Disease relevance of Mfi2

• Melanotransferrin (MTf) is a transferrin homologue initially identified in melanoma cells [1].

Psychiatry related information on Mfi2

• Membrane-bound transferrin-like protein (MTf), a glycosylphosphatidylinositol-anchored protein, is expressed at high levels in many tumors and in several fetal and adult tissues including cartilage and the intestine, as well as in the amyloid plaques of Alzheimer's disease, although its role remains unknown [2].

High impact information on Mfi2

• Incubation of non-Mtf alpha target cells with synthetic peptide ND1 alpha 1-17 (the first 17 amino acid of the ND1 protein of Mtf alpha mice) rendered them susceptible to lysis by MTF alpha-specific cytotoxic T cells (CTLs) [3].
• Assessment of Fe indices, tissue Fe levels, hematology, and serum chemistry parameters demonstrated no differences between MTf-/- and wild-type (MTf+/+) mice, suggesting MTf was not essential for Fe metabolism [4].
• These findings suggest that the expression of MTf on the cell surface facilitates the differentiation of prechondrogenic cells, although MTf overexpression alone seems to be insufficient to commit pluripotent mesenchymal cells to the chondrocyte lineage [5].
• MTf overexpression in C3H10T1/2 cells also induced aggrecan and/or type II collagen mRNA but not the spherical phenotype [5].
• The higher permeability of RAP compared with that of melanotransferrin and transferrin show that the LRP receptor is a high capacity transport system [6].

Chemical compound and disease context of Mfi2

• In vitro cytotoxicity assays with 3677 human melanoma cells demonstrated that C-Mel was 40-fold less toxic than melphalan and was activated in an immunologically specific manner by L49-sFv-bL, a recombinant fusion protein that binds to the melanotransferrin antigen on melanomas and on some carcinomas [7].

Biological context of Mfi2

• The findings suggest that the crosslinking of MTf changes the cell shape and induces chondrogenic differentiation [2].
• In this study, we examined the effects of anti-MTf antibodies and concanavalin A on cell shape and gene expression, using cultures of chondrocytes and MTf-overexpressing ATDC5 and C3H10T1/2 cells [2].
• In this study, we isolated the MTf gene from a constructed mouse genomic library [8].
• The chondrocyte-specific expression of the MTf gene could be regulated via these regulatory elements in the promoter region [8].
• The mouse MTf gene was encoded by a single-copy gene spanning approximately 26 kb and consisting of 16 exons [8].

Anatomical context of Mfi2

• Using primary chondrocytes, SK-MEL-28 (melanoma cell line), ATDC5 (chondrogenic cell line) and NIH3T3 (fibroblast cell line) cells, we carried out transient expression studies on various lengths of the 5' flanking region of the MTf gene fused to the luciferase reporter gene [8].
• These findings were consistent with the levels of expression of MTf mRNA in these cells cultured under similar conditions [8].
• MTf mRNA was expressed only at very low levels in the brain, spleen, thymus, muscle, lung, skin and intestine, and hardly detected in the heart, kidney, stomach and liver [9].
• Among various adult mouse tissues, MTf mRNA was expressed at the highest level in cartilage and at a moderate level in the testis [9].
• OBJECTIVE: This study was undertaken to assess the role of p97 (also known as melanotransferrin) in the transfer of iron into the brain, because the passage of most large molecules is limited by the presence of the blood-brain barrier, including that of the serum iron transporter transferrin [10].

Regulatory relationships of Mfi2

• In cultures of the mouse ATDC5 cell line, MTf is developmentally expressed in parallel with the expression of type II collagen and aggrecan, in the pattern commensurate with the onset of chondrogenesis to form cartilage nodules [9].

Other interactions of Mfi2

• Membrane-bound transferrin-like protein (MTf): structure, evolution and selective expression during chondrogenic differentiation of mouse embryonic cells [9].
• Phylogenetic analysis indicated that the MTf gene diverged from the common ancestor gene earlier than the genes of the other transferrins such as serum transferrin, lactoferrin and ovotransferrin, and that the divergence occurred after the divergence of vertebrates and invertebrates [9].

Analytical, diagnostic and therapeutic context of Mfi2

• The mouse MTf gene was mapped on the B3 band of chromosome 16 by fluorescence in situ hybridization [8].
• As the Mta type of a mouse cannot be influenced by embryo transfer or foster nursing, we concluded that it was determined by a cytoplasmic factor (Mtf), transmitted through the egg [11].
• Flow cytometry and immunocytochemical analyses demonstrated that the cells expressed melanotransferrin and S-100 protein [12].

References