Disease relevance of GUCY2C

• The heat-stable enterotoxin (STa) of Escherichia coli causes intestinal secretion by stimulating guanylate cyclase, an enzyme believed to be distinct from the STa receptor [1].
• A review of the measures relating to the monitoring of disease progression in Duchenne muscular dystrophy was undertaken as part of the work of the North Star Clinical Network for Paediatric Neuromuscular Disease Management developing a standardized assessment protocol for ambulant children in the UK [2].
• This assay confirmed that GCC mRNA was overexpressed by colorectal tumors from 41 patients, which correlated with increased GCC protein quantified by immunohistochemistry [3].

High impact information on GUCY2C

• Stable mammalian cell lines over-expressing the STa receptor specifically bind 125I-STa (Kd approximately 1.0 nM) and respond to STa by dramatically increasing (approximately 50-fold) cellular cGMP levels [4].
• A 60 kDa protein was also specifically immunoprecipitated from solubilized human brush border membranes using antisera raised against a cloned STa receptor fusion protein [5].
• Our observations of multiple crosslinked proteins in human intestine and Caco-2 cells could be explained by the existence of several members of a family of STa receptors and/or the existence of smaller STa binding proteins generated by the protease cleavage of a larger complete STa receptor [5].
• This suggested that a guanine nucleotide regulatory protein (G protein) coupled the STa receptor to guanylate cyclase, a function not previously recognized for G proteins [1].
• The putative STa receptor was radiolabeled with 431 125I-STa and solubilized with sodium deoxycholate [6].

Biological context of GUCY2C

• The predicted amino acid sequence of the human STa receptor is 81% identical with the previously cloned enterotoxin receptor (GC-C) from rat intestine [7].
• GC-C is modified by N-linked glycosylation and, at least in the small intestine, by proteolysis, resulting in a STa receptor that is coupled non-covalently to the intracellular domain [8].
• We investigated whether PKC causes phosphorylation of the STa receptor in vivo and in vitro [9].
• An assessment of the Kemble Star 700 sample processor for the automation of complement fixation and ELISA tests in a microbiology laboratory [10].

Anatomical context of GUCY2C

• 125I-STa-binding assay suggested that the stronger fluorescence intensity on enterocytes from younger mice is due to higher STa receptor density and higher receptor affinity to STa [11].
• The guanylin/STa receptor is expressed in crypts and apical epithelium throughout the mouse intestine [12].

Associations of GUCY2C with chemical compounds

• Although GC-C, the STa receptor, may also be a receptor for guanylin, other receptors may exist that may be more specific for guanylin.(ABSTRACT TRUNCATED AT 250 WORDS)[13]
• It is likely that guanylin and uroguanylin are indeed endogenous ligands for the STa receptor and may be modulators of Cl- secretion in the intestine, kidney, and perhaps in other organs [13].
• D-dimers plasma concentrations were measured with the STA Liatest D-Di on the STA-R coagulation analyzer, with a reference ELISA technique (Asserachrom), with an automated quantitative latex-based immunoassay (Tinaquant) and with the VIDAS D-dimer test [14].
• The double-leg lowering test was measured in degrees, and the Star Excursion Balance Test was measured in 4 directions as a percentage of the subject's leg length [15].
• The probability of receiving a Purple Heart, Bronze Star, Commendation Medal and Combat Infantry Badge is associated strongly with the combat exposure index [16].

Physical interactions of GUCY2C

• Recently an endogenous ligand called guanylin has been extracted from mammalian intestine and shown to bind the STa receptor [13].

Other interactions of GUCY2C

• These cells possess transcripts for cystic fibrosis transmembrane conductance regulator, Na+-K+-2Cl- cotransporter, STa receptor, and intestine-specific cGMP-dependent protein kinase II [17].

Analytical, diagnostic and therapeutic context of GUCY2C

• Flow cytometry and indirect immunofluorescence analyses suggested that insulin had an up-regulatory effect on the STa-receptor level [18].

References