosphate-linked sugar phosphate antiporters.
Mansfield et al., Bethesda, United States. In Mol Aspects Med, 2013
The best characterized family member is SLC37A4, better known as the glucose-6-phosphate (G6P) transporter (G6PT).
AA Amyloidosis in a patient with glycogen storage disorder and progressive chronic kidney disease.
Jayawardene et al., London, United Kingdom. In Clin Kidney J, 2012
Type 1 glycogen storage diseases (GSD) are inherited metabolic diseases caused by defects in the activity of the glucose-6-phosphate transporter.
[Mutation in the SLC37A4 gene of glycogen storage disease type Ib in 15 families of the mainland of China].
Wei et al., Beijing, China. In Zhonghua Er Ke Za Zhi, 2011
A total of 11 SLC37A4 gene mutations were identified in 15 families of the mainland of China. The frequent mutations are p.Pro191Leu, p.Gly149Glu and c.870 + 5G > A.
Tissue-specific dysregulation of hexose-6-phosphate dehydrogenase and glucose-6-phosphate transporter production in db/db mice as a model of type 2 diabetes.
Liu et al., Los Angeles, United States. In Diabetologia, 2011
Findings suggest that increased hepatic H6PDH and G6PT production contribute to 11beta-HSD1 upregulation of local glucocorticoid action that may be related to the development of type 2 diabetes.
Glycogen storage disease type I and G6Pase-β deficiency: etiology and therapy.
Mansfield et al., Bethesda, United States. In Nat Rev Endocrinol, 2010
Glycogen storage disease type I (GSD-I) consists of two subtypes: GSD-Ia, a deficiency in glucose-6-phosphatase-α (G6Pase-α) and GSD-Ib, which is characterized by an absence of a glucose-6-phosphate (G6P) transporter (G6PT).
Two new variants of G6PD deficiencies in Singapore.
Matsuo et al., Kōbe, Japan. In Nepal Med Coll J, 2010
Two novel mutations were identified in these samples: one had a novel mutation (25C>T); the remaining sample carried a 49 bp deletion in intron 12.
Quantitative determination and tissue distribution of human 11β-hydroxysteroid dehydrogenase, hexose-6-phosphate dehydrogenase, glucose-6-phosphate transporter, glucocorticoid receptor and mineralocorticoid receptor mRNAs.
Nakajin et al., In Horm Mol Biol Clin Investig, 2010
METHODS: An absolute comparison of mRNA expression of human 11β-HSD isozymes, hexose-6-phosphate dehydrogenase (H6PDH), glucose-6-phosphate transporter (G6PT), glucocorticoid receptors (GRs), and mineralocorticoid receptor (MR) was performed by real-time RT-PCR.
Molecular analysis of glycogen storage disease type Ib in Sardinian population: evidence for a founder effect.
Loudianos et al., Cagliari, Italy. In Genet Test Mol Biomarkers, 2010
Our results suggest that in Sardinia, Glycogen storage disease Ib is caused by only one mutational event in the G6PT gene, further suggesting that Sardinia is a founder population.
Evidence for transcriptional regulation of the glucose-6-phosphate transporter by HIF-1alpha: Targeting G6PT with mumbaistatin analogs in hypoxic mesenchymal stromal cells.
Annabi et al., Montréal, Canada. In Stem Cells, 2009
Data suggest that G6PT may account for the metabolic flexibility that enables MSCs to survive under conditions characterized by hypoxia and could be specifically targeted within developing tumors.
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