This process is called metacyclogenesis. The ovarian stimulation protocol used for IVF/ICSI women causes the development of several follicles with a wide range of sizes and at different developmental stages. The observed increase in follicular fluid AEA concentrations with increased follicle size and lower AEA concentrations in follicles from which oocytes were not retrieved indicate that AEA is probably involved in the maturation of follicles or the oocyte. Since oocyte maturity is currently assessed subjectively by embryologists there is a need for a more objective method of assessment. The complex molecular events that underlie most neurodegenerative diseases are poorly understood. In prion diseases the mechanism by which PrPc is converted to PrPsc is central to disease transmission and pathophysiology. Indeed, deposition of PrPsc in the absence of endogenous PrPc is insufficient to cause disease. Consequently, the disruption of PrPc to PrPsc conversion and concomitant cellular events provides a useful basis for therapeutic intervention. The structural change from primarily alpha-helical PrPc to beta-sheet PrPsc is thought to underpin the aggregation status, protease resistance and replication capacity of PrPsc. The PrPsc template is necessary to promote conversion of PrPc in transmitted disease, but mutations in the PrP gene can impart intrinsic changes in PrPc primary structure that fosters spontaneous conformational conversion that leads to abnormal protein aggregation and prion diseases. The existence of multiple prion strains with differing biochemical and pathophysiological signatures suggests that a range of stabilized structural isoforms of PrPsc can be transmitted to PrPc. This functional diversity likely reflects the unique properties of stabilized prion structures and their ability to complex with distinct compliments of endogenous factors. Moreover, the neuropathological variability observed among prion strains may result from a selective targeting of a strain-specific PrPsc complex to unique cellular or extracellular sites within the brain. A C-terminus ubiquitin binding CUE domain identified by Shih et al. as a ubiquitin binding site that mediates intramolecular monoubiquitylation. At the amino-terminus , a GAT/TOM1 interacting domain is also described. So far, Pazopanib Tollip has been involved in two main functions. The first, proposed by Burns and collaborators , indicates Tollip as an interactor of the IL-1 receptor TIR domain, mediating the binding of the serine/ threonine kinase IRAK-1 to the activated receptor complex, thus being integral part of the IL-1RI signaling cascade. Later, Yamakami & Yokosawa proposed a negative regulatory role of Tollip on the IL-1b and TNF-a signaling pathways, in agreement with the inhibition of NF-kB activation observed following Tollip overexpression. The second function, described by Yamakami et al. , concerns the interaction of Tollip with Tom1, Ubiquitin and Clathrin in a high molecular mass complex involved in protein sorting.