Mgll Antibody

Code CSB-PA013787ZA01MO
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Product Details

Full Product Name
Rabbit anti-Mus musculus (Mouse) Mgll Polyclonal antibody
Uniprot No.
Target Names
Mgll
Alternative Names
MgllMonoglyceride lipase antibody; MGL antibody; EC 3.1.1.23 antibody; Monoacylglycerol lipase antibody; MAGL antibody
Raised in
Rabbit
Species Reactivity
Mus musculus
Immunogen
Recombinant Mus musculus Mgll protein
Immunogen Species
Mus musculus (Mouse)
Conjugate
Non-conjugated
Clonality
Polyclonal
Isotype
IgG
Purification Method
Antigen Affinity Purified
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Tested Applications
ELISA, WB (ensure identification of antigen)
Protocols
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Value-added Deliverables
① 200ug * antigen (positive control);
② 1ml * Pre-immune serum (negative control);
Quality Guarantee
① Antibody purity can be guaranteed above 90% by SDS-PAGE detection;
② ELISA titer can be guaranteed 1: 64,000;
③ WB validation with antigen can be guaranteed positive;
Lead Time
Made-to-order (12-14 weeks)

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Target Background

Function
Converts monoacylglycerides to free fatty acids and glycerol. Hydrolyzes the endocannabinoid 2-arachidonoylglycerol, and thereby contributes to the regulation of endocannabinoid signaling, nociperception and perception of pain. Regulates the levels of fatty acids that serve as signaling molecules and promote cancer cell migration, invasion and tumor growth.
Gene References into Functions
  1. Neuronal and astrocytic monoacylglycerol lipase contributes to 2-arachidonoylglycerol clearance and prevent CB1 receptor over-stimulation in the cerebellum. PMID: 27775008
  2. Results provide evidence that MGL deficiency causes complex changes in cholesterol metabolism and in the regulation of gut transit. PMID: 28380440
  3. N-arachidonoyl ethanolamine and 2-arachidonoyl glycerol hydrolyzing enzymes, FAAH and MAGL, and the CB1 receptor link the endocannabinoid system to broader lipid signaling networks in contrasting ways, potentially altering neurotransmission and behavior independently of cannabinoid receptor signaling. PMID: 27109320
  4. Results suggest that neuronal and astrocytic MAGL collaborate to terminate endocannabinoid-mediated synaptic suppression and prompt synapse-specificity of endocannabinoid signaling in the cerebellum. PMID: 27182552
  5. Activities of adipose triglyceride lipase (ATGL), hormone sensitive lipolitic enzyme (HSL) and monoacylglycerol lipase (MGL) were significantly higher (51 %, 38 %, 49 %) in the DE group than the HF group (p < 0.05). MGL, there were no differences between the CO group, HF group, and DC group, with the DE group (70 %) being significantly higher (p < 0.05). PMID: 27596982
  6. MGL in astrocytes is an important regulator of 2-arachidonoylglyerol levels, arachidonic acid availability, and neuroinflammation. PMID: 26565024
  7. Genetic and pharmacological ablation of Magl attenuated centrally-mediated fever response. PMID: 26287872
  8. the results indicate that global MGL deletion leads to systemic changes that produce a leaner phenotype and an improved serum metabolic profile. PMID: 25842377
  9. This study showed that Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CBR signaling and anxiety-like behavior. PMID: 26223500
  10. Suggest that organophosphate agents induce plasma hypertriglyceridemia in mouse through single or dual inhibition of FAAH or/and MAGL, apparently leading to overstimulation of cannabinoid signal regulating energy metabolism. PMID: 24361246
  11. Inactivation of Monoacylglycerol lipase robustly suppressed production and accumulation of beta-amyloid (Abeta) associated with reduced expression of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) in a mouse model of Alzheimer's disease. PMID: 23122958
  12. Data indicate that nerve growth factor (NGF) controls monoacylglycerol lipase (MGL) degradation in vitro and in vivo. PMID: 23319656
  13. The results therefore suggest a role for intestinal MGL in whole body energy balance via regulation of food intake as well as metabolic rate. PMID: 22937137
  14. MGL regulates 2-arachidonoylglycerol signaling rather broadly within a certain range of neural tissue, although MGL expression is heterogeneous and limited to a subset of nerve terminals and astrocytes. PMID: 22783023
  15. results indicate that genetic deletion of MAGL causes profound changes in eCB signaling, long-term synaptic plasticity, and learning behavior. PMID: 21940435
  16. pathway exists in brain where MAGL hydrolyzes 2-arachidonoylglycerol to generate arachidonate precursor pool for neuroinflammatory prostaglandins; found MAGL as metabolic node coupling endocannabinoid to prostaglandin signaling networks in nervous system PMID: 22021672
  17. MGL deficiency impairs lipolysis and attenuates diet-induced insulin resistance PMID: 21454566
  18. MAGL is the major regulator of 2- arachidonoylglycerol (2-AG) levels and signaling. PMID: 20855465
  19. spatially confined MGL activity generates a 2-arachidonoyl glycerol sensing microdomain and configures 2-arachidonoyl glycerol signaling to promote axonal growth PMID: 20962221
  20. sustained inactivation of monoacylglycerol lipase impairs specific endocannabinoid-mediated forms of synaptic plasticity; ligand diversification may be important for shaping the distinct functions and properties of endocannabinoid signaling pathways PMID: 20729846
  21. Astrocytes express monoacylglycerol lipase, the main hydrolyzing enzyme of 2-arachidonoylglycerol. Pharmacological inhibition of MGL potentiates ATP-induced 2-AG production. PMID: 15371507
  22. analysis of developmental and nutritional regulation of monoacylglycerol lipase and monoacylglycerol acyltransferase PMID: 17848545

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Subcellular Location
Cytoplasm, cytosol. Membrane; Peripheral membrane protein.
Protein Families
AB hydrolase superfamily, Monoacylglycerol lipase family
Tissue Specificity
Ubiquitous.
Database Links
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