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guanylyl cyclase\; functions as receptor for heat-stable enterotoxin responsible for acute diarrhea [RGD, Feb 2006]..
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Findings show how caloric suppression of the guanylin (show GUCA2A Antibodies)-GUCY2C signaling axis links obesity to negation of a universal tumor suppressor pathway in colorectal cancer.
The GC-C signaling pathway blunts colonic mucosal inflammation that is initiated by systemic cytokine burst or loss of mucosal immune cell immunosuppression.
GC-C signaling is an essential component of host defense during murine enteric infection by reducing bacterial load and preventing systemic dissemination of attaching/effacing-lesion forming bacterial pathogens such as C. rodentium.
Intestinal cell proliferation and senescence are regulated by receptor guanylyl cyclase C and p21 (show D4S234E Antibodies).
GUCY2C opposes systemic genotoxic tumorigenesis by regulating AKT (show AKT1 Antibodies)-dependent intestinal barrier integrity
The role for GUCY2C-directed CD8 (show CD8A Antibodies)(+) T cells targeting specific epitopes in antitumor efficacy.
Data show that silencing of GUCY2C in mice disrupts satiation, resulting in hyperphagia and subsequent obesity and metabolic syndrome.
a novel role for GC-C signaling in facilitating mucosal wounding and inflammation, and further suggest that this may be mediated, in part, through control of RELMbeta (show RETNLB Antibodies) production
midbrain dopamine neurons express GC-C; GC-C activation potentiates excitatory response mediated by glutamate (show GRIN1 Antibodies) and acetylcholine receptors via activity of PKG (show PRKG1 Antibodies); GC-C knockout mice exhibit hyperactivity and attention deficit
guanylyl cyclase\; functions as receptor for heat-stable enterotoxin responsible for acute diarrhea
, guanylyl cyclase C
, heat stable enterotoxin receptor
, heat-stable enterotoxin receptor
, intestinal guanylate cyclase
, Guanylate cyclase 2C (heat stable enterotoxin receptor)