Another study has Serotonin hydrochloride demonstrated the utility of IQGAP2 IQ motif-mimicking peptides as antibacterial agents. In addition to IBD, our findings maybe applicable to other chronic inflammation-associated disorders, including diabetes, cardiovascular diseases, osteoporosis, and cancer. A fragment of prion protein, PrP106-126, is highly conserved among Ifenprodil Tartrate various species and displays similar characteristics to the full-length prion protein. PrP106-126 is thought to be one of the most critical domains involved in fibril formation and structural transition from cellular prion to its scrapie form. This peptide can induce neuro-pathological alterations observed in prion diseases such as apoptosis of nerve cells, prolife ration and hypertrophy of astrocytes. It has been also reported that the selective deletion of residues along with residues can prevent the formation of PrPSc, while only removing residues 23�C88 does not inhibit structural conversion, which indicate that PrP106-126 may play an important role in PrPC-PrPSc transition. Furthermore, the peptide tends to aggregate into amyloid fibrils that are resistant to protease. More interestingly, the toxicity of PrP106126 requires the expression of PrPC, which is similar to PrPSc and further indicates that the toxic mechanism of PrP106-126 may reflect the pathology of PrPSc. Many efforts have been made to investigate the properties of PrP106-126. The physicochemical nature, aggregating propensity and conformational properties of PrP106-126 have been studied by applying biophysical techniques such as circular dichroism spectrum, nuclear magnetic resonance, ion mobility mass spectrometry, as well as molecular simulations. It has been shown that PrP106-126 displays structural diversity and different physical chemical conditions such as solvent composition, ionic strength and pH affect the secondary structure and aggregating propensity of PrP106-126. Mutations of some residues in the peptide also change the conformations and fibrillogenic propensity of PrP106-126. A substitution of alanine by valine at position117 is related to Gerstmann-Straussler-Scheinker disease.