AKT3 + AKT1 Antibody [L21G14]

Catalog No.: F3150

Application: Reactivity: Human

Lane 1: 293T (transfected with Empty vector), Lane 2: 293T (transfected with GFP tagged AKT1), Lane 3: 293T (transfected with GFP tagged AKT2), Lane 4: 293T (transfected with GFP tagged AKT3)

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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
WB1:10000 IHC1:250-1:1000 IF1:500

Application
WB, IHC, IF

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
54 kDa 82kDa, 56kDa
^*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
AKT3 + AKT1 Antibody [L21G14] detects endogenous levels of total AKT3 and AKT1 protein.

Clone
L21G14

Synonym(s)
PKB; RAC; AKT1; RAC‑alpha serine/threonine‑protein kinase; Protein kinase B; Protein kinase B alpha; Proto‑oncogene c‑Akt; RAC‑PK‑alpha; PKB alpha; PKBG; AKT3; Protein kinase B gamma; RAC‑PK‑gamma; STK‑2; PKB gamma

Background
AKT1 and AKT3 are closely related serine/threonine kinases of the protein kinase B (PKB) family that function as central nodes in the PI3K–AKT–mTOR signaling axis, integrating growth factor, insulin, and nutrient inputs to regulate cell survival, proliferation, metabolism, and neuronal development. Both isoforms adopt a conserved modular architecture that positions regulatory hydrophobic and pleckstrin homology domains upstream of the kinase domain, enabling membrane recruitment and allosteric activation through phosphorylation at key regulatory sites such as threonine 308 and serine 473, which together stabilize the active kinase conformation and promote interaction with downstream substrates. Upon PI3K dependent phosphoinositide generation at the plasma membrane, AKT1 and AKT3 are recruited and phosphorylated by PDK1 and mTORC2, initiating site specific phosphorylation of effectors such as mTORC1, GSK 3β, FOXO transcription factors, and BAD, thereby enhancing protein synthesis, cell cycle progression, and survival signaling while attenuating glycogen synthesis and autophagy linked catabolism. In most tissues, AKT1 driven signaling supports growth factor–dependent proliferation, glucose utilization, and suppression of apoptosis, whereas in the brain AKT3 rich activity modulates neuronal migration, axon guidance, and synaptic plasticity, contributing to cortical lamination and higher order connectivity during development. Dysregulation of AKT1 or AKT3 activity, arising from upstream lesions in PI3K, PTEN, or receptor tyrosine kinases or from gain of function mutations in AKT genes, is associated with malignant transformation in carcinomas and hematologic neoplasms as well as with neurodevelopmental and neuropsychiatric disorders.

Background

AKT1 and AKT3 are closely related serine/threonine kinases of the protein kinase B (PKB) family that function as central nodes in the PI3K–AKT–mTOR signaling axis, integrating growth factor, insulin, and nutrient inputs to regulate cell survival, proliferation, metabolism, and neuronal development. Both isoforms adopt a conserved modular architecture that positions regulatory hydrophobic and pleckstrin homology domains upstream of the kinase domain, enabling membrane recruitment and allosteric activation through phosphorylation at key regulatory sites such as threonine 308 and serine 473, which together stabilize the active kinase conformation and promote interaction with downstream substrates. Upon PI3K dependent phosphoinositide generation at the plasma membrane, AKT1 and AKT3 are recruited and phosphorylated by PDK1 and mTORC2, initiating site specific phosphorylation of effectors such as mTORC1, GSK 3β, FOXO transcription factors, and BAD, thereby enhancing protein synthesis, cell cycle progression, and survival signaling while attenuating glycogen synthesis and autophagy linked catabolism. In most tissues, AKT1 driven signaling supports growth factor–dependent proliferation, glucose utilization, and suppression of apoptosis, whereas in the brain AKT3 rich activity modulates neuronal migration, axon guidance, and synaptic plasticity, contributing to cortical lamination and higher order connectivity during development. Dysregulation of AKT1 or AKT3 activity, arising from upstream lesions in PI3K, PTEN, or receptor tyrosine kinases or from gain of function mutations in AKT genes, is associated with malignant transformation in carcinomas and hematologic neoplasms as well as with neurodevelopmental and neuropsychiatric disorders.

References
[1] Manning BD, et al. Cell. 2017 Apr 20;169(3):381-405. [2] Levenga J, et al. Elife. 2017 Nov 27;6:e30640.

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%