Fibronectin Antibody [P19B9] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

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

Usage Information

Dilution
WB1:1000-1:10000 IF1:500 FCM1:150

Application
WB, IF, FCM

Reactivity
Mouse, Rat, Human

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
262 kDa, 272 kDa 238-268 kDa, 272 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
Fibronectin Antibody [P19B9] detects endogenous levels of total Fibronectin protein.

Clone
P19B9

Synonym(s)
FN; FN1; Fibronectin; Cold‑insoluble globulin; CIG

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.

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.

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

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%