Tyrosinase Antibody [P8H17]

Catalog No.: F2481

Application: Reactivity: Mouse, Human

Lane 1: Mewo

当該製品は品切れ状态で、ごメールアドレスを教えていただければ、在庫があると、メールで顧客様に伝えます。

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

使用情報

Dilution
WB1:1000-1:5000 IHC1:100-1:500

Application
WB, IHC

Source
Rabbit Monoclonal Antibody

Reactivity
Mouse, 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
60 kDa 50-80 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
Tyrosinase Antibody [P8H17] detects endogenous levels of total Tyrosinase protein.

Clone
P8H17

Synonym(s)
Tyrosinase; LB24-AB; Monophenol monooxygenase; SK29-AB; Tumor rejection antigen AB; TYR

Background
Tyrosinase, the rate-limiting copper-containing monooxygenase of the tyrosinase family alongside TRP1 and TRP2, catalyzes the initial steps of melanogenesis by hydroxylating L-tyrosine to L-DOPA and oxidizing L-DOPA to dopaquinone through a type-3 dicopper active site featuring oxy-tyrosinase (Cu2O2) and met-tyrosinase (Cu2(OH)) intermediates. Binuclear copper coordination at His residues enables electrophilic aromatic attack, where dioxygen activation produces the μ-η2:η2-peroxo dicopper core that delivers the hydroxyl equivalent to the ortho position of monophenols, followed by two-electron oxidation of diphenols via substrate-assisted proton transfer; conformational shifts between syn/anti ligand geometries gate substrate access while latent zymogen activation by proteolysis exposes the catalytic cleft. The enzyme integrates within melanosomal complexes where TRP2 (DCT) accelerates dopachrome tautomerization, and TRP1 isomerizes quinone methides to 5,6-dihydroxyindoles, with MITF-driven transcriptional synergy at E-box/CATGTG motifs amplifying expression under UV/cAMP/PKA signaling. Tyrosinase governs constitutive and UV-inducible pigmentation in melanocytes, protecting basal keratinocytes from ROS while establishing retinal pigment epithelium barrier function critical for photoreceptor outer segment phagocytosis. OCA1A mutations abolish copper loading/trafficking, causing complete albinism with foveal hypoplasia, while hypomorphic OCA1B variants retain partial activity; conversely, melanoma exploits PKC-β phosphorylation and TPC2-mediated melanosome pH for hyperactivation, driving aberrant pigmentation that aids immunoevasion through melanin-mediated ROS quenching.

Background

Tyrosinase, the rate-limiting copper-containing monooxygenase of the tyrosinase family alongside TRP1 and TRP2, catalyzes the initial steps of melanogenesis by hydroxylating L-tyrosine to L-DOPA and oxidizing L-DOPA to dopaquinone through a type-3 dicopper active site featuring oxy-tyrosinase (Cu2O2) and met-tyrosinase (Cu2(OH)) intermediates. Binuclear copper coordination at His residues enables electrophilic aromatic attack, where dioxygen activation produces the μ-η2:η2-peroxo dicopper core that delivers the hydroxyl equivalent to the ortho position of monophenols, followed by two-electron oxidation of diphenols via substrate-assisted proton transfer; conformational shifts between syn/anti ligand geometries gate substrate access while latent zymogen activation by proteolysis exposes the catalytic cleft. The enzyme integrates within melanosomal complexes where TRP2 (DCT) accelerates dopachrome tautomerization, and TRP1 isomerizes quinone methides to 5,6-dihydroxyindoles, with MITF-driven transcriptional synergy at E-box/CATGTG motifs amplifying expression under UV/cAMP/PKA signaling. Tyrosinase governs constitutive and UV-inducible pigmentation in melanocytes, protecting basal keratinocytes from ROS while establishing retinal pigment epithelium barrier function critical for photoreceptor outer segment phagocytosis. OCA1A mutations abolish copper loading/trafficking, causing complete albinism with foveal hypoplasia, while hypomorphic OCA1B variants retain partial activity; conversely, melanoma exploits PKC-β phosphorylation and TPC2-mediated melanosome pH for hyperactivation, driving aberrant pigmentation that aids immunoevasion through melanin-mediated ROS quenching.

References
[1] Matoba Y, et al. PLoS Biol. 2018 Dec 31;16(12):e3000077. [2] Yasumoto K, et al. Mol Cell Biol. 1994 Dec;14(12):8058-70.

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

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

* 必須

* 大学・企業名 大学・企業名を記入してください

* 名前 名前を記入してください

* 電子メール 電子メール・アドレスを記入してください 有効なメールアドレスを入力してください

電話番号

* 内容 お問い合わせ内容をご入力ください

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%