LASS5

Official Full Name

ceramide synthase 5

Organism

Homo sapiens

GeneID

91012

Background

This gene encodes a protein that belongs to the TLC (TRAM, LAG1 and CLN8 homology domains) family of proteins. The encoded protein functions in the synthesis of ceramide, a lipid molecule that is involved in a several cellular signaling pathways. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Aug 2013]

Synonyms

CERS5; Trh4; LASS5;

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Detailed Information

Recent Progress

LASS gene encodes proteins that are involved in ceramide synthesis by hydrolyzing sphingomyelin and thereby mediating apoptosis. The involvement of these proteins in ceramide synthesis substantiates their relationship to apoptosis.

Researchers have found that LASS5 is a genuine dihydroceramide synthase, and demonstrated that mammalian dihydroceramide synthases do not require additional subunits for their activity. Upon over-expression in human embryonic kidney cells, LASS5 elevates the synthesis of (dihydro) ceramides selectively enriched in palmitic acid. The results have shown that solubilized LASS5-HA has the same fatty acid selectivity as the membrane-bound enzyme. After elution from agarose beads, only one band of LASS5 can be detected by SDS-PAGE. Dihydroceramide synthase activity of the eluted LASS5-HA protein is completely dependent on exogenously added phospholipids. Moreover, eluted LASS5-HA was highly selective toward palmitoyl-CoA as acyl donor and was inhibited by the (dihydro) ceramide synthase inhibitor, fumonisin B1.

Fig. 1. Domain architecture of the LASS5. (Robert et al, 2015)

LASS5 gene plays a key role in de novo synthesis of ceramide, the backbone of sphingolipids, which is also a key component of atherosclerotic changes through its important second-messenger role. LASS5 gene also has an indirect effect on AMPK gene, AMP-activated protein kinase genes, which protects against atherosclerosis and hypertension. Previous studies in cell culture and mice experiments have also shown that antagonizing CERS5 could be helpful in treating diabetic cardiomyopathy. Downregulation of LASS5 was found to attenuate ceramide production and increase expression of some AMPK target genes in HUVEC. It has also demonstrated that LASS5 is involved in the negative regulation of atherosclerosis-related genes, such as AMPK-alpha. These preliminary findings provide insight into molecular mechanism of atherosclerosis and are important for development of potential therapeutic agents for the treatment of atherosclerosis.

References:

Çoban N, et al. "[Investigating the role of ceramide metabolism-associated CERS5 (LASS5) gene in atherosclerosis pathogenesis in endothelial cells]." Turk Kardiyol Dern Ars 45.2(2017):118-125.
Jiang, Z., et al. "LASS5 Interacts with SDHB and Synergistically Represses p53 and p21 Activity." Current Molecular Medicine 16.6(2016):-.
Mojakgomo, Rahaba Makgotso. "Molecular analysis of longevity assurance genes (LASS)/ Ceramide Synthases (CerS) 4 and 5 in endomentrial and colon cancer." Thesis (2013).
Robertsrapp, L., et al. "28PDIdentifying the correct patient (pt) population for ABT-414: Biomarker assays for epidermal growth factor receptor (EGFR) in pts with glioblastoma (GBM)." European Journal of Cancer 9(2015):S585-S586.
Li, Xiao Lin, et al. "Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase." Plos One 9.11(2014):e108192.

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