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Intestinal Alkaline Phosphatase Rabbit mAb

Catalog No.: F3426

Application: Reactivity: Mouse, Human

Usage Information

Dilution
WB1:1000 - 1:10000 IHC1:100 - 1:500

Application
WB, IHC

Reactivity
Mouse, Human

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
57 kDa 57 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Datasheet & SDS

Biological Description

Specificity
Intestinal Alkaline Phosphatase Rabbit mAb detects endogenous levels of total Intestinal Alkaline Phosphatase protein.

Clone
M14M3

Synonym(s)
Intestinal-type alkaline phosphatase, IAP, Intestinal alkaline phosphatase, ALPI

Background
Intestinal alkaline phosphatase (IAP) is a membrane-bound, zinc-dependent metalloenzyme belonging to the alkaline phosphatase (AP) family, encoded in humans by the ALPI gene on chromosome 2. Structurally, it shares high amino acid sequence homology with placental AP, and also with tissue-nonspecific AP (TNAP), reflecting an evolutionary divergence between tissue-specific and nonspecific isoforms. IAP is predominantly expressed and secreted by enterocytes of the small intestine, with highest mRNA expression in the duodenum and maximal enzymatic activity in the terminal ileum; it is also released into the intestinal lumen and, to a lesser extent, the circulation, where it remains catalytically active. Functionally, IAP plays a central role in maintaining gut homeostasis by dephosphorylating and detoxifying pathogen-associated molecular patterns such as lipopolysaccharide (LPS), flagellin, unmethylated CpG DNA, and extracellular nucleotides (ATP, ADP, UDP), thereby dampening pro-inflammatory signaling. It supports commensal bacterial colonization, limits bacterial translocation across the epithelium, modulates duodenal pH and bicarbonate secretion, facilitates long-chain fatty acid absorption, and shapes microbiome composition in response to diet. Reduced IAP expression—seen in conditions like prematurity, starvation, inflammation, and certain surgical states—has been linked to dysbiosis, intestinal inflammation, and systemic sepsis risk, making recombinant or exogenous IAP a promising therapeutic candidate for inflammatory, infectious, and postoperative complications.

Background

Intestinal alkaline phosphatase (IAP) is a membrane-bound, zinc-dependent metalloenzyme belonging to the alkaline phosphatase (AP) family, encoded in humans by the ALPI gene on chromosome 2. Structurally, it shares high amino acid sequence homology with placental AP, and also with tissue-nonspecific AP (TNAP), reflecting an evolutionary divergence between tissue-specific and nonspecific isoforms. IAP is predominantly expressed and secreted by enterocytes of the small intestine, with highest mRNA expression in the duodenum and maximal enzymatic activity in the terminal ileum; it is also released into the intestinal lumen and, to a lesser extent, the circulation, where it remains catalytically active. Functionally, IAP plays a central role in maintaining gut homeostasis by dephosphorylating and detoxifying pathogen-associated molecular patterns such as lipopolysaccharide (LPS), flagellin, unmethylated CpG DNA, and extracellular nucleotides (ATP, ADP, UDP), thereby dampening pro-inflammatory signaling. It supports commensal bacterial colonization, limits bacterial translocation across the epithelium, modulates duodenal pH and bicarbonate secretion, facilitates long-chain fatty acid absorption, and shapes microbiome composition in response to diet. Reduced IAP expression—seen in conditions like prematurity, starvation, inflammation, and certain surgical states—has been linked to dysbiosis, intestinal inflammation, and systemic sepsis risk, making recombinant or exogenous IAP a promising therapeutic candidate for inflammatory, infectious, and postoperative complications.

References
https://pubmed.ncbi.nlm.nih.gov/27083970/ https://pubmed.ncbi.nlm.nih.gov/25400448/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%