Disease relevance of GMFB

• AIMS: To investigate whether Glia maturation factor-beta (GMFB) is expressed in thymomas and is associated with T-cell development [1].
• These data show that PKCiota can confer partial resistance to cisplatin in glioblastoma cells by suppressing GMFbeta-mediated enhancement of p38 MAP kinase signaling [2].
• This polypeptide, human recombinant glia maturation factor-beta, has been expressed in Escherichia coli and found to possess structural characteristics and biological activity indistinguishable from those of the native bovine protein [3].
• The proliferation of medulloblastoma cells was arrested 24-48 hr after exposure to human recombinant GMF-beta [4].
• GMF-beta promotes growth arrest and morphological alteration of cultured glioma and neuroblastoma cells [4].

High impact information on GMFB

• The BHC locus in this family was located between markers D14S49 and D14S1064, a region spanning approximately 20.6 cM that contains several interesting candidate genes involved in the development and/or maintenance of the CNS: glia maturation factor-beta, GTP cyclohydrolase 1 and the survival of motor neurons (SMN)-interacting protein 1 [5].
• These results show that the expression of GMF-beta in Schwann cells, as is the case with the NGF receptor, is induced by the loss of the normal axon-Schwann cell contact [6].
• Axonal signals regulate expression of glia maturation factor-beta in Schwann cells: an immunohistochemical study of injured sciatic nerves and cultured Schwann cells [6].
• Transient overexpression of GMFbeta increased cisplatin-activated p38 MAP kinase signaling and also sensitised cells to cisplatin cytotoxicity [2].
• Using oligonucleotide probes based on the sequences of three tryptic peptides derived from bovine glia maturation factor-beta, we screened a human brainstem cDNA library in lambda gt11 [3].

Biological context of GMFB

• These assay systems enabled us to identify GMFB and GMFG (GMFs) in both human and rat samples and they were used to investigate the tissue distribution and serum concentrations of human and rat GMFs [7].
• The deduced amino acid sequences of its putative product is highly homologous to human GMF-beta (82% identity) and named for GMF-gamma [8].
• Within the set of genes that were negatively regulated by PKCiota, the function of the gene coding for GMFbeta, an enhancer of p38 mitogen-activated protein kinase (MAP kinase) signaling, was investigated further, as the p38 MAP kinase pathway has been previously identified as a key mediator of cisplatin cytotoxicity [2].
• We cloned a full-length, 4,311-bp mouse cDNA containing a 270-bp 5' UTR, a 3,615-bp 3' UTR, and an open reading frame of 426 nucleotides encoding a putative 142 amino-acid protein, identical to human GMFB, with the exception of two amino acids [9].
• The presence of A2, cde, CwDe, Kpa, AK2, pc, Gmfb, and Gmfnb genes or haplotypes in low or moderate frequencies was observed [10].

Anatomical context of GMFB

• In the case of rat, relatively high levels of GMFB were found in the central nervous system, except for the spinal cord, and in thymus and colon [7].
• There was a significant correlation between GMFB expression and the amount of accompanying non-neoplastic T cells [1].
• Identification and isolation of a full-length clone of mouse GMFB (Gmfb), a putative intracellular kinase regulator, differentially expressed in telencephalon [9].
• Many but not all neurons in the central and peripheral nervous system were positive for GMF-beta [11].
• We have investigated the consequences of treating cell lines derived from a human medulloblastoma with glia maturation factor-beta (GMF-beta), a protein found in mammalian brain [4].

Associations of GMFB with chemical compounds

• The expression of both GMFbeta mRNA and protein increased upon PKCiota depletion, and this was accompanied by an increase in cisplatin-activated p38 MAP kinase signaling [2].

Other interactions of GMFB

• Human glia maturation factor-gamma (hGMFG) was recently identified as a gene that is homologous to glia maturation factor-beta (GMFB) [12].
• CONCLUSIONS: The present study suggests that T-cell development in thymoma may be maintained partly by GMFB produced by the tumour cells [1].
• Expression of glial fibrillary acidic protein in human medulloblastoma cells treated with recombinant glia maturation factor-beta [4].

Analytical, diagnostic and therapeutic context of GMFB

• Sensitive immunoassays for human and rat GMFB and GMFG, tissue distribution and age-related changes [7].
• Northern blot analysis indicated that a message of 0.9 kb long, but not 4.1 kb of GMF-beta, is predominantly expressed in human lung, heart, and placenta [8].
• GMFB promoted T-cell differentiation into CD4-/CD8+ cells when analysed by two-colour flow cytometry [1].
• METHODS AND RESULTS: We investigated the expression of GMFB by immunohistochemistry in 86 cases of thymoma classified into five type A, 35 type AB, 11 type B1, 26 type B2, and nine type B3 thymomas according to the World Health Organization classification system [1].
• Molecular cloning and expression of biologically active human glia maturation factor-beta [3].

References