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There are at least four distinct but related alkaline phosphatases: intestinal, placental, placental-like, and liver/bone/kidney (tissue non-specific). Additionally we are shipping Intestinal Alkaline Phosphatase Antibodies (207) and Intestinal Alkaline Phosphatase Proteins (14) and many more products for this protein.
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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.
Expressions of human intestinal alkaline phosphatase and sucrase-isomaltase, which are intestinal differentiation markers, were highly enhanced in Caco-2 cells by menaquinone-4.
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.
Intestinal alkaline phosphatase is a major regulator of gut (show GUSB ELISA Kits) mucosal permeability and appears to work at least partly through improving tight junction protein (show OCLN ELISA Kits) levels and localization.
A High Level of Intestinal Alkaline Phosphatase Is Protective Against Type 2 Diabetes Mellitus Irrespective of Obesity
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.
The expression of ALPi and MUC5AC in cocultures of Caco-2 and HT29 cells developed for permeability studies is reported.
Data indicate that histone deacetylase (show HDAC1 ELISA Kits) inhibitors (HDACi) induce intestinal alkaline phosphatase (ALPi) in a subset of colon cancer cell lines in a Kruppel-like factor 5 (KLF5 (show KLF5 ELISA Kits))-dependent manner.
Report lowered intestinal alkaline phosphatase in the colonic mucosa of children with inflammatory bowel disease.
we are the first to demonstrate the alteration of protein expression of iAP in the duodenal mucosa of children with newly diagnosed coeliac disease
It is concluded that CD36 (show CD36 ELISA Kits) exists in its phosphorylated and dephosphorylated states in mouse enterocytes and that pCD36 is a substrate of global intestinal alkaline phosphatase (gIAP).
Suggest role for lysophosphatidylcholine in brush-border intestinal alkaline phosphatase release and restoration.
Mechanism of IAP action appears to be through dephosphorylation of specific bacterial components, including LPS, CpG DNA, and flagellin (show FliC ELISA Kits), and not on live bacteria. IAP likely targets these bacterially derived molecules as gut (show GUSB ELISA Kits) mucosal defense factor.
Secondary structure of CIP after reaction with Co2+ in different conditions.
There are at least four distinct but related alkaline phosphatases: intestinal, placental, placental-like, and liver/bone/kidney (tissue non-specific). The intestinal alkaline phosphatase gene encodes a digestive brush-border enzyme. This enzyme is upregulated during small intestinal epithelial cell differentiation.
, alkaline phosphomonoesterase
, intestinal alkaline phosphatase
, intestinal-type alkaline phosphatase
, Alkaline phosphatase 1, intestinal, defined by SSR
, intestinal alkaline phosphatase 1
, intestinal alkaline phosphatase I IAP-I
, intestinal-type alkaline phosphatase 1
, alkaline phosphatase 6
, intestinal alkaline phosphatase V
, alkaline phosphatase, intestinal.1
, alkaline phosphatase, intestinal
, intestinal-type alkaline phosphatase-like