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Phosphoglycerate Mutase (Phosphoglyceromutase)

An enzyme that catalyzes the conversion of 2-phospho-D-glycerate to 3-phospho-D-glycerate. EC 5.4.2.1.
Also Known As:
Phosphoglyceromutase; Phosphoglycerate Phosphomutase; Mutase, Phosphoglycerate; Phosphomutase, Phosphoglycerate; Glycerate (3-2)-Phosphomutase; D-Phosphoglycerate 2,3-phosphomutase
Networked: 71 relevant articles (0 outcomes, 6 trials/studies)

Bio-Agent Context: Research Results

Experts

1. Carreras, José: 4 articles (06/2005 - 01/2003)
2. Climent, Fernando: 4 articles (06/2005 - 01/2003)
3. DiMauro, Salvatore: 3 articles (03/2010 - 11/2006)
4. Vissing, John: 3 articles (03/2009 - 08/2002)
5. Rakus, Dariusz: 2 articles (07/2015 - 06/2012)
6. Inagaki, Nobuya: 2 articles (05/2015 - 10/2014)
7. Yokode, Masayuki: 2 articles (05/2015 - 10/2014)
8. Kondoh, Hiroshi: 2 articles (05/2015 - 10/2014)
9. Chen, Georgia Z: 2 articles (01/2013 - 11/2012)
10. Khoury, Hanna J: 2 articles (01/2013 - 11/2012)

Related Diseases

1. Muscular Diseases (Myopathy)
2. Glycogen Storage Disease (Glycogenosis)
03/01/2009 - "Phosphoglycerate mutase (PGAM) deficiency (glycogen storage disease type X) has been reported in 12 patients of whom 9 were African American. "
10/01/1999 - "Muscle-specific phosphoglycerate mutase (PGAM-M) deficiency results in a metabolic myopathy (glycogenosis type X). "
10/01/2007 - "Phosphoglycerate Kinase, Phosphoglycerate Mutase, Lactate Dehydrogenase, beta-Enolase and Aldolase A deficiencies have been described as distal glycogenoses. "
12/01/1986 - "Six glycogen storage diseases (resulting from deficiencies of acid maltase, phosphorylase, phosphofructokinase, phosphoglycerate kinase, phosphoglycerate mutase, and lactate dehydrogenase) and one mitochondrial myopathy (cytochrome c oxidase deficiency) are reviewed to illustrate: clinical heterogeneity, biochemical heterogeneity, evidence for tissue-specific and developmentally controlled isozymes, and molecular genetic studies."
06/01/1996 - "Disorders of glycogen, lipid or mitochondrial metabolism may cause two main clinical syndromes, namely (1) progressive weakness (eg, acid maltase, debrancher enzyme, and brancher enzyme deficiencies among the glycogenoses; long- and very-long-chain acyl-CoA dehydrogenase (LCAD, VLCAD), and trifunctional enzyme deficiencies among the fatty acid oxidation (FAO) defects; and mitochondrial enzyme deficiencies) or (2) acute, recurrent, reversible muscle dysfunction with exercise intolerance and acute muscle breakdown or myoglobinuria (with or without cramps) (eg, phosphorylase (PPL), phosphorylase b kinase (PBK), phosphofructokinase (PFK), phosphoglycerate kinase (PGK), phosphoglycerate mutase (PGAM), and lactate dehydrogenase (LDH) among the glycogenoses and carnitine palmitoyltransferase II (CPT II) deficiency among the disorders of FAO or (3) both (eg, PPL, PBK, PFK among the glycogenoses; LCAD, VLCAD, short-chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD), and trifunctional enzyme deficiencies among the FAO defects; and multiple mitochondrial DNA (mtDNA) deletions). "
3. Cytochrome-c Oxidase Deficiency
4. Autoimmune Hepatitis
5. Mitochondrial Myopathies (Mitochondrial Myopathy)

Related Drugs and Biologics

1. Proteins (Proteins, Gene)
2. Phosphoglycerate Kinase (Kinase, Phosphoglycerate)
3. L-Lactate Dehydrogenase (Lactate Dehydrogenase)
4. Phosphopyruvate Hydratase (Enolase)
5. Isoenzymes
6. Autoantibodies
7. alpha-Glucosidases (Acid Maltase)
8. CAP18 lipopolysaccharide-binding protein (Bac4)
9. Leukocyte L1 Antigen Complex (Calgranulin)
10. Proteome

Related Therapies and Procedures

1. Lenses