Cd5l
entrez
11801
canonical
uniprot
Q9QWK4
canonical
ensembl
ENSMUSG00000015854
resolver
ensp
ENSMUSP00000015998
resolver
enst
ENSMUST00000015998
resolver
genesymbol
Cd5l
resolver
genesymbol_syn
Aim
resolver
genesymbol_syn
Api6
resolver
uniprot
O35300
resolver
uniprot
O35301
resolver
uniprot
Q3TXN5
resolver
uniprot
Q505P6
resolver
uniprot
Q91W05
resolver
uniprot_entry
CD5L_MOUSE
resolver
uniprot_sec
O35300
resolver
uniprot_sec
O35301
resolver
uniprot_sec
Q3TXN5
resolver
uniprot_sec
Q505P6
resolver
uniprot_sec
Q91W05
resolver
amino_acid_sequence
MAPLFNLMLAILSIFVGSCFSESPTKVQLVGGAHRCEGRVEVEHNGQWGTVCDDGWDRRDVAVVCRELNCGAVIQTPRGASYQPPASEQRVLIQGVDCNGTEDTLAQCELNYDVFDCSHEEDAGAQCENPDSDLLFIPEDVRLVDGPGHCQGRVEVLHQSQWSTVCKAGWNLQVSKVVCRQLGCGRALLTYGSCNKNTQGKGPIWMGKMSCSGQEANLRSCLLSRLENNCTHGEDTWMECEDPFELKLVGGDTPCSGRLEVLHKGSWGSVCDDNWGEKEDQVVCKQLGCGKSLHPSPKTRKIYGPGAGRIWLDDVNCSGKEQSLEFCRHRLWGYHDCTHKEDVEVICTDFDV
uniprot
proteins
function
FUNCTION: Secreted protein that acts as a key regulator of lipid synthesis: mainly expressed by macrophages in lymphoid and inflamed tissues and regulates mechanisms in inflammatory responses, such as infection or atherosclerosis (PubMed:26048980). Able to inhibit lipid droplet size in adipocytes (PubMed:20519120, PubMed:22579686). Following incorporation into mature adipocytes via CD36-mediated endocytosis, associates with cytosolic FASN, inhibiting fatty acid synthase activity and leading to lipolysis, the degradation of triacylglycerols into glycerol and free fatty acids (FFA) (PubMed:20519120). CD5L-induced lipolysis occurs with progression of obesity: participates in obesity-associated inflammation following recruitment of inflammatory macrophages into adipose tissues, a cause of insulin resistance and obesity-related metabolic disease (PubMed:21730133). Regulation of intracellular lipids mediated by CD5L has a direct effect on transcription regulation mediated by nuclear receptors ROR-gamma (RORC) (PubMed:22579686, PubMed:26607793). Acts as a key regulator of metabolic switch in T-helper Th17 cells (PubMed:26607793, PubMed:26607794). Regulates the expression of pro-inflammatory genes in Th17 cells by altering the lipid content and limiting synthesis of cholesterol ligand of RORC, the master transcription factor of Th17-cell differentiation (PubMed:26607793). CD5L is mainly present in non-pathogenic Th17 cells, where it decreases the content of polyunsaturated fatty acyls (PUFA), affecting two metabolic proteins MSMO1 and CYP51A1, which synthesize ligands of RORC, limiting RORC activity and expression of pro-inflammatory genes (PubMed:26607793). Participates in obesity-associated autoimmunity via its association with IgM, interfering with the binding of IgM to Fcalpha/mu receptor and enhancing the development of long-lived plasma cells that produce high-affinity IgG autoantibodies (PubMed:23562157). Also acts as an inhibitor of apoptosis in macrophages: promotes macrophage survival from the apoptotic effects of oxidized lipids in case of atherosclerosis (PubMed:16054063, PubMed:9892623). Involved in early response to microbial infection against various pathogens by acting as a pattern recognition receptor and by promoting autophagy (By similarity). Promotes recovery from acute kidney injury (AKI) by accumulating on necrotic cell debris within the kidney proximal tubules following AKI and interacting with HAVCR1 expressed on the surface of injured kidney tubular epithelial cells (PubMed:26726878). This enhances HAVCR1-mediated phagocytosis of intraluminal necrotic debris and contributes to kidney tissue repair (PubMed:26726878). Also enhances necrotic debris uptake by kidney macrophages in a HAVCR1-independent manner (PubMed:26726878). {ECO:0000250|UniProtKB:O43866, ECO:0000269|PubMed:16054063, ECO:0000269|PubMed:20519120, ECO:0000269|PubMed:21730133, ECO:0000269|PubMed:22579686, ECO:0000269|PubMed:23562157, ECO:0000269|PubMed:26607793, ECO:0000269|PubMed:26607794, ECO:0000269|PubMed:26726878, ECO:0000269|PubMed:9892623, ECO:0000303|PubMed:26048980}.
uniprot
proteins
mass_dalton
38863
uniprot
proteins
mutagenesis
MUTAGEN 99; /note="N->Q: Decreased glycosylation."; /evidence="ECO:0000269|PubMed:23236605"; MUTAGEN 194; /note="C->S: Abolishes interaction with IgM."; /evidence="ECO:0000269|PubMed:30324136"; MUTAGEN 229; /note="N->Q: Decreased glycosylation."; /evidence="ECO:0000269|PubMed:23236605"; MUTAGEN 316; /note="N->Q: Does not affect glycosylation."; /evidence="ECO:0000269|PubMed:23236605
uniprot
proteins
post_translational_modification
PTM: N-glycosylated (PubMed:10651944, PubMed:23236605). N-glycan at Asn-99 possesses only alpha2,6-sialylated terminals, while Asn-229 possesses both alpha2,6-sialylated and non-sialylated terminals (PubMed:23236605). N-glycosylation increases secretion. {ECO:0000269|PubMed:10651944, ECO:0000269|PubMed:23236605}.
uniprot
proteins
pubmed
10651944
uniprot
proteins
pubmed
15489334
uniprot
proteins
pubmed
16054063
uniprot
proteins
pubmed
16141072
uniprot
proteins
pubmed
20519120
uniprot
proteins
pubmed
21730133
uniprot
proteins
pubmed
22579686
uniprot
proteins
pubmed
23236605
uniprot
proteins
pubmed
23562157
uniprot
proteins
pubmed
26048980
uniprot
proteins
pubmed
26607793
uniprot
proteins
pubmed
26607794
uniprot
proteins
pubmed
26726878
uniprot
proteins
pubmed
30324136
uniprot
proteins
pubmed
9892623
uniprot
proteins
sequence_length
352
uniprot
proteins
subcellular_location
SUBCELLULAR LOCATION: Secreted {ECO:0000269|PubMed:20519120, ECO:0000269|PubMed:23236605, ECO:0000269|PubMed:26726878, ECO:0000269|PubMed:9892623}. Cytoplasm {ECO:0000269|PubMed:20519120}. Note=Secreted by macrophages and circulates in the blood (PubMed:20519120). Transported into the cytoplasm via CD36-mediated endocytosis (PubMed:20519120). Following acute kidney injury, dissociates from IgM in the blood and is excreted into urine, leading to its accumulation at intraluminal debris in the kidney proximal tubules (PubMed:26726878). {ECO:0000269|PubMed:20519120, ECO:0000269|PubMed:26726878}.
uniprot
proteins