API5-FGF2 complex
Crystal structure of API5-FGF2 complex
This is a default text for your page API5-FGF2 complex. Click above on edit this page to modify. Be careful with the < and > signs. You may include any references to papers as in: the use of JSmol in Proteopedia [1] or to the article describing Jmol [2] to the rescue. FunctionApi5 is an anti-apoptotic clone that increases the survival of the cells in growth factor deprivation. Apoptosis, a highly regulated programmed cell death process, is important in maintaining tissue homeostasis and eliminating damaged or potentially abnormal cells and various pro- and anti-apoptotic proteins regulate apoptosis. Api5 (Anti-apoptotic clone 5) is an anti-apoptotic protein which is known to inhibit cell death by various methods which includes Api5-FGF2 mediated Bim degradation. FGF2 (Fibroblast Growth Factor 2) is a protein that helps regulate proliferation, cell differentiation, morphogenesis, wound healing, and various other cellular processes. FGF2 is produced in both low and high-molecular-weight isoforms, all translated from a single mRNA using alternative translation start sites. The low molecular weight (LMW) form, an 18 kDa protein, is synthesized from a conventional AUG codon. This isoform is distributed in the cytoplasm and nucleus and can also be secreted by cells. The high molecular weight (HMW) isoforms (22, 22.5, 24, 34 kDa) are generated by translation initiation at upstream CUG codons. Disease and Biological RelevanceAPI5 is a predominantly nuclear protein that forms a complex with nuclear FGF2, a form of FGF2 associated with poor clinical outcomes in cancer. The crystal structure of the API5–FGF2 complex defines how these two proteins interact and identifies the specific residues involved in their binding. Subsequent analyses revealed an unanticipated function for the complex: API5 and FGF2 associate with the essential RNA helicase UAP56, a core component of mRNA export pathways. Through this interaction, they contribute to the export and expression of select oncogenic mRNAs. Recent studies have shown that overexpression of Api5 in a non-tumorigenic breast epithelial cell line, increased the levels of FGF2 during the initial stages of morphogenesis and it also led to the activation of the Akt and ERK pathway during the initial and later stages of morphogenesis, respectivily. These findings establish API5 and nuclear FGF2 as previously unrecognized factors in mRNA export and highlight their potential relevance to cancer biology. Structural highlightsThis is a sample scene created with SAT to color by Group, and another to make a transparent representation of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.
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