GSK-3-α Antibody [G23H20]

Catalog No.: F4609

Application: Reactivity: Human, Mouse, Rat, Hamster, Monkey

Lane 1: Hela, Lane 2: CHO, Lane 3: C6, Lane 4: COS

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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 IP1:200 IF1:50 - 1:100

Application
WB, IP, IF

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Mouse, Rat, Hamster, Monkey

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
51 kDa

Datasheet & SDS

生物学的記述

Specificity
GSK-3-α Antibody [G23H20] detects endogenous levels of total GSK-3-α protein.

Clone
G23H20

Synonym(s)
Glycogen synthase kinase-3 alpha; GSK-3 alpha; Serine/threonine-protein kinase GSK3A; GSK3A

Background
GSK-3α (Glycogen Synthase Kinase-3α) is a constitutively active serine/threonine protein kinase isoform of the GSK-3 family, distinguished from GSK-3β by an N-terminal extension, ubiquitously expressed to regulate metabolism, signaling, and development. GSK-3α features a bilobal kinase domain with N-lobe β-barrel (7 strands), glycine-rich loop (ATP lid), hinge region, and C-lobe α-helices; the ATP-binding cleft accommodates primed substrates via a positively charged pocket (Arg96, Lys205, Arg220) binding the priming phosphate 4 residues C-terminal to the target Ser/Thr, with key residues Asp133 (catalysis), Tyr279 (activation loop), and Ser21 (inhibitory Akt site). GSK-3α phosphorylates >100 substrates (e.g., glycogen synthase inactivating it, β-catenin for Wnt degradation, APP for amyloid-β cleavage, tau, cyclin D1) after priming, integrating into PI3K/Akt (inhibited at Ser21), Wnt/β-catenin, mTORC1/autophagy, and p53 pathways to control glycogen synthesis, proliferation, apoptosis, and neural progenitor dynamics. Dysregulated GSK-3α drives Alzheimer's (amyloid/tau), cancer, diabetes, and aging via unchecked substrate phosphorylation.

Background

GSK-3α (Glycogen Synthase Kinase-3α) is a constitutively active serine/threonine protein kinase isoform of the GSK-3 family, distinguished from GSK-3β by an N-terminal extension, ubiquitously expressed to regulate metabolism, signaling, and development. GSK-3α features a bilobal kinase domain with N-lobe β-barrel (7 strands), glycine-rich loop (ATP lid), hinge region, and C-lobe α-helices; the ATP-binding cleft accommodates primed substrates via a positively charged pocket (Arg96, Lys205, Arg220) binding the priming phosphate 4 residues C-terminal to the target Ser/Thr, with key residues Asp133 (catalysis), Tyr279 (activation loop), and Ser21 (inhibitory Akt site). GSK-3α phosphorylates >100 substrates (e.g., glycogen synthase inactivating it, β-catenin for Wnt degradation, APP for amyloid-β cleavage, tau, cyclin D1) after priming, integrating into PI3K/Akt (inhibited at Ser21), Wnt/β-catenin, mTORC1/autophagy, and p53 pathways to control glycogen synthesis, proliferation, apoptosis, and neural progenitor dynamics. Dysregulated GSK-3α drives Alzheimer's (amyloid/tau), cancer, diabetes, and aging via unchecked substrate phosphorylation.

References
[1] Beurel E, et al. Pharmacol Ther. 2015 Apr;148:114-31. [2] Buescher JL, et al. J Biol Chem. 2010 Mar 12;285(11):7957-63.

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%