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Study provides evidence that GAL and GALR1/2 genes were identified as aberrantly methylated in head and neck squamous cell carcinoma.
GAL and its receptors, GALR1 and GALR2, play a role in head and neck squamous cell carcinoma tumorigenesis
The G protein-coupled receptor GALR2 promotes angiogenesis in head and neck cancer
In HEp-2 cells, GALR2-mediated apoptosis was caspase-independent.
Data from ligand-receptor interaction studies suggest that human spexin-1 and zebrafish spexin-2 activate galanin receptors GALR2/GALR3 (but not GALR1); thus spexins appear to be natural ligands for human/Xenopus/zebrafish GALR2/GALR3.
Variants in genes for galanin (GAL) and its receptors (GALR1, GALR2, GALR3), despite their disparate genomic loci, conferred increased risk of depression and anxiety in people who experienced childhood adversity or recent negative life events.
Activation of GalR2 leads to elevation of intracellular Ca(2+) due to Ca(2+) efflux from endoplasmic reticulum through IP3R sequentially opening BK alpha channels.
The expression of GALR2 mRNA is lost in head and neck squamous cell carcinoma as a consequence of DNA methylation.Silencing of the GALR2 gene by methylation may be a critical event in head and neck squamous cell carcinoma.
galanin receptor 2 promotes cell proliferation and survival, and promotes tumor growth, consistent with an oncogenic role for GALR2 in squamous cell carcinoma of the head and neck
Elevated expression of galanin receptors in childhood neuroblastic tumors
study indicates that a high level of GalR2 galanin receptor expression is able to inhibit cell proliferation and induce apoptosis in neuroblastoma cells
There was no effect of GALR2 on alcoholism risk.
point to GalR2 as a possible target for therapeuthic interventions in pheochromocytoma
these results identify that GALR2 is a regulator of insulin resistance and activation of GALR2 represents a promising strategy against obesity-induced insulin resistance.
In chronic restraint stress, the expression of GalR2 is increased in the nucleus accumbens following antidepressant administration.
Three age groups of the Galr2 overexpressing mice demonstrated decreased levels of immobility in the forced swim test, indicative of antidepressive-like behavior and/or increased stress resistance.
High level of endogenous galanin in injured primary afferents activates peripheral GalR2, which leads to an increase in C-fibre mechanical activation thresholds and a marked reduction in evoked and ongoing nociceptive responses.
To gain insight into the possible physiological significance of GALR2, phenotypic analysis of mice deficient in GALR2 was determined.
lack of GalR2 activation in galanin knockout and GalR2-MUT animals is responsible for the observed developmental deficits in the dorsal root ganglia
the discovery of an anxiogenic phenotype specific to the elevated plus-maze highlights the potential therapeutic efficacy of targeting GalR2 receptors in treating anxiety disorders
These findings imply that the rise in endogenous galanin observed either after brain injury or in various disease states is an adaptive response that reduces apoptosis by the activation of GalR2, and hence Akt and ERK.
Galr2 receptors stimulate vagal afferent mechanosensitivity in the gastro-esophageal afferent preparation.
The present findings are consistent with a predicted antidepressant-like effect of GalR2 signaling, suggesting that GalR2 might be a valid drug target for depressive disorders.
The result indicate that galanin and its receptors (GalR1 and GalR2) might regulate neurite extension in differentiating neural stem cells and even participate in the development of the nervous system.
Galanin is an important neuromodulator present in the brain, gastrointestinal system, and hypothalamopituitary axis. It is a 30-amino acid non-C-terminally amidated peptide that potently stimulates growth hormone secretion, inhibits cardiac vagal slowing of heart rate, abolishes sinus arrhythmia, and inhibits postprandial gastrointestinal motility. The actions of galanin are mediated through interaction with specific membrane receptors that are members of the 7-transmembrane family of G protein-coupled receptors. GALR2 interacts with the N-terminal residues of the galanin peptide. The primary signaling mechanism for GALR2 is through the phospholipase C/protein kinase C pathway (via Gq), in contrast to GALR1, which communicates its intracellular signal by inhibition of adenylyl cyclase through Gi. However, it has been demonstrated that GALR2 couples efficiently to both the Gq and Gi proteins to simultaneously activate 2 independent signal transduction pathways.
, galanin receptor type 2
, galanin receptor 2
, galanin receptor type 2-like
, galactose operon repressor
, DNA-binding transcriptional regulator GalR