CERS5
Ceramide synthase 5
Also known as: CERS5_HUMAN, FLJ25304, LASS5, MGC45411, Trh4
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8N5B7
- Gene
- CERS5
- Ensembl
- ENSG00000139624
- Chromosome
- 12
- Canonical length
- 392 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted membrane proteins
- Subcellular location
- Nuclear membrane,Endoplasmic reticulum,Primary cilium
OverviewNCBI Gene
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]
Canonical amino-acid sequenceUniProt
392 residues, UniProt reviewed canonical sequence.
>Q8N5B7|CERS5
1 MATAAQGPLS LLWGWLWSER FWLPENVSWA DLEGPADGYG YPRGRHILSV FPLAAGIFFV
61 RLLFERFIAK PCALCIGIED SGPYQAQPNA ILEKVFISIT KYPDKKRLEG LSKQLDWNVR
121 KIQCWFRHRR NQDKPPTLTK FCESMWRFTF YLCIFCYGIR FLWSSPWFWD IRQCWHNYPF
181 QPLSSGLYHY YIMELAFYWS LMFSQFTDIK RKDFLIMFVH HLVTIGLISF SYINNMVRVG
241 TLIMCLHDVS DFLLEAAKLA NYAKYQRLCD TLFVIFSAVF MVTRLGIYPF WILNTTLFES
301 WEIIGPYASW WLLNGLLLTL QLLHVIWSYL IARIALKALI RGKVSKDDRS DVESSSEEED
361 VTTCTKSPCD SSSSNGANRV NGHMGGSYWA EELocalizationUniProt · AlphaFold · HPA
Whether an antibody against CERS5 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Other membrane
- Secreted
- No
- Transmembrane segments
- 6
- Mean surface accessibility (rSASA)
- 0.32
- Highest tissue expression
- 32 nTPM
Expression across tissuesHPA
Tissue
- pituitary gland: 32 nTPM
- choroid plexus: 27 nTPM
- kidney: 27 nTPM
- blood vessel: 26 nTPM
- cervix: 26 nTPM
- ovary: 26 nTPM
Single-cell type
- cardiomyocytes: 188 nCPM
- extravillous trophoblasts: 127 nCPM
- retinal ganglion cells: 100 nCPM
- brain inhibitory neurons: 95 nCPM
- neutrophils: 89 nCPM
- other brain neurons: 89 nCPM
Immune cell
- non-classical monocyte: 56 nTPM
- eosinophil: 43 nTPM
- neutrophil: 43 nTPM
- NK-cell: 40 nTPM
- intermediate monocyte: 38 nTPM
- total PBMC: 38 nTPM
Brain region
- hypothalamus: 16 nTPM
- cerebellum: 16 nTPM
- pons: 15 nTPM
- midbrain: 15 nTPM
- white matter: 14 nTPM
- medulla oblongata: 14 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.96
- gnomAD pLI
- 0
- gnomAD missense Z
- 1.19
- DepMap mean gene effect
- -0.01
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of CERS5 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads CERS5 as an antibody target. Whether an autoantibody or antibody against CERS5 could matter depends on whether native CERS5 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CERS5 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label CERS5 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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