Alkaline Phosphatase, Intestinal (ALPI) ELISA Kits

Human Alkaline Phosphatase, Intestinal (ALPI) interaction partners

1. Data confirm that, in enterocytes (Caco-2 cells), 1-alpha,25-dihydroxy-vitamin-D3 up-regulates expression of 2 isoforms of IAP, alternative splicing variants.

2. Expressions of human intestinal alkaline phosphatase and sucrase-isomaltase, which are intestinal differentiation markers, were highly enhanced in Caco-2 cells by menaquinone-4.

3. Data indicate alkaline phosphatase (AP) as the primary soluble ectonucleotidase in infants undergoing cardiopulmonary bypass and show decreased capacity to clear AMP when AP activity decreases post-bypass.

4. Intestinal alkaline phosphatase is a major regulator of gut mucosal permeability and appears to work at least partly through improving tight junction protein levels and localization.

5. A High Level of Intestinal Alkaline Phosphatase Is Protective Against Type 2 Diabetes Mellitus Irrespective of Obesity

6. Review of the role of intestinal alkaline phosphatase in inflammatory diseases. Loss of IAP expression or function is associated with increased intestinal inflammation, dysbiosis, bacterial translocation and subsequently systemic inflammation.

7. The expression of ALPi and MUC5AC in cocultures of Caco-2 and HT29 cells developed for permeability studies is reported.

8. Data indicate that histone deacetylase inhibitors (HDACi) induce intestinal alkaline phosphatase (ALPi) in a subset of colon cancer cell lines in a Kruppel-like factor 5 (KLF5)-dependent manner.

9. Report lowered intestinal alkaline phosphatase in the colonic mucosa of children with inflammatory bowel disease.

10. we are the first to demonstrate the alteration of protein expression of iAP in the duodenal mucosa of children with newly diagnosed coeliac disease

11. Mechanism of IAP action appears to be through dephosphorylation of specific bacterial components, including LPS, CpG DNA, and flagellin, and not on live bacteria. IAP likely targets these bacterially derived molecules as gut mucosal defense factor.

12. the structural differences in human AP isoforms are demonstrated through models

13. intestinal alkaline transactivation by Kruppel-like factor-4 is likely mediated through a critical region located within the proximal IAP promoter region

14. Northern blotting detected expression of two IAP transcripts, which were increased approximately 3-fold in response to thyroid hormone

15. receptor for Aeromonas sobria hemolysin

16. Cdx1 activates the IAP gene via a novel cis element, whereas Cdx2 inhibits the Cdx1 effects

17. Cotransfection with an HNF-4alpha expression vector demonstrated a direct activation of the ALPI promoter through -94 to -82 element

18. Crohn's disease increases the alkaline phosphatase activity in the intestine. Use histochemistry to differentiate Crohn's disease/ulcerative colitis.

19. has the ability to detoxify lipopolysaccharide and prevent bacterial invasion across the gut mucosal barrier. IAP expression and function are lost with starvation and maintained by enteral feeding

20. Cathepsin C propeptide interacts with intestinal alkaline phosphatase (IAP) and heat shock cognate protein 70. The propeptide of cathepsin C may stimulate the sorting to the lysosome contributing to the degradation of IAP in Caco-2 cells.

Mouse (Murine) Alkaline Phosphatase, Intestinal (ALPI) interaction partners

1. Intestinal alkaline phosphatase is a major regulator of gut mucosal permeability and appears to work at least partly through improving tight junction protein levels and localization.

2. It is concluded that CD36 exists in its phosphorylated and dephosphorylated states in mouse enterocytes and that pCD36 is a substrate of global intestinal alkaline phosphatase (gIAP).

3. Suggest role for lysophosphatidylcholine in brush-border intestinal alkaline phosphatase release and restoration.

Cow (Bovine) Alkaline Phosphatase, Intestinal (ALPI) interaction partners

1. Intravenous bolus administration plus 8 hours continuous infusion of alkaline phosphatase in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass results in endogenous alkaline phosphatase release.

2. Mechanism of IAP action appears to be through dephosphorylation of specific bacterial components, including LPS, CpG DNA, and flagellin, and not on live bacteria. IAP likely targets these bacterially derived molecules as gut mucosal defense factor.

3. differences in metal binding between bovine and Escherichia coli alkaline phosphatases

4. Secondary structure of CIP after reaction with Co2+ in different conditions.