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DUB-DECODE Report Summary

Project ID: 648039
Funded under: H2020-EU.1.1.

Periodic Reporting for period 1 - DUB-DECODE (Systematic Decoding of Deubiquitylase-Regulated Signaling Networks)

Reporting period: 2015-10-01 to 2017-03-31

Summary of the context and overall objectives of the project

The overall goal of the DUB-DECODE project is to understand how ubiquitylation, a type of protein modification, regulates function of proteins. In particular, we are interested in understanding the functions of deubiquitylases (DUBs) - the enzymes that remove ubiquitin that is conjugated to its substrates.

Work performed from the beginning of the project to the end of the period covered by the report and main results achieved so far

Since the starting of the project, we have generated human cell line models to investigate DUB functions. In one of recently published paper, we identified a novel mechanism by which the deubiquitylase CYLD is recruited to tumor necrosis factor alpha (TNFa) receptor. TNFa is a key cytokine that functions in regulating innate immunity and inflammation. Binding of TNFa to its receptor can activate pro-survival signaling, or signaling that lead to cell death, and CYLD is implicated as a key regulator of these decisions. We showed that a novel protein SPATA2 constitutively binds to CYLD and recruits it to TNFa receptor, thus, serving a key role in determining the outcomes of TNFa receptor signaling.

Progress beyond the state of the art and expected potential impact (including the socio-economic impact and the wider societal implications of the project so far)

Dysregulated TNFa signaling is implicated in human immune disorders, and understanding the mechanistic basis of TNFa will aid in designing improved therapeutic strategies for treating such disorders.
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