Fibronectin Antibody [P19B9]

Catalog No.: F4898

Application: Reactivity: Mouse, Rat, Human

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

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

Application
WB, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Mouse, Rat, Human

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
^*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
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
[1] You R, et al. Matrix Biol. 2009 Mar;28(2):101-9. [2] Yi M, et al. Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):620-4.

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%