Fibronectin Antibody [P19B9] Datasheet

Biological Description

Specificity	Fibronectin Antibody [P19B9] detects endogenous levels of total Fibronectin protein.
Background	Fibronectin, a versatile glycoprotein central to extracellular matrix assembly, facilitates cell adhesion, migration, and tissue organization by binding integrins, collagen, fibrin, heparin, DNA, and actin to orchestrate dynamic matrix remodeling. Its modular architecture includes type I, II, and III repeats, with the RGD loop in the 10th type III domain mediating integrin engagement and N-terminal modules driving cell-directed fibrillogenesis through conformational unfolding. Upon integrin α5β1 or αvβ3 ligation, fibronectin activates FAK-Src signaling, recruiting PI3K to inhibit Hippo kinases MST1/2-LATS1/2, thereby dephosphorylating YAP/TAZ for nuclear entry and transcription of proliferative genes like CTGF and CYR61, while RhoA effector ROCK promotes actin bundling essential for fibril extension and force transmission. The fragment anastellin binds fibronectin to catalyze rapid polymerization into superfibronectin, a super-adhesive matrix that heightens integrin clustering, potently activates p38 MAPK independently of β1 integrins, even in suspension, while suppressing lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) signaling through Ras/ERK inhibition, curtailing endothelial migration and vessel sprouting. These actions drive physiological processes like osteoblast compaction for bone mineralization, wound closure via directed motility, and muscle-secreted induction of hepatic autophagy through ITGA5-ITGB1 for insulin sensitization during exercise. Excessive fibril deposition underlies fibrosis and tumor progression, where aberrant signaling fosters invasion.

Specificity

Fibronectin Antibody [P19B9] detects endogenous levels of total Fibronectin protein.

Background

Fibronectin, a versatile glycoprotein central to extracellular matrix assembly, facilitates cell adhesion, migration, and tissue organization by binding integrins, collagen, fibrin, heparin, DNA, and actin to orchestrate dynamic matrix remodeling. Its modular architecture includes type I, II, and III repeats, with the RGD loop in the 10th type III domain mediating integrin engagement and N-terminal modules driving cell-directed fibrillogenesis through conformational unfolding. Upon integrin α5β1 or αvβ3 ligation, fibronectin activates FAK-Src signaling, recruiting PI3K to inhibit Hippo kinases MST1/2-LATS1/2, thereby dephosphorylating YAP/TAZ for nuclear entry and transcription of proliferative genes like CTGF and CYR61, while RhoA effector ROCK promotes actin bundling essential for fibril extension and force transmission. The fragment anastellin binds fibronectin to catalyze rapid polymerization into superfibronectin, a super-adhesive matrix that heightens integrin clustering, potently activates p38 MAPK independently of β1 integrins, even in suspension, while suppressing lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) signaling through Ras/ERK inhibition, curtailing endothelial migration and vessel sprouting. These actions drive physiological processes like osteoblast compaction for bone mineralization, wound closure via directed motility, and muscle-secreted induction of hepatic autophagy through ITGA5-ITGB1 for insulin sensitization during exercise. Excessive fibril deposition underlies fibrosis and tumor progression, where aberrant signaling fosters invasion.

Usage Information

Application

WB, IF, FCM

Dilution

WB	IF	FCM
1:1000-1:10000	1:500	1:150

Reactivity

Mouse, Rat, Human

Source

Rabbit Monoclonal Antibody

MW

262 kDa, 272 kDa

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

References

https://pubmed.ncbi.nlm.nih.gov/19379667/
https://pubmed.ncbi.nlm.nih.gov/11209058/

Application Data

WB

Validated by Selleck

Lane 1: MCF7, Lane 2: MCF7 (KO Human FN1), Lane 3: HepG2, Lane 4: PC-3