CD5L report

I. Expression across cell types

II. Expression across tissues

sc-RNAseq data

Insufficient scRNA-seq data for expression of CD5L at tissue level.

III. Associated gene sets

GO_0006915Biological processapoptotic process
GO_0002376Biological processimmune system process
GO_0006954Biological processinflammatory response
GO_0006968Biological processcellular defense response
GO_0030449Biological processregulation of complement activation
GO_1903661Biological processpositive regulation of complement-dependent cytotoxicity
GO_0031638Biological processzymogen activation
GO_0005615Cellular componentextracellular space
GO_0009986Cellular componentcell surface
GO_0072562Cellular componentblood microparticle
GO_0005576Cellular componentextracellular region
GO_0005886Cellular componentplasma membrane
GO_0005737Cellular componentcytoplasm
GO_0004252Molecular functionserine-type endopeptidase activity

IV. Literature review

[source]
Gene nameCD5L
Protein nameCD5 antigen-like (Apoptosis inhibitor expressed by macrophages) (hAIM) (CT-2) (IgM-associated peptide) (SP-alpha)
SynonymsAPI6
UNQ203/PRO229
DescriptionFUNCTION: 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. Able to inhibit lipid droplet size in adipocytes. 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). 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. Regulation of intracellular lipids mediated by CD5L has a direct effect on transcription regulation mediated by nuclear receptors ROR-gamma (RORC). Acts as a key regulator of metabolic switch in T-helper Th17 cells. 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. 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. 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 (By similarity). Also acts as an inhibitor of apoptosis in macrophages: promotes macrophage survival from the apoptotic effects of oxidized lipids in case of atherosclerosis . Involved in early response to microbial infection against various pathogens by acting as a pattern recognition receptor and by promoting autophagy . .

AccessionsO43866
ENST00000368174.5