AFP Antibody [M19A22]

Catalog No.: F1021

Application: Reactivity: Human

Lane 1: Huh7, Lane 2: HepG2, Lane 3: Human fetal liver, Lane 4: Human plasma

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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 IP1:10 - 1:100 IHC1:50 - 1:100 IF1:100 - 1:250 FCM1:50

Application
WB, IP, IHC, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
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
68 kDa 70 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
AFP Antibody [M19A22] detects endogenous levels of total AFP protein.

Clone
M19A22

Synonym(s)
HPAFP; AFP; Alpha-fetoprotein; Alpha-1-fetoprotein; Alpha-fetoglobulin

Background
Alpha-fetoprotein (AFP), also known as alpha-1-fetoprotein, is a fetal-specific glycoprotein and oncofetal biomarker belonging to the albumin gene family. It is primarily synthesized in the embryonic yolk sac, fetal liver, and gastrointestinal tract during development, with expression silenced in adults except for low hepatic levels. Reactivation of AFP occurs in hepatocellular carcinoma (HCC), germ cell tumors, and nonseminomatous testicular cancers, making it a key marker for diagnosis and monitoring. AFP is a single polypeptide chain folded into three conserved domains (I, II, III) that form a V-shaped molecule stabilized by 15-16 disulfide bridges. It contains four fatty acid-binding pockets (subdomains IIA, IIA/IIB, IIIA, IIIB) with key ligand-orienting residues (Lys242, Lys246, Arg233, Tyr435), a metal-ion binding site in Domain IA (His22, His264, His268, Asp280), N-glycosylation at Asn251 (the fucosylated AFP-L3 isoform is clinically relevant for aggressive HCC), and C-terminal motifs for protein-receptor interactions. AFP serves biological roles in fetal plasma transport of bilirubin, fatty acids, and metals, maintenance of osmotic pressure, and modulation of immune tolerance by suppressing maternal T, NK, and dendritic cell responses through estrogen and growth factor binding. It also regulates liver cell proliferation and differentiation. AFP promotes tumor growth by activating PI3K/Akt/mTOR and cAMP/PKA pathways, inhibits apoptosis via caspase-3 binding, drives angiogenesis and metastasis through Wnt/β-catenin signaling, enables immune evasion, and is regulated by p53 and β-catenin mutations in HCC.

Background

Alpha-fetoprotein (AFP), also known as alpha-1-fetoprotein, is a fetal-specific glycoprotein and oncofetal biomarker belonging to the albumin gene family. It is primarily synthesized in the embryonic yolk sac, fetal liver, and gastrointestinal tract during development, with expression silenced in adults except for low hepatic levels. Reactivation of AFP occurs in hepatocellular carcinoma (HCC), germ cell tumors, and nonseminomatous testicular cancers, making it a key marker for diagnosis and monitoring. AFP is a single polypeptide chain folded into three conserved domains (I, II, III) that form a V-shaped molecule stabilized by 15-16 disulfide bridges. It contains four fatty acid-binding pockets (subdomains IIA, IIA/IIB, IIIA, IIIB) with key ligand-orienting residues (Lys242, Lys246, Arg233, Tyr435), a metal-ion binding site in Domain IA (His22, His264, His268, Asp280), N-glycosylation at Asn251 (the fucosylated AFP-L3 isoform is clinically relevant for aggressive HCC), and C-terminal motifs for protein-receptor interactions. AFP serves biological roles in fetal plasma transport of bilirubin, fatty acids, and metals, maintenance of osmotic pressure, and modulation of immune tolerance by suppressing maternal T, NK, and dendritic cell responses through estrogen and growth factor binding. It also regulates liver cell proliferation and differentiation. AFP promotes tumor growth by activating PI3K/Akt/mTOR and cAMP/PKA pathways, inhibits apoptosis via caspase-3 binding, drives angiogenesis and metastasis through Wnt/β-catenin signaling, enables immune evasion, and is regulated by p53 and β-catenin mutations in HCC.

References
[1] Ucdal M, et al. Euroasian J Hepatogastroenterol. 2025 Jan-Jun;15(1):72-82. [2] Kim H, et al. Int J Mol Sci. 2025 May 19;26(10):4863.

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%