anti-Guanylate Cyclase Activator 2B (Uroguanylin) (GUCA2B) Antibodies

Mouse (Murine) Guanylate Cyclase Activator 2B (Uroguanylin) (GUCA2B) interaction partners

1. guanylin (show GUCA2A Antibodies) and uroguanylin are produced by mouse intestinal epithelial cells of columnar and secretory lineage

2. In obese mice UGN expression was decreased, whereas leptin (show LEP Antibodies) treatment up-regulated UGN levels in duodenum in these genetically modified mice compared to WT.

3. UGN exerts its inhibitory activity on the prendrin gene promoter likely via heat shock factor 1 action at a defined heat shock element site.

4. findings establish a role for uroguanylin in an enteric-renal communication axis as well as a fundamental principle of this axis in the maintenance of salt homeostasis in vivo

5. act on the mouse kidney, in part, through a cGMP-dependent, GC-C (show GUCY2C Antibodies)-independent mechanism, causing significant natriuresis by renal tubular processes.

6. existence of two signaling pathways for guanylin (show GUCA2A Antibodies) peptides in principal cells of mouse cortical collecting duct of kidney

7. Role for uroguanylin in fluid homeostasis and as an integral component of a signaling mechanism that mediates changes in Na excretion in response to an enteral salt loading.

Human Guanylate Cyclase Activator 2B (Uroguanylin) (GUCA2B) interaction partners

1. Both guanylin (show GUCA2A Antibodies) and uroguanylin trigger lipolysis in human visceral adipocytes. Given the lipolytic action of the guanylin (show GUCA2A Antibodies) system on visceral adipocytes, the herein reported decrease of circulating prouroguanylin concentrations in obese patients may have a role in excessive fat accumulation in obesity.

2. Results demonstrate that GC-C (show GUCY2C Antibodies) and its ligands, guanylin (show GUCA2A Antibodies) and uroguanylin are downregulated in ulcerative colitis (UC), and this downregulation is more significant with aggravation of the clinical condition. Therefore, the GC-C (show GUCY2C Antibodies) signaling pathway may be implicated in the progression of UC.

3. The simulations suggested that all missense SNPs considered as convergent deleterious caused some kind of structural change to the uroguanylin peptide. Additionally, four of these SNPs were also shown to cause modifications in peptide flexibility, possibly resulting in functional changes.

4. The specific cellular distribution of both GN and UGN differs between duodenum and colon and between human and rat intestines.

5. Uroguanylin concentrations are increased in patients with chronic renal failure, nephrotic syndrome, or those on dialysis.