Disease relevance of FGFR1OP

• The t(6;8)(q27;p11) translocation in a stem cell myeloproliferative disorder fuses a novel gene, FOP, to fibroblast growth factor receptor 1 [1].

High impact information on FGFR1OP

• FOP-FGFR1 tyrosine kinase, the product of a t(6;8) translocation, induces a fatal myeloproliferative disease in mice [2].
• In this study, we show that expression of FOP-FGFR1 in primary bone marrow cells induced by retroviral transduction generates a MPD in mice [2].
• This survival effect is dependent upon the constitutive tyrosine phosphorylation of FOP-FGFR1 [3].
• These results demonstrate that FOP-FGFR1 is capable of protecting cells from apoptosis by using the same effectors as the wild-type FGFR1 [3].
• In the present study, we have cloned the t(6;8)(q27;p11) translocation in two patients and found a fusion between FGFR1 and a novel gene, FOP (FGFR1 Oncogene Partner), located on chromosome band 6q27 [1].

Biological context of FGFR1OP

• Structure of the N-terminal domain of the FOP (FGFR1OP) protein and implications for its dimerization and centrosomal localization [4].
• We show that the C-terminal domain of CAP350 interacts directly with FOP and that both proteins localize to the centrosome throughout the cell cycle [5].
• A subsequent proteomics screen identified FOP as a component of the centrosome [4].
• The fibroblast growth factor receptor 1 (FGFR1) oncogene partner, FOP, is a centrosomal protein that is involved in the anchoring of microtubules (MTS) to subcellular structures [4].
• The low FOP prevalence cannot be considered a public health problem and is not perceived as such by the population [6].

Anatomical context of FGFR1OP

• These results have implications for the mechanisms underlying MT anchoring at the centrosome and they attribute a key MT anchoring function to two novel centrosomal proteins, CAP350 and FOP [5].
• A complex of two centrosomal proteins, CAP350 and FOP, cooperates with EB1 in microtubule anchoring [5].

Associations of FGFR1OP with chemical compounds

• Postero-anterior (PA) cephalograms of 187 pre-orthodontic treatment subjects (aged 18-45 years, mean 23.9 years) were used to investigate the inclination of the frontal occlusal (FOP) and frontal mandibular (FMP) planes to determine vertical asymmetry [7].
• The prevalences of fluoride-associated opacities (FOP) and nonfluoride-associated opacities (non-FOP) were assessed in two cantons of Switzerland with different salt fluoridation schemes [6].

Other interactions of FGFR1OP

• We report two new cases with the t(6;8)(q27;p12) and FGFR1OP-FGFR1 fusion [8].

Analytical, diagnostic and therapeutic context of FGFR1OP

• Constitutive FOP-FGFR1 kinase activity was both essential and sufficient to cause a chronic myeloproliferative syndrome in the murine bone marrow transplantation model [2].

References