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anti-Human MGLL Antikörper:
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Human Polyclonal MGLL Primary Antibody für ELISA, WB - ABIN409119
Blankman, Simon, Cravatt: A comprehensive profile of brain enzymes that hydrolyze the endocannabinoid 2-arachidonoylglycerol. in Chemistry & biology 2007
Human Polyclonal MGLL Primary Antibody für WB - ABIN250940
Tang, Wang: YAP-mediated induction of monoacylglycerol lipase restrains oncogenic transformation. in Cellular signalling 2015
Mammalian Monoclonal MGLL Primary Antibody für - ABIN1304818
Iannotti, Silvestri, Mazzarella, Martella, Calvigioni, Piscitelli, Ambrosino, Petrosino, Czifra, Bíró, Harkany, Taglialatela, Di Marzo: The endocannabinoid 2-AG controls skeletal muscle cell differentiation via CB1 receptor-dependent inhibition of Kv7 channels. in Proceedings of the National Academy of Sciences of the United States of America 2014
Human Polyclonal MGLL Primary Antibody für IHC, IHC (p) - ABIN4335291
Kirkedal, Elfving, Müller, Moreira, Bindila, Lutz, Wegener, Liebenberg: Hemisphere-dependent endocannabinoid system activity in prefrontal cortex and hippocampus of the Flinders Sensitive Line rodent model of depression. in Neurochemistry international 2019
Study utilizing colorectal cancer patients tissue samples, mouse tumor cell lines and xenograft models identify MGLL as a switch for CB2/TLR4-dependent macrophage activation and provide potential targets for cancer therapy.
Using a multimethod approach, the authors show that the dynamically relevant Trp-289 and Leu-232 residues serve as communication hubs within an allosteric protein network that controls signal propagation to the active site, and thus, regulates active-inactive interconversion of human MGL.
RNA interference, specific pharmacological inhibitor JZL-184 and gene knock-in of MAGL were utilized to investigate the effects of MAGL on hepatocellular carcinoma (HCC) cell proliferation, apoptosis, and invasion. MAGL played important roles in both proliferation and invasion of HCC cells.
This review summarizes the basics of monoglyceride metabolism and provides an overview on the therapeutic potential of MGL. [Review]
MGLL may have a role in progression of gastrointestinal stromal tumors
the upregulation of MAGL in hepatocellular carcinoma cells promoted cell growth and invasiveness abilities, and mediated epithelial-mesenchymal transition
we clarify the key role of Phe159 and Ile179, two conserved residues within the lid domain, in regulating substrate specificity in MAGL. We conclude by proposing that other structurally related lipases may share this lid-domain-mediated mechanism for substrate specificity.
the presence and differential distribution of fatty acid amide hydrolase (FAAH) and monoglyceride lipase (MGLL) in relation to CB1 during the maturation of human oocytes, was investigated.
there was evidence that MGLL rs604300 genotype interacts with early life adversity to predict threat-related basolateral amygdala habituation, a neural phenotype linked to the endocannabinoid system and addiction
This study unravels a novel mechanism of SND1 function and identifies MGLL as a unique tumor suppressor for HCC. MGLL might function as a homeostatic regulator of Akt restraining its activation.
The data highlight specific inter-residue interactions within hMGL
Monoacylglycerol lipase sulfenylation might act as an intrinsic neuroprotective mechanism by potentiating 2-AG signaling at CB1 receptors.
The study identified monoacylglycerol lipase as a YAP transcriptional target and an inhibitor of anchorage-dependent cell growth.
Molecular dynamics and nudged elastic band simulations were used to explore the conformational transition pathway of the helix alpha4 of human monoacylglycerol lipase.
role of monoacylglycerol lipase (MAGL) in the cancer progress
Our findings establish that MAGL promotes metastases in nasopharyngeal carcinoma
In subcutaneous adipose tissue, DAGL-a mRNA was upregulated and fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) mRNAs were down-regulated in obese subjects, but the diets had no influence.
In obese humans, FAAH or MGL activity in adipocytes is not affected by diabetes, dyslipidaemia or other markers of metabolic dysfunction.
Mutation of Cys242 was also found to impair inhibition of monoacylglycerol lipase.
MGL interaction with a phospholipid membrane bilayer induces regional changes in the enzyme's conformation that favor its recruiting lipophilic substrate from membrane stores to the active site resulting in enhanced MGL catalytic activity.
The study reveals changes in gene expression of members of the endocannabinoid system in situ attesting particularly GPR55 and MGL a distinct cellular role in the regulation of the immune response to intestinal and systemic inflammation.
Neuronal and astrocytic monoacylglycerol lipase contributes to 2-arachidonoylglycerol clearance and prevent CB1 receptor over-stimulation in the cerebellum.
Results provide evidence that MGL deficiency causes complex changes in cholesterol metabolism and in the regulation of gut transit.
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.
Results suggest that neuronal and astrocytic MAGL collaborate to terminate endocannabinoid-mediated synaptic suppression and prompt synapse-specificity of endocannabinoid signaling in the cerebellum.
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).
MGL in astrocytes is an important regulator of 2-arachidonoylglyerol levels, arachidonic acid availability, and neuroinflammation.
Genetic and pharmacological ablation of Magl attenuated centrally-mediated fever response.
the results indicate that global MGL deletion leads to systemic changes that produce a leaner phenotype and an improved serum metabolic profile.
This study showed that Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CBR signaling and anxiety-like behavior.
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.
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.
Data indicate that nerve growth factor (NGF) controls monoacylglycerol lipase (MGL) degradation in vitro and in vivo.
The results therefore suggest a role for intestinal MGL in whole body energy balance via regulation of food intake as well as metabolic rate.
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.
results indicate that genetic deletion of MAGL causes profound changes in eCB signaling, long-term synaptic plasticity, and learning behavior.
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
MGL deficiency impairs lipolysis and attenuates diet-induced insulin resistance
MAGL is the major regulator of 2- arachidonoylglycerol (2-AG) levels and signaling.
This gene encodes a serine hydrolase of the AB hydrolase superfamily that catalyzes the conversion of monoacylglycerides to free fatty acids and glycerol. The encoded protein plays a critical role in several physiological processes including pain and nociperception through hydrolysis of the endocannabinoid 2-arachidonoylglycerol. Expression of this gene may play a role in cancer tumorigenesis and metastasis. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
, Monoglyceride lipase
, lysophospholipase homolog
, monoacylglycerol lipase