| LANCL2 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | LANCL2 , GPR69B, TASP, LanC like 2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 612919 MGI: 1919085 HomoloGene: 23116 GeneCards: LANCL2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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LanC-like protein 2 is a protein that in humans is encoded by the LANCL2 gene. [5] [6] It is a protein broadly expressed in the plasma a nuclear membranes of immune, epithelial and muscle cells and a potential therapeutic target for chronic inflammatory, metabolic and immune-mediated diseases such as Crohn's disease and diabetes. [7]
The natural ligand of LANCL2, abscisic acid (ABA), has been identified as a new endogenous mammalian hormone implicated in glycemic control. The mammalian ABA receptor has been identified as LANCL2 on the basis of (1) modeling predictions, [8] (2) direct and specific ABA binding to the purified recombinant protein, [9] and (3) abrogation of the functional effects of ABA by silencing of LANCL2 expression in ABA-sensitive cells. [10]
Selective binding between LANCL2 and ABA or other ligands such as the benzimidazole NSC61610 and piperazine BT-11, [11] lead to elevation of intracellular cAMP, activation of PKA [12] and suppression of inflammation [12] in macrophages. In hepatocytes, LANCL2 regulates cell survival by phosphorylation of Akt through its interaction with the Akt kinase mTORC2. [13] Active mTORC2 causes translocation of GLUT4 to the plasma membrane and stimulates glucose uptake. [14] LANCL2 expression in immune cells, adipose tissue, skeletal muscle and pancreas, and the potential to manipulate LANCL2 signaling and GLUT4 translocation with ABA make this G protein-coupled receptor a novel therapeutic target for glycemic control. [7] In humans, ABA release was detected with increasing glycemia, although this mechanism failed in people suffering from type 2 and gestational diabetes. Also, plasma ABA concentrations increase after oral glucose load (OGTT) in healthy subjects. [15] ABA stimulates glucose-dependent insulin release from human and rodent pancreatic β-cells. [15] At a low dose (micrograms/Kg body weight) oral ABA significantly reduces both glycemia and insulinemia in rats and in humans undergoing an OGTT [16] indicating that ABA reduces the amount of insulin required to control hyperglycemia. This insulin-sparing effect suggests that LANCL2 can be used as a therapeutic target for the treatment of inflammatory and metabolic diseases such as metabolic syndrome, prediabetes and diabetes.
Novel LANCL2 ligands such as BT-11 significantly decrease disease activity in the Dextran Sodium Sulfate (DSS)-induced model of acute colitis and the IL-10-/- mice and CD4+ T cell transfer-induced chronic colitis models. [11] BT-11 treatment decreased leukocytic infiltration, mucosal thickening and epithelial erosion in the colon, decreased Th1 and Th17 CD4+ T cells and TNFα while increasing regulatory T cells, LANCL2 and IL-10 expression. [11]
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