TMEM18 seems to affect energy levels through insulin and glucagon signaling, and in flies, its downregulation induces a metabolic state resembling type-II diabetes[6]
Overexpression of the TMEM18 protein increases the migration capacity of neural stem cells while inactivation of TMEM18 results in almost complete loss of migration activity.[7]
The TMEM18 gene is ubiquitously expressed in both mammalian and fly tissues,[6] which suggests a basic cellular function. In the mouse brain, it is found in the majority of all cells, but is more abundant in neurons than other cell types.[8]
The TMEM18 gene has a long evolutionary history as it is present in both plants and animals.[6][8] The TMEM18 protein's amino acid sequence is well conserved, which suggests that it has retained its function since the divergence of human and plants. The gene seems to have been lost in two separate lineages, but is not found duplicated in any analyzed genomes. Hence, it is not essential for eukaryotic organisms, but there appears to be selection against multiple copies of the TMEM18 gene.[6]
^Thorleifsson G, Walters GB, Gudbjartsson DF, et al. (January 2009). "Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity". Nat. Genet. 41 (1): 18–24. doi:10.1038/ng.274. PMID19079260. S2CID764409.
Brandys MK, van Elburg AA, Loos RJ, et al. (2010). "Are recently identified genetic variants regulating BMI in the general population associated with anorexia nervosa?". Am. J. Med. Genet. B Neuropsychiatr. Genet. 153B (2): 695–699. doi:10.1002/ajmg.b.31026. PMID19746409. S2CID45793585.
Thorleifsson G, Walters GB, Gudbjartsson DF, et al. (2009). "Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity". Nat. Genet. 41 (1): 18–24. doi:10.1038/ng.274. PMID19079260. S2CID764409.