ENPP2/ATX Antibody [J20P19]

Catalog No.: F3713

Application: Reactivity: Human, Mouse

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

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IF1:50 FCM1:500

Application
WB, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Mouse

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
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

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
[1] Laface C, et al. Int J Mol Sci. 2024 Jul 15;25(14):7737. [2] Ninou I, et al. Front Med (Lausanne). 2018 Jun 13;5:180.

PVDFメンブレン孔径参考表

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%