| Field | Specification |
|---|---|
| Mfr No | |
| Alternative Names | Macrophage migration inhibitory factor|MIF|Glycosylation-inhibiting factor|GIF|L-dopachrome isomerase|L-dopachrome tautomerase|Phenylpyruvate tautomerase|MIF|GLIF|MMIF |
| Assay Time | |
| Detection Method | |
| Detection Range | |
| Product Type | |
| Reactivity | |
| Sample Type(s) | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
| Sensitivity | |
| Species | |
| Storage | |
| Target | |
| UniProt # |
Background
human MIF (Macrophage migRation inhibitory factor) is a molecular target commonly studied in immunology, cardiovascular, and metabolism research. Many proteins are studied as molecular readouts that can change with cellular state, tissue remodeling, or stress responses.
Biological role and mechanism
The biological role of MIF is typically understood in terms of its molecular category and interaction network. Depending on the model system, it may participate in cell–cell communication, intracellular signaling, enzymatic processing, or regulation of gene expression programs. Mechanistic interpretation is often strengthened by considering upstream regulators and downstream readouts rather than relying on a single marker.
Expression and abundance of MIF can vary by tissue, cell type, and physiological state. In many systems, levels are influenced by factors such as developmental stage, immune activation, metabolic status, and cellular stress. Because sample matrix and pre-analytical handling can affect measured concentrations, interpretation is typically strongest when experiments keep collection and processing consistent across groups.
Nomenclature and related terms
MIF (Macrophage migRation inhibitory factor) may also be referenced as Macrophage migration inhibitory factor, MIF, and Glycosylation-inhibiting factor in the literature or in databases. When comparing results across studies, confirm that the reported analyte refers to the same molecule, species context, and molecular form (e.g., precursor vs mature protein, or soluble vs membrane-associated forms).
Why it matters in research
- Understanding how MIF relates to innate and adaptive immune responses, cytokine signaling networks, host–pathogen interactions, and immune cell activation and trafficking in immunology, cardiovascular, and metabolism research.
- Interpreting shifts in MIF levels alongside other pathway components or complementary markers.
- Connecting molecular changes to phenotypes such as inflammation, remodeling, metabolism shifts, or cell-state transitions (context-dependent).
Molecular forms and interpretation
For some targets, isoforms, proteolytic processing, or post-translational modifications (such as phosphorylation or glycosylation) can influence function and apparent abundance. If multiple molecular forms are expected in your model, align interpretation with the form most relevant to the biological question.
Disease and translational relevance
MIF has been investigated across diverse physiological and disease contexts, and changes in its abundance have been reported in areas aligned with immunology, cardiovascular, and metabolism studies. These associations are interpreted as research findings rather than diagnostic or therapeutic claims, and they should be evaluated alongside model-specific covariates and study design.
Can’t Find What You’re Looking For? We can help you source the best match or customize an ELISA solution for your study. Options may include alternative target synonyms, different species reactivity, sample type/matrix compatibility (serum/plasma/lysate/supernatant), assay format (sandwich/competitive), sensitivity/range, detection chemistry (colorimetric/fluorescent/chemiluminescent), plate format (pre-coated/uncoated, strips vs full plate), and bulk or custom packaging. Click Talk to a Scientist to submit a request form, email us at support@biohippo.com, or explore our Research Services for additional support. Our team will be in contact with you shortly.
Chemotherapy awakens dormant cancer cells in lung by inducing neutrophil extracellular traps
IF: 44.5 Journal: Cancer Cell Author: CAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. Cited Date: 2025-07-11
Sulforaphane effectively inhibits HBV by altering Treg/Th17 immune balance and the MIF-macrophages polarizing axis in vitro and in vivo
IF: 5 Journal: Virus Research Author: Laboratory Animal Center of Chongqing Medical University, Chongqing, China Cited Date: 2024-01-19
MIF/CD74 axis in hepatic stellate cells mediates HBV-related liver fibrosis
IF: 4.8 Journal: International Immunopharmacology Author: Department of Bioengineering, Jilin University School of Pharmaceutical Sciences, Changchun, Jilin Province 130021. Cited Date: 2025-01-10
Macrophage Migration Inhibitory Factor as a Potential Plasma Biomarker of Cognitive Impairment in Cerebral Small Vessel Disease
IF: 4.1 Journal: ACS Omega Author: Department of Neurology, the Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi 214023, China. Cited Date: 2024-04-12