anti-Guanylate Cyclase 2C (Heat Stable Enterotoxin Receptor) (GUCY2C) Antibodies

Human Guanylate Cyclase 2C (Heat Stable Enterotoxin Receptor) (GUCY2C) interaction partners

1. The results support a role of guanylate cyclase C signaling and disturbed electrolyte homeostasis in development of IBD. Furthermore, downregulation of metallothioneins in the ileal mucosa of familial GUCY2C diarrhea syndrome patients may contribute to inflammatory bowel disease development, possibly alongside effects from NOD2 risk variants.

2. Human GUCY2C-targeted murine CAR-T cells promoted antigen-dependent T-cell activation quantified by activation marker upregulation, cytokine production, and killing of GUCY2C-expressing, but not GUCY2C-deficient, cancer cells in vitro GUCY2C CAR-T cells provided long-term protection against lung metastases of murine colorectal cancer cells engineered to express human GUCY2C in a syngeneic mouse model.

3. High Expressions of guanylyl cyclase C is associated with rectal cancer.

4. The findings support that the activating mutation in GUCY2C creates an intestinal environment with a major influence on the microbiota, which could contribute to the increased susceptibility to inflammatory bowel disease in patients with Familial GUCY2C diarrhea syndrome.

5. Results demonstrate that GC-C and its ligands, guanylin and uroguanylin are downregulated in ulcerative colitis (UC), and this downregulation is more significant with aggravation of the clinical condition. Therefore, the GC-C signaling pathway may be implicated in the progression of UC.

6. the expression of GCC is maintained throughout the process of tumor progression and formation of metastatic disease.

7. To investigate gut motility and hormones before and after a meal in Familial GUCY2C diarrhea syndrome patients and compare with healthy controls

8. Mutations in GUCY2C indicate a role for this receptor in the pathogenesis of sporadic Congenital secretory diarrhea.

9. these data support Ad5-GUCY2C-PADRE as a safe and effective vaccination strategy in preclinical models and position Ad5-GUCY2C-PADRE for Phase I clinical testing in colorectal cancer patients.

10. Familial GUCY2C diarrhoea syndrome is caused by an activating mutation in the GUCY2C gene, which causes impaired contractility and fluid stagnation in the small bowel

11. Findings show how caloric suppression of the guanylin-GUCY2C signaling axis links obesity to negation of a universal tumor suppressor pathway in colorectal cancer.

12. Data show that individuals affected with meconium ileus (MI) had either homozygous or compound heterozygous variants in enterotoxin receptor GUCY2C.

13. High guanylyl cyclase C expression is associated with colon cancer recurrence.

14. Transmission disequilibrium tests (TDT), case-control studies and quantitative analyses indicated association between GUC2C with Attention-deficit/hyperactivitydisorder and its core symptoms.

15. Intestinal cell proliferation and senescence are regulated by receptor guanylyl cyclase C and p21.

16. GUCY2C signaling constitutes a direct link between the initiation of colorectal cancer and the induction of its associated desmoplastic stromal niche.

17. Data show that lower survival (OS) and disease-free survival (DFS) rates were significantly associated with guanylate cyclase C (GCC) and CK20 mRNA levels.

18. Interaction with VIP36 is dependent on glycosylation at the same sites that allow GC-C to fold and bind ligand.

19. GUCY2C opposes systemic genotoxic tumorigenesis by regulating AKT-dependent intestinal barrier integrity

20. Mutations in GUCY2C were associated with the Meconium ileus phenotype. downregulation of GUCY2C leads to a cystic fibrosis-like intestinal phenotype.

Mouse (Murine) Guanylate Cyclase 2C (Heat Stable Enterotoxin Receptor) (GUCY2C) interaction partners

1. Gucy2c knockout mice have a moderate cognitive and startle phenotype but have no ADHD-like phenotype.

2. This retrogenic model can be employed to define self-tolerance mechanisms restricting T and B cell responses to GUCY2C to optimize colorectal cancer immunotherapy without autoimmunity.

3. Activation of guanylate cyclase-C attenuates stretch responses and sensitization of mouse colorectal afferents.

4. Relative to controls, guanylate cyclase C knockout mice develop severe systemic illness following oral Salmonella infection, characterized by disrupted intestinal mucus layer, elevated cytokines and organ bacterial load, and reduced animal survival.

5. Loss of Gucy2c expression is associated with Acute Radiation-Induced GI Syndrome.

6. Findings show how caloric suppression of the guanylin-GUCY2C signaling axis links obesity to negation of a universal tumor suppressor pathway in colorectal cancer.

7. The GC-C signaling pathway blunts colonic mucosal inflammation that is initiated by systemic cytokine burst or loss of mucosal immune cell immunosuppression.

8. 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.

9. Intestinal cell proliferation and senescence are regulated by receptor guanylyl cyclase C and p21.

10. GUCY2C opposes systemic genotoxic tumorigenesis by regulating AKT-dependent intestinal barrier integrity

11. The role for GUCY2C-directed CD8(+) T cells targeting specific epitopes in antitumor efficacy.

12. Data show that silencing of GUCY2C in mice disrupts satiation, resulting in hyperphagia and subsequent obesity and metabolic syndrome.

13. 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 production

14. midbrain dopamine neurons express GC-C; GC-C activation potentiates excitatory response mediated by glutamate and acetylcholine receptors via activity of PKG; GC-C knockout mice exhibit hyperactivity and attention deficit

15. GCC signaling plays a protective role in the integrity of the intestinal mucosal barrier by regulating myosin light chain kinase activation and tight junction disassembly.

16. There is a previously unappreciated interaction between sex and GCC signaling restricting crypt cell proliferation.

17. GUCY2C is a tumor suppressor that controls proliferation and metabolism of intestinal epithelial cells by inactivating AKT signaling

18. transmembrane guanylyl cyclase C is a key mediator of acid-stimulated duodenal bicarbonate secretion

19. guanylin, uroguanylin, and E coli enterotoxin act on the mouse kidney, in part, through a cGMP-dependent, GC-C-independent mechanism, causing significant natriuresis by renal tubular processes

20. two signaling pathways for guanylin peptides in principal cells of mouse cortical kidney collecting duct is not mediated by guanylate cyclase C