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Characterizing the influence of YB-1 on tumor necrosis factor-α signaling in inflammatory renal disease
Tumor necrosis factor-alpha (TNF) is a cytokine that plays a central role in initiating inflammatory processes. Inflammation plays a key role in the pathology of many immune-mediated kidney diseases and is thought to be a driving factor in the development of fibrosis, which results in a reduced kidney funtion. TNF has been identified as a central molecule associated with poor outcome in patiets with Nephrotic syndrome. Further more, plasma levels of soluble TNF receptors are a predictive factor for progression to end-stage kidney disease within 10 years in patients.
Studies have demonstrated a beneficial effect of anti-TNF therapy in kidney disease. However, experience with the use of anti-TNF therapy in the clinic over the past 25 years has demonstrated that only 50% of patients respond to therapy.
We have demonstrated that the cold shock protein Y-box binding protein-1 (YB-1) is an abundant serum protein and that it possesses the ability to compete with TNF for TNFR binding. This project aims to investigate whether YB-1 is responsible for setting the threshold of TNFR signaling.

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