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PRKAG3
Purified Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC, ICC, E |
|---|---|
| Primary Accession | Q9UGI9 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | 1C5D10 |
| Isotype | Mouse IgG1 |
| Calculated MW | 54.3kDa |
| Immunogen | Purified recombinant fragment of human PRKAG3 (AA: 9-151) expressed in E. Coli. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
| Gene ID | 53632 |
|---|---|
| Other Names | AMPKG3 |
| Dilution | E~~ 1/10000 WB~~ 1/500 - 1/2000 |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | PRKAG3 is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | PRKAG3 |
|---|---|
| Synonyms | AMPKG3 |
| Function | AMP/ATP-binding subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism (PubMed:14722619, PubMed:17878938, PubMed:24563466). 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. AMPK also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. The AMPK gamma3 subunit is a non-catalytic subunit with a regulatory role in muscle energy metabolism (PubMed:17878938). It mediates binding to AMP, ADP and ATP, leading to AMPK activation or inhibition: AMP-binding results in allosteric activation of alpha catalytic subunit (PRKAA1 or PRKAA2) both by inducing phosphorylation and preventing dephosphorylation of catalytic subunits. ADP also stimulates phosphorylation, without stimulating already phosphorylated catalytic subunit. ATP promotes dephosphorylation of catalytic subunit, rendering the AMPK enzyme inactive. |
| Tissue Location | Skeletal muscle, with weak expression in heart and pancreas |
Research Areas
Citations (0)
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Application Protocols
Provided below are standard protocols that you may find useful for product applications.
References
1.Diabetologia. 2010 Sep;53(9):1986-97.2.PLoS One. 2007 Sep 19;2(9):e903.
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$ 385.00
Cat# AO2518a
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