Glutamate-Ammonia Ligase (Glutamine Synthetase)

An enzyme that catalyzes the conversion of ATP, L-glutamate, and NH3 to ADP, orthophosphate, and L-glutamine. It also acts more slowly on 4-methylene-L-glutamate. (From Enzyme Nomenclature, 1992) EC 6.3.1.2.

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Networked: 491 relevant articles (6 outcomes, 40 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Eid, Tore: 7 articles (10/2015 - 01/2008)
2.	Lee, Tih-Shih W: 7 articles (10/2015 - 01/2008)
3.	Gonçalves, Carlos-Alberto: 5 articles (10/2015 - 09/2006)
4.	Kakar, Sanjay: 5 articles (11/2014 - 11/2011)
5.	Schwarz, Michael: 5 articles (03/2011 - 10/2002)
6.	Ferrell, Linda D: 4 articles (11/2015 - 05/2013)
7.	Zaveri, Hitten P: 4 articles (10/2015 - 08/2008)
8.	Quincozes-Santos, André: 4 articles (10/2015 - 07/2009)
9.	Rosenstein, Ruth E: 4 articles (02/2013 - 10/2009)
10.	Enosawa, Shin: 4 articles (12/2012 - 01/2005)

Related Diseases

1.	Liver Cell Adenoma (Hepatocellular Adenoma) 10/01/2014 - "Glutamine synthetase interpretation in hepatocellular adenoma." 08/01/2014 - "Diffuse glutamine synthetase overexpression restricted to areas of peliosis in a β-catenin-activated hepatocellular adenoma: a potential pitfall in glutamine synthetase interpretation." 01/01/2014 - "The majority of inflammatory hepatocellular adenomas demonstrated perivascular and/or patchy glutamine synthetase staining (73.6%), while the remaining cases had diffuse (7.5%), negative (3.8%), or patchy pattern of staining (15%) that showed subtle differences from the classic map-like staining pattern and was designated as pseudo map-like staining. " 01/01/2013 - "Value and limits of routine histology alone or combined with glutamine synthetase immunostaining in the diagnosis of hepatocellular adenoma subtypes on surgical specimens." 06/01/2011 - "We report a case of hepatocellular carcinoma arising within a pigmented telangiectatic hepatocellular adenoma in a noncirrhotic man with diffuse glutamine synthetase and nuclear β-catenin positivity. "
2.	Neoplasms (Cancer) 08/01/1989 - "Marked decrease in glutamine synthetase activity was observed in the tumor cells. " 04/01/1993 - "[Immunohistochemical study of glutamine synthetase expression in normal human brain and intracranial tumors]." 11/01/2015 - "Immunohistochemically, increased expression of glutamine synthetase in tumor cells and CD34 expression in sinusoidal endothelial cells were seen in the HCC component. " 11/01/2014 - "Tumors with nuclear β-catenin and/or diffuse glutamine synthetase were considered β-catenin activated. " 08/01/2014 - "The tumor lacked nuclear β-catenin positivity and demonstrated a hitherto undescribed pattern of glutamine synthetase overexpression restricted to areas of peliosis with mostly negative staining in non-peliotic areas. "
3.	Hyperammonemia 09/01/1997 - "Developmental study of hepatic glutamine synthetase in a mouse model of congenital hyperammonemia." 10/01/2015 - "Hyperammonemia induces significant changes in the central nervous system (CNS) in direct association with astroglial functions, such as oxidative damage, glutamatergic excitotoxicity, and impaired glutamine synthetase (GS) activity and pro-inflammatory cytokine release. " 04/28/2015 - "Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase." 01/01/2015 - "A baculovirus, termed Bac-GS, containing the glutamine synthetase (GS) gene was constructed for the in vitro and in vivo treatment of hyperammonemia. " 01/01/2015 - "Delivery of glutamine synthetase gene by baculovirus vectors: a proof of concept for the treatment of acute hyperammonemia."
4.	Acidosis 10/03/2003 - "Inhibition of glutamine synthetase in the mouse kidney: a novel mechanism of adaptation to metabolic acidosis." 01/01/1984 - "Renal recovery from metabolic acidosis in the rat: no role for glutamine synthetase." 11/15/1983 - "Glutamine synthetase activity of muscle in acidosis." 02/15/2014 - "Metabolic acidosis increased phosphenolpyruvate carboxykinase (PEPCK) and Na(+)/H(+) exchanger NHE-3 and decreased glutamine synthetase (GS) expression in both genotypes, and these changes were significantly greater in CD-Rhbg/Rhcg-KO than in C mice. " 11/01/2010 - "We conclude 1) intercalated cell Rhbg contributes to acidosis-stimulated renal ammonia excretion, 2) Rhbg in CNT and principal cells may contribute to renal ammonia excretion, and 3) decreased glutamine synthetase expression may enable normal rates of ammonia excretion under both basal conditions and on day 5 of acid loading in IC-Rhbg-KO mice."
5.	Focal Nodular Hyperplasia 01/01/2014 - "The glutamine synthetase staining pattern was map-like in 90% of focal nodular hyperplasia cases, with the remaining 10% of cases showing pseudo map-like staining. " 12/01/2012 - "Immunostaining of glutamine synthetase is a sensitive and specific marker for diagnosing focal nodular hyperplasia in needle biopsy." 03/01/2009 - "Over-expression of glutamine synthetase in focal nodular hyperplasia: a novel easy diagnostic tool in surgical pathology." 01/01/2014 - "Three cases were labeled as indeterminate and showed focal nodular hyperplasia-like morphology but lacked map-like glutamine synthetase staining pattern; these cases demonstrated a patchy pseudo map-like glutamine synthetase pattern along with the expression of serum amyloid-associated protein. " 01/01/2014 - "Expression of serum amyloid-associated protein in inflammatory hepatocellular adenoma and map-like pattern of glutamine synthetase in focal nodular hyperplasia can be helpful in this distinction, but the pitfalls and limitations of these markers have not been established. "

Related Drugs and Biologics

1.	Amyloid (Amyloid Fibrils)
2.	Glutamine (L-Glutamine)
3.	Fatty Acid-Binding Proteins
4.	Sodium-Hydrogen Antiporter
5.	C-Reactive Protein
6.	Glutamic Acid (Glutamate)
7.	Glutaminase
8.	Ammonia
9.	Retinaldehyde (Retinal)
10.	Glial Fibrillary Acidic Protein

Related Therapies and Procedures

1.	Bioreactors
2.	Artificial Liver (Bioartificial Liver)
3.	Transplantation (Transplant Recipients)
4.	Surgical Portacaval Shunt (Portacaval Anastomosis)
5.	Ischemic Postconditioning