Ceramide synthase that catalyzes the transfer of the acyl chain from acyl-CoA to a sphingoid base, with high selectivity toward palmitoyl-CoA (hexadecanoyl-CoA; C16:0-CoA) (PubMed:12912983, PubMed:15823095, PubMed:16100120, PubMed:17977534, PubMed:17609214, PubMed:26853464). Can use other acyl donors, but with less efficiency (PubMed:15823095). N-acylates sphinganine and sphingosine bases to form dihydroceramides and ceramides in de novo synthesis and salvage pathways, respectively (PubMed:12912983, PubMed:15823095, PubMed:15772421, PubMed:17977534). Plays a role in de novo ceramide synthesis and surfactant homeostasis in pulmonary epithelia (PubMed:15772421). a sphingoid base + hexadecanoyl-CoA = an N-hexadecanoyl-sphingoid base + CoA + H(+) hexadecanoyl-CoA + sphinganine = CoA + H(+) + N-hexadecanoylsphinganine hexadecanoyl-CoA + hexadecasphinganine = CoA + H(+) + N-hexadecanoylhexadecasphinganine hexadecanoyl-CoA + sphing-4-enine = CoA + H(+) + N-hexadecanoylsphing-4-enine 2-hydroxyhexadecanoyl-CoA + sphinganine = CoA + H(+) + N-(2-hydroxyhexadecanoyl)-sphinganine sphinganine + tetradecanoyl-CoA = CoA + H(+) + N-(tetradecanoyl)-sphinganine octadecanoyl-CoA + sphinganine = CoA + H(+) + N-(octadecanoyl)-sphinganine (9Z)-octadecenoyl-CoA + sphinganine = CoA + H(+) + N-(9Z-octadecenoyl)-sphinganine a fatty acyl-CoA + sphing-4-enine = an N-acylsphing-4-enine + CoA + H(+) Inhibited by fumonisin B1. Lipid metabolism; sphingolipid metabolism. Ubiquitously expressed, with highest levels in testis and kidney (PubMed:12912983, PubMed:15823095). Expressed in pulmonary epithelia (PubMed:15772421). Expressed in lungs of 15 days old fetuses followed by a modest peak at day 17, thereafter decreasing in adult lungs. The last loop motif confers selectivity toward palmitoyl-CoA (hexadecanoyl-CoA; C16:0-CoA) as acyl donor. Phosphorylated at the C-terminus by CK2. Mice are viable and show no apparent morphological alterations in normal conditions (PubMed:26853464). Decreased palmitoyl (C16:0) ceramide pools (PubMed:26853464). According to a report, deletion of Cers5 protects from obesity: knockout mice are associated with reduced weight gain and improved systemic health after high fat diet challenge (PubMed:26853464). This result was however not confirmed by another study, which did not observe any protection from diet-induced obesity in knockout mice (PubMed:31150623). Effects observed in the first study might be indirect and caused by a large deletion that affects neighboring genes and/or deletes non-coding RNAs (PubMed:26853464, PubMed:31150623). Some prediction bioinformatics tools predict the presence of a homeobox domain (By similarity). However, the domain is degenerate and residues that are important for DNA-binding are absent (By similarity). Moreover, the protein localizes in the endoplasmic reticulum and not in the nucleus, strongly suggesting that it does not constitute a canonical homeobox domain (PubMed:12912983).