AMPK alpha Antibody - #DF6361

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产品: AMPK alpha 抗体
货号: DF6361
描述: Rabbit polyclonal antibody to AMPK alpha
应用: WB IHC IF/ICC
文献验证: WB, IHC
反应: Human, Mouse, Rat
预测: Zebrafish, Bovine, Sheep, Rabbit, Dog, Chicken
蛋白号: Q13131 | P54646
RRID: AB_2838325

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 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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说明书
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实验方案
WB Handbook
IHC Protocol
IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
AMPK alpha Antibody detects endogenous levels of total AMPK alpha.
RRID:
AB_2838325
引用格式: Affinity Biosciences Cat# DF6361, RRID:AB_2838325.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

5 AMP activated protein kinase alpha 1catalytic subunit; 5 AMP activated protein kinase catalytic alpha 1 chain; 5' AMP activated protein kinase catalytic subunit alpha 1; 5'-AMP-activated protein kinase catalytic subunit alpha-1; AAPK1; AAPK1_HUMAN; ACACA kinase; acetyl CoA carboxylase kinase; AI194361; AI450832; AL024255; AMP -activate kinase alpha 1 subunit; AMP-activated protein kinase, catalytic, alpha -1; AMPK 1; AMPK alpha 1; AMPK alpha 1 chain; AMPK; AMPK subunit alpha-1; AMPK1; AMPKa1; AMPKalpha1; C130083N04Rik; cb116; EC 2.7.11.1; HMG CoA reductase kinase; HMGCR kinase; hormone sensitive lipase kinase; Hydroxymethylglutaryl CoA reductase kinase; im:7154392; kinase AMPK alpha1; MGC33776; MGC57364; OTTHUMP00000161795; OTTHUMP00000161796; PRKAA 1; PRKAA1; Protein kinase AMP activated alpha 1 catalytic subunit; SNF1-like protein AMPK; SNF1A; Tau protein kinase PRKAA1; wu:fa94c10; 5'-AMP-activated protein kinase catalytic subunit alpha-2; AAPK2_HUMAN; ACACA kinase; Acetyl-CoA carboxylase kinase; AMPK alpha 2 chain; AMPK subunit alpha-2; AMPK2; AMPKa2; AMPKalpha2; HMGCR kinase; Hydroxymethylglutaryl-CoA reductase kinase; PRKAA; PRKAA2; Protein kinase AMP activated alpha 2 catalytic subunit; Protein kinase AMP activated catalytic subunit alpha 2;

抗原和靶标

免疫原:

A synthesized peptide derived from human AMPK alpha, corresponding to a region within C-terminal amino acids.

基因/基因ID:
PRKAA1(5562) | PRKAA2(5563)
描述:
AMP-activated protein kinase (AMPK) is highly conserved from yeast to plants and animals and plays a key role in the regulation of energy homeostasis (1). AMPK is a heterotrimeric complex composed of a catalytic α subunit and regulatory β and γ subunits, each of which is encoded by two or three distinct genes (α1, 2; β1, 2; γ1, 2, 3) (2). The kinase is activated by an elevated AMP/ATP ratio due to cellular and environmental stress, such as heat shock, hypoxia, and ischemia (1). The tumor suppressor LKB1, in association with accessory proteins STRAD and MO25, phosphorylates AMPKα at Thr172 in the activation loop, and this phosphorylation is required for AMPK activation (3-5). AMPKα is also phosphorylated at Thr258 and Ser485 (for α1; Ser491 for α2). The upstream kinase and the biological significance of these phosphorylation events have yet to be elucidated (6). The β1 subunit is post-translationally modified by myristoylation and multi-site phosphorylation including Ser24/25, Ser96, Ser101, Ser108, and Ser182 (6,7). Phosphorylation at Ser108 of the β1 subunit seems to be required for the activation of AMPK enzyme, while phosphorylation at Ser24/25 and Ser182 affects AMPK localization (7). Several mutations in AMPKγ subunits have been identified, most of which are located in the putative AMP/ATP binding sites (CBS or Bateman domains). Mutations at these sites lead to reduction of AMPK activity and cause glycogen accumulation in heart or skeletal muscle (1,2). Accumulating evidence indicates that AMPK not only regulates the metabolism of fatty acids and glycogen, but also modulates protein synthesis and cell growth through EF2 and TSC2/mTOR pathways, as well as blood flow via eNOS/nNOS (1).

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Tight junction.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Cardiovascular diseases > Hypertrophic cardiomyopathy (HCM).

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species.   (View pathway)

· Organismal Systems > Environmental adaptation > Circadian rhythm.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Oxytocin signaling pathway.

· Organismal Systems > Endocrine system > Glucagon signaling pathway.

文献引用

1). High expressions of LDHA and AMPK as prognostic biomarkers for breast cancer. BREAST, 2016 (PubMed: 27598996) [IF=5.7]

Application: WB    Species: human    Sample:

Fig. 1. LDHA and AMPK were up-regulated synchronously in breast cancer. A. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer cell lines, including four NTNBC cell lines and four TNBC cell lines. GAPDH was used as a loading control. B. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The differences between TNBC and NTNBC cell lines were analyzed (below). GAPDH was used as an internal control. C. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer tissues, including four NTNBC tissues and four TNBC tissues. GAPDH was used as a loading control. D. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The diffe

Application: IHC    Species: human    Sample:

Fig. 2. The expression of LDHA and AMPK showed a positive correlation in breast cancer. A. The expression of LDHA and AMPK were detected by IHC using breast cancer TMAs of 112 patients. Representative IHC images of four staining degrees (no-weak-medium-strong) of LDHA and AMPK expression under a microscope were showed (400). B. The correlation between LDHA and AMPK expression scores of 112 breast cancer patients was analyzed and a positive correlation between them was showed.
2). Gastrodin induces lysosomal biogenesis and autophagy to prevent the formation of foam cells via AMPK‐FoxO1‐TFEB signalling axis. Journal of Cellular and Molecular Medicine, 2021 (PubMed: 33973365) [IF=5.3]

Application: WB    Species: Mice    Sample: macrophages

FIGURE 6 AMPK is a critical upstream regulator of FoxO1 and TFEB. A and B, Gastrodin activated AMPK in the foam cells. A, Representative blots of AMPK and p‐AMPK in macrophages. B, Immunofluorescence analysis of p‐AMPK in macrophages. C and D, The inhibition of AMPK activity decreased the phosphorylation of FoxO1 and nuclear translocation of TFEB. Macrophages were treated with CC (10μM) for 1 h. The phosphorylation level of FoxO1 was analysed by Western blotting C, and nuclear translocation of TFEB was determined by immunofluorescence D. *P < .05; **P < .01. Results are presented as mean ± SD of three independent experiments. The value represents fold of vehicle. CC, Dorsomorphin dihydrochloride
3). Asiatic acid attenuates hypertrophic and fibrotic differentiation of articular chondrocytes via AMPK/PI3K/AKT signaling pathway. ARTHRITIS RESEARCH & THERAPY, 2020 (PubMed: 32398124) [IF=4.9]

Application: WB    Species: human    Sample: human OA chondrocytes

Fig. 5| AA treatment activated the AMPK and inhibited PI3K/AKT signaling pathway. The cells were treated with or without AA (5 μM) for 3 days. aRepresentative western blot of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, and AKT. GAPDH was served as a loading control.

Application: WB    Species: Human    Sample: OA chondrocytes

Fig. 5 AA treatment activated the AMPK and inhibited PI3K/AKT signaling pathway. The cells were treated with or without AA (5 μM) for 3 days. a Representative western blot of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, and AKT. GAPDH was served as a loading control. b Relative protein expression of p-AMPK/AMPK, p-PI3K/PI3K, and p-AKT/AKT. Unpaired t test, *P < 0.05, ***P < 0.001. Each experiment was repeated three times (p-AMPK, phosphorylated AMP-activated protein kinase; AMPK, AMP-activated protein kinase; p-PI3K, phosphorylated phosphoinositide-3 kinase; PI3K, phosphoinositide-3 kinase; p-AKT, phosphorylated protein kinase B; AKT, protein kinase B)
4). Gold nanoclusters eliminate obesity induced by antipsychotics. Scientific Reports, 2022 (PubMed: 35365730) [IF=3.8]

Application: WB    Species: Rat    Sample: hypothalamus

Figure 3 Effects of olanzapine and AuNCs co-treatment on H1R-AMPK signaling, POMC protein expression and POMC immunofluorescence staining in the hypothalamus. (a) TEM image of a hypothalamic slice at 6th h after IP injection of 20 mg/kg AuNCs in rats. The presence of AuNCs was marked by red arrows. (b) Representative western blot figures of H1R, AMPK, pAMPK and POMC in the hypothalamus after co-treatment of olanzapine and AuNCs. (c–e) Densitometry analysis of H1R expression (c), pAMPK/AMPK (d) and POMC expression (e). (f–k) POMC immunofluorescence staining in the hypothalamic Arc of rats in CON (f), OLZ (g), O + AuNCs H (h), O + AuNCs L (i), AuNCs H (j) group and the corresponding quantification of POMC fluorescence intensity (k). n = 4/group. All data were presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.0001, OLZ vs. CON; #p < 0.05, ##p < 0.01, ###p < 0.0001, OLZ + AuNCs H vs. OLZ; $p < 0.05, OLZ + AuNCs L vs. OLZ. Original figures were shown in Fig. S8.
5). FGF1 reduces cartilage injury in osteoarthritis via regulating AMPK/Nrf2 pathway. Journal of Molecular Histology, 2023 (PubMed: 37659992) [IF=2.9]
6). Myostatin inhibits eEF2K-eEF2 by regulating AMPK to suppress protein synthesis. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2017 (PubMed: 29024627) [IF=2.5]

Application: WB    Species: mouse    Sample:

Fig. 4. Myostatin regulated translation elongation through AMP. C2C12 myotubes were treated with various concentration recombinant myostatin (0, 0.01,0.1, 1, 2, 3 µg/ml) for 48 h andthen lysed and cellular extracts were analyzed by Western blot with anti-AMPK(A).

Application: WB    Species: mouse    Sample: C2C12 myotubes

Fig. 4. |Myostatin regulated translation elongation through AMPK.C2C12 myotubes were treated with various concentration recombinant myostatin (0, 0.01,429 0.1, 1, 2, 3 µg/ml) for 48 h andthen lysed and cellular extracts were analyzed by Western blot with 430 anti-AMPK(A).

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