GTP-Binding Protein alpha Subunits

The GTPase-containing subunits of heterotrimeric GTP-binding proteins. When dissociated from the heterotrimeric complex these subunits interact with a variety of second messenger systems. Hydrolysis of GTP by the inherent GTPase activity of the subunit causes it to revert to its inactive (heterotrimeric) form. The GTP-Binding protein alpha subunits are grouped into families according to the type of action they have on second messenger systems.

Also Known As:

Networked: 49 relevant articles (0 outcomes, 3 trials/studies)

Bio-Agent Context: Research Results

Experts

1.	Edwards, Robert A: 3 articles (08/2009 - 06/2007)
2.	Birnbaumer, Lutz: 3 articles (08/2009 - 06/2007)
3.	Kilic, E: 2 articles (07/2013 - 09/2009)
4.	Vaarwater, J: 2 articles (07/2013 - 09/2009)
5.	de Klein, A: 2 articles (07/2013 - 09/2009)
6.	Wang, Kehui: 2 articles (08/2009 - 07/2008)
7.	Weinstein, Lee S: 2 articles (03/2007 - 09/2003)
8.	Özsu, Elif: 1 article (06/2015)
9.	Çizmecioğlu, Filiz Mine: 1 article (06/2015)
10.	Mutlu, Gül Yeşiltepe: 1 article (06/2015)

Related Diseases

1.	Adenoma (Adenomas) 06/01/1996 - "Low incidence of the stimulatory G protein alpha-subunit mutations in autonomously functioning thyroid adenomas in Japan." 03/01/2008 - "Some studies have found better responses to somatostatin analogues in G-protein alpha subunit (Gsalpha) mutation (gsp oncogene)-positive adenomas. " 02/15/1993 - "Stimulation of human thyroid growth via the inhibitory guanine nucleotide binding (G) protein Gi: constitutive expression of the G-protein alpha subunit Gi alpha-1 in autonomous adenoma."
2.	Cardiomyopathies (Cardiomyopathy) 01/01/1997 - "The goal of this study was to determine whether chronic endogenous sympathetic stimulation resulting from the overexpression of cardiac stimulatory G protein alpha subunit (Gs alpha) in transgenic mice (15.3 +/- 0.1 mo old) resulted in a clinical picture of cardiomyopathy. "
3.	Malaria 12/01/2008 - "Functional studies have demonstrated an interaction between the stimulatory G protein alpha subunit (G-alpha-s) and the malaria parasite at a cellular level. "
4.	Pseudohypoparathyroidism 12/01/2006 - "Moreover, alteration in genes encoding for second messengers may cause forms of resistance other than those due to receptor mutations, the most important one being that of an inactivating mutation in the G-protein alpha-subunit leading to TSH resistance in the setting of pseudohypoparathyroidism type 1a. " 05/01/2006 - "Most loss of function mutations of GNAS identified in different forms of pseudohypoparathyroidism disrupt not only the stimulatory G protein alpha-subunit (Gsalpha), but also its paternally expressed variant, XLalphas. " 09/01/2003 - "The stimulatory G protein alpha-subunit Gs alpha is imprinted in human thyroid glands: implications for thyroid function in pseudohypoparathyroidism types 1A and 1B." 03/01/2002 - "Pseudohypoparathyroidism: a multitude of mutations in the stimulatory G protein alpha subunit (Gsalpha)." 07/01/2001 - "Pseudohypoparathyroidism Ia (PHP Ia) is characterized by resistance to PTH and many other stimuli because of deficiency of stimulatory G protein alpha-subunit. "
5.	Obesity 05/01/2009 - "A missense mutation in the non-neural G-protein alpha-subunit isoforms modulates susceptibility to obesity." 03/01/2007 - "Obesity is a prominent feature of Albright hereditary osteodystrophy (AHO), a disorder caused by heterozygous GNAS mutations that disrupt the stimulatory G protein alpha-subunit Galpha(s). " 07/21/1998 - "Albright hereditary osteodystrophy (AHO), an autosomal dominant disorder characterized by short stature, obesity, and skeletal defects, is associated with heterozygous inactivating mutations of GNAS1, the gene encoding the heterotrimeric G protein alpha-subunit (Gsalpha) that couples multiple receptors to the stimulation of adenylyl cyclase. "

Related Drugs and Biologics

1.	Somatostatin (Somatotropin Release-Inhibiting Factor)
2.	GTP-Binding Proteins (G-Protein)
3.	Adenylate Cyclase (Adenylyl Cyclase)
4.	Messenger RNA (mRNA)
5.	Human Growth Hormone (Saizen)
6.	Guanine
7.	Albright's hereditary osteodystrophy
8.	Ghrelin Receptors
9.	Type 4 Fibroblast Growth Factor Receptor
10.	Aromatase Inhibitors