ENPP2/ATX Antibody [J20P19] | Primary Antibodies

Application: Reactivity: Human, Mouse

Lane 1: Hela, Lane 2: U-87 MG, Lane 3: A375, Lane 4: Mouse placenta

Usage Information

Dilution
WB1:1000 IF1:50 FCM1:500

Application
WB, IF, FCM

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

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
98 kDa 100 kDa,36 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
ENPP2/ATX Antibody [J20P19] detects endogenous levels of total ENPP2/ATX protein.

Clone
J20P19

Synonym(s)
ATX; PDNP2; ENPP2; Autotaxin; Ectonucleotide pyrophosphatase/phosphodiesterase family member 2; Extracellular lysophospholipase D; E‑NPP 2; LysoPLD

Background
ENPP2, widely known as autotaxin (ATX), functions as a secreted ectonucleotide pyrophosphatase/phosphodiesterase that hydrolyzes lysophosphatidylcholine into bioactive lysophosphatidic acid (LPA), driving critical signaling in cell motility, vascular maturation, and tissue repair. ATX generates LPA gradients that engage LPAR1-6 G-protein-coupled receptors, activating Gαq/PLCβ for calcium release and RhoA/ROCK-mediated actomyosin contraction, alongside Gαi/PI3K/Akt for survival and Gα12/13/PKA for chemotaxis, while direct ATX-integrin αvβ3/α5β1 interactions localize LPA delivery at leading edges to amplify FAK/Src signaling for focal adhesion turnover. This fuels directional migration during embryonic angiogenesis, where ATX-LPA promotes endothelial sprouting and vessel stabilization, and orchestrates wound healing by recruiting fibroblasts and macrophages through autocrine LPA loops that sustain proliferation and ECM deposition. In muscle regeneration, ATX expression surges post-injury to license satellite cell fusion via LPA-WNT/β-catenin crosstalk, ensuring myofiber hypertrophy, while in immunity it shapes B cell trafficking and platelet activation for thrombus resolution. ATX deficiency phenocopies vascular defects and impairs lymphangiogenesis, making it essential for studying chemotactic gradients in vivo via plasma LPA profiling or neutralizing antibodies in migration chambers. Overproduction drives pancreatic cancer desmoplasia through CAF-derived LPA stimulating CTGF/TGF-β, while in pulmonary fibrosis ATX-LPA sustains myofibroblast differentiation and TIF1 deposition; both contexts reveal therapeutic vulnerability to ATX inhibitors that collapse LPA signaling without toxicity.

Background

ENPP2, widely known as autotaxin (ATX), functions as a secreted ectonucleotide pyrophosphatase/phosphodiesterase that hydrolyzes lysophosphatidylcholine into bioactive lysophosphatidic acid (LPA), driving critical signaling in cell motility, vascular maturation, and tissue repair. ATX generates LPA gradients that engage LPAR1-6 G-protein-coupled receptors, activating Gαq/PLCβ for calcium release and RhoA/ROCK-mediated actomyosin contraction, alongside Gαi/PI3K/Akt for survival and Gα12/13/PKA for chemotaxis, while direct ATX-integrin αvβ3/α5β1 interactions localize LPA delivery at leading edges to amplify FAK/Src signaling for focal adhesion turnover. This fuels directional migration during embryonic angiogenesis, where ATX-LPA promotes endothelial sprouting and vessel stabilization, and orchestrates wound healing by recruiting fibroblasts and macrophages through autocrine LPA loops that sustain proliferation and ECM deposition. In muscle regeneration, ATX expression surges post-injury to license satellite cell fusion via LPA-WNT/β-catenin crosstalk, ensuring myofiber hypertrophy, while in immunity it shapes B cell trafficking and platelet activation for thrombus resolution. ATX deficiency phenocopies vascular defects and impairs lymphangiogenesis, making it essential for studying chemotactic gradients in vivo via plasma LPA profiling or neutralizing antibodies in migration chambers. Overproduction drives pancreatic cancer desmoplasia through CAF-derived LPA stimulating CTGF/TGF-β, while in pulmonary fibrosis ATX-LPA sustains myofibroblast differentiation and TIF1 deposition; both contexts reveal therapeutic vulnerability to ATX inhibitors that collapse LPA signaling without toxicity.

References
https://pubmed.ncbi.nlm.nih.gov/39062979/ https://pubmed.ncbi.nlm.nih.gov/29951481/

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

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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%