Key features and details
- Mouse monoclonal [34.2] to AMPK alpha 1 + AMPK alpha 2 - BSA and Azide free
- Suitable for: WB, IP, ELISA, IHC-Fr, ICC/IF
- Reacts with: Rat, Human
- Isotype: IgG2a
Product nameAnti-AMPK alpha 1 + AMPK alpha 2 antibody [34.2] - BSA and Azide free
See all AMPK alpha 1 + AMPK alpha 2 primary antibodies
DescriptionMouse monoclonal [34.2] to AMPK alpha 1 + AMPK alpha 2 - BSA and Azide free
Tested applicationsSuitable for: WB, IP, ELISA, IHC-Fr, ICC/IFmore details
Species reactivityReacts with: Rat, Human
Synthetic peptide corresponding to Drosophila melanogaster AMPK alpha 1 + AMPK alpha 2 (N terminal).
- WB: Rat heart lysate; HepG2 and HEK-293T whole cell lysates.
Storage instructionsShipped at 4°C. Store at +4°C. Do Not Freeze.
Storage bufferConstituent: PBS
Concentration information loading...
PurityImmunogen affinity purified
- Pathways and Processes
- Metabolic signaling pathways
- Lipid and lipoprotein metabolism
- Fatty acids
- Pathways and Processes
- Metabolic signaling pathways
- Energy transfer pathways
- Integration of energy
Our Abpromise guarantee covers the use of ab187408 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 1 µg/ml. Detects a band of approximately 62 kDa (predicted molecular weight: 62 kDa).|
|IP||Use at an assay dependent concentration.|
|ELISA||Use at an assay dependent concentration.|
|IHC-Fr||Use at an assay dependent concentration.|
|ICC/IF||Use at an assay dependent concentration.|
FunctionCatalytic subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Regulates lipid synthesis by phosphorylating and inactivating lipid metabolic enzymes such as ACACA, ACACB, GYS1, HMGCR and LIPE; regulates fatty acid and cholesterol synthesis by phosphorylating acetyl-CoA carboxylase (ACACA and ACACB) and hormone-sensitive lipase (LIPE) enzymes, respectively. Regulates insulin-signaling and glycolysis by phosphorylating IRS1, PFKFB2 and PFKFB3. AMPK stimulates glucose uptake in muscle by increasing the translocation of the glucose transporter SLC2A4/GLUT4 to the plasma membrane, possibly by mediating phosphorylation of TBC1D4/AS160. Regulates transcription and chromatin structure by phosphorylating transcription regulators involved in energy metabolism such as CRTC2/TORC2, FOXO3, histone H2B, HDAC5, MEF2C, MLXIPL/ChREBP, EP300, HNF4A, p53/TP53, SREBF1, SREBF2 and PPARGC1A. Acts as a key regulator of glucose homeostasis in liver by phosphorylating CRTC2/TORC2, leading to CRTC2/TORC2 sequestration in the cytoplasm. In response to stress, phosphorylates 'Ser-36' of histone H2B (H2BS36ph), leading to promote transcription. Acts as a key regulator of cell growth and proliferation by phosphorylating TSC2, RPTOR and ATG1: in response to nutrient limitation, negatively regulates the mTORC1 complex by phosphorylating RPTOR component of the mTORC1 complex and by phosphorylating and activating TSC2. In response to nutrient limitation, promotes autophagy by phosphorylating and activating ULK1. AMPK also acts as a regulator of circadian rhythm by mediating phosphorylation of CRY1, leading to destabilize it. May regulate the Wnt signaling pathway by phosphorylating CTNNB1, leading to stabilize it. Also has tau-protein kinase activity: in response to amyloid beta A4 protein (APP) exposure, activated by CAMKK2, leading to phosphorylation of MAPT/TAU; however the relevance of such data remains unclear in vivo. Also phosphorylates CFTR, EEF2K, KLC1, NOS3 and SLC12A1.
Sequence similaritiesBelongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. SNF1 subfamily.
Contains 1 protein kinase domain.
DomainThe AIS (autoinhibitory sequence) region some sequence similarity with the ubiquitin-associated domains and represses kinase activity.
Phosphorylated at Thr-183 by STK11/LKB1 in complex with STE20-related adapter-alpha (STRADA) pseudo kinase and CAB39. Also phosphorylated at Thr-183 by CAMKK2; triggered by a rise in intracellular calcium ions, without detectable changes in the AMP/ATP ratio. CAMKK1 can also phosphorylate Thr-183, but at a much lower level. Dephosphorylated by protein phosphatase 2A and 2C (PP2A and PP2C). Phosphorylated by ULK1 and ULK2; leading to negatively regulate AMPK activity and suggesting the existence of a regulatory feedback loop between ULK1, ULK2 and AMPK.
Cellular localizationCytoplasm. Nucleus. In response to stress, recruited by p53/TP53 to specific promoters.
- Information by UniProt
- 5''-AMP-activated protein kinase catalytic subunit alpha-1 antibody
- AAPK1_HUMAN antibody
- ACACA kinase antibody
All lanes : Anti-AMPK alpha 1 + AMPK alpha 2 antibody [34.2] (ab80039) at 1 µg/ml
Lane 1 : Heart (Rat) Tissue Lysate
Lane 2 : ab29466
Lane 3 : HepG2 (Human hepatocellular liver carcinoma cell line) Whole Cell Lysate
Lane 4 : HEK293 (Human embryonic kidney cell line) Whole Cell Lysate
Lysates/proteins at 10 µg per lane.
All lanes : Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/10000 dilution
Developed using the ECL technique.
Predicted band size: 62 kDa
Observed band size: 62 kDa
Additional bands at: 75 kDa, 80 kDa. We are unsure as to the identity of these extra bands.
Exposure time: 20 minutes
This data was developed using the same antibody clone in a different formulation containing PBS, Azide and arginine (ab80039).
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab187408 has not yet been referenced specifically in any publications.