Mouse Anti-MIF Recombinant Antibody (CBYJL-2299) (CBMAB-L2585-YJ)

Macrophage Migration Inhibitory Factor

MIF is a lymphokine involved in cell-mediated immunity, immunoregulation, and inflammation. It functions in the regulation of macrophage function in host defense through the suppression of anti-inflammatory effects of glucocorticoids. This lymphokine and the JAB1 protein form a complex in the cytosol near the peripheral plasma membrane, which may indicate an additional role in integrin signaling pathways.

Macrophage Migration Inhibitory Factor; Macrophage Migration Inhibitory Factor (Glycosylation-Inhibiting Factor); Glycosylation-Inhibiting Factor; Phenylpyruvate Tautomerase; L-Dopachrome Tautomerase; L-Dopachrome Isomerase

Pro-inflammatory cytokine involved in the innate immune response to bacterial pathogens (PubMed:15908412, PubMed:17443469, PubMed:23776208).

The expression of MIF at sites of inflammation suggests a role as mediator in regulating the function of macrophages in host defense (PubMed:15908412, PubMed:17443469, PubMed:23776208).

Counteracts the anti-inflammatory activity of glucocorticoids (PubMed:15908412, PubMed:17443469, PubMed:23776208).

Has phenylpyruvate tautomerase and dopachrome tautomerase activity (in vitro), but the physiological substrate is not known (PubMed:11439086, PubMed:17526494).

It is not clear whether the tautomerase activity has any physiological relevance, and whether it is important for cytokine activity (PubMed:11439086, PubMed:17526494).

Carboxylic acid metabolic process Source: BHF-UCL
Cell aging Source: Ensembl
Cell surface receptor signaling pathway Source: UniProtKB
DNA damage response, signal transduction by p53 class mediator Source: Ensembl
Inflammatory response Source: UniProtKB-KW
Innate immune response Source: UniProtKB-KW
Negative regulation of apoptotic process Source: UniProtKB
Negative regulation of cell aging Source: BHF-UCL
Negative regulation of cell migration Source: ARUK-UCL
Negative regulation of cellular protein metabolic process Source: Ensembl
Negative regulation of DNA damage response, signal transduction by p53 class mediator Source: BHF-UCL
Negative regulation of gene expression Source: BHF-UCL
Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source: BHF-UCL
Negative regulation of macrophage chemotaxis Source: BHF-UCL
Negative regulation of mature B cell apoptotic process Source: Ensembl
Negative regulation of myeloid cell apoptotic process Source: Ensembl
Positive regulation of arachidonic acid secretion Source: Ensembl
Positive regulation of B cell proliferation Source: BHF-UCL
Positive regulation of cell population proliferation Source: BHF-UCL
Positive regulation of chemokine (C-X-C motif) ligand 2 production Source: Ensembl
Positive regulation of cytokine production Source: BHF-UCL
Positive regulation of ERK1 and ERK2 cascade Source: BHF-UCL
Positive regulation of fibroblast proliferation Source: BHF-UCL
Positive regulation of lipopolysaccharide-mediated signaling pathway Source: Ensembl
Positive regulation of MAP kinase activity Source: Ensembl
Positive regulation of myeloid leukocyte cytokine production involved in immune response Source: Ensembl
Positive regulation of peptidyl-serine phosphorylation Source: BHF-UCL
positive regulation of peptidyl-tyrosine phosphorylation Source: BHF-UCL
Positive regulation of phosphorylation Source: BHF-UCL
Positive regulation of prostaglandin secretion involved in immune response Source: Ensembl
Positive regulation of protein kinase A signaling Source: BHF-UCL
Positive regulation of tumor necrosis factor production Source: BHF-UCL
Prostaglandin biosynthetic process Source: UniProtKB
Protein homotrimerization Source: UniProtKB
Regulation of macrophage activation Source: UniProtKB

Cytoplasm
Secreted
Note: Does not have a cleavable signal sequence and is secreted via a specialized, non-classical pathway. Secreted by macrophages upon stimulation by bacterial lipopolysaccharide (LPS), or by M.tuberculosis antigens.

Rheumatoid arthritis systemic juvenile (RASJ):
An inflammatory articular disorder with systemic onset beginning before the age of 16. It represents a subgroup of juvenile arthritis associated with severe extraarticular features and occasionally fatal complications. During active phases of the disorder, patients display a typical daily spiking fever, an evanescent macular rash, lymphadenopathy, hepatosplenomegaly, serositis, myalgia and arthritis.