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anti-Human MGLL Antibodies:
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Mammalian Monoclonal MGLL Primary Antibody for - 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 for 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 for WB - ABIN250940
Tang, Wang: YAP-mediated induction of monoacylglycerol lipase restrains oncogenic transformation. in Cellular signalling 2015
This review summarizes the basics of monoglyceride metabolism and provides an overview on the therapeutic potential of MGL (show CLEC10A Antibodies). [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 (show FAAH Antibodies)) and monoglyceride lipase (MGLL) in relation to CB1 (show CNR1 Antibodies) 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 (show SND1 Antibodies) function and identifies MGLL as a unique tumor suppressor for HCC (show FAM126A Antibodies). MGLL might function as a homeostatic regulator of Akt (show AKT1 Antibodies) restraining its activation.
Monoacylglycerol lipase sulfenylation might act as an intrinsic neuroprotective mechanism by potentiating 2-AG signaling at CB1 (show CNR1 Antibodies) receptors.
The study identified monoacylglycerol lipase as a YAP (show YAP1 Antibodies) 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.
Results provide evidence that MGL (show CLEC10A Antibodies) deficiency causes complex changes in cholesterol metabolism and in the regulation of gut (show GUSB Antibodies) transit.
N-arachidonoyl ethanolamine and 2-arachidonoyl glycerol hydrolyzing enzymes, FAAH (show FAAH Antibodies) and MAGL, and the CB1 (show CNR1 Antibodies) 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 (show PNPLA2 Antibodies)), hormone sensitive lipolitic enzyme (HSL (show LIPE Antibodies)) and monoacylglycerol lipase (MGL) were significantly higher (51 %, 38 %, 49 %) in the DE group than the HF group (p < 0.05). MGL (show CLEC10A Antibodies), 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 (show CLEC10A Antibodies) 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 (show CLEC10A Antibodies) deletion leads to systemic changes that produce a leaner (show CACNA1A Antibodies) phenotype and an improved serum metabolic profile.
This study showed that Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CBR (show CBR1 Antibodies) signaling and anxiety-like behavior.
Suggest that organophosphate agents induce plasma hypertriglyceridemia in mouse through single or dual inhibition of FAAH (show FAAH Antibodies) 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 (show APP Antibodies)) associated with reduced expression of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1 (show BACE Antibodies)) in a mouse model of Alzheimer's disease.
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