TRAF3

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TRAF3

A gene on chromosome 14q32.32 that encodes TNF receptor-associated factor 3, which regulates NF-kappaB kinase and MAP kinase activation, plays a central role in regulating B-cell survival, and is part of signalling pathways leading to cytokine and interferon production. TRAF3 is required for normal antibody isotype switching from IgM to IgG, and it plays a role in T-cell dependent immune responses as well as antiviral responses. It is an essential constituent of several E3 ubiquitin-protein ligase complexes and may promote Lys-63-linked ubiquitination of target proteins. It inhibits NF-kappaB activation in response to LTBR stimulation, as well as TRAF2-mediated NF-kappaB activation, and it downregulates proteolytic processing of NFKB2 and NF-kappaB activation. It promotes ubiquitination and proteasomal degradation of MAP3K14.
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Figure 3]d shows that IL-4/13 significantly induced CAP1 in both NHK and HaCaT cells.
sup][14] The precursor pro-FLG is dephosphorylated with increasing calcium concentration and proteolytically cleaved by proteases, such as matriptase,[sup][22] CAP1,[sup][23] KLK7, and KLK5[sup][24] to release FLG protein during keratinocyte differentiation.
Both internal and external infectious disease medical and regulatory reviewers have now assessed many possible factors that could have contributed to the unexpected overall outcome of the CAP1 study.
Cubist has also announced preliminary results from the first of two pivotal, Phase III trials investigating the safety and efficacy of CIDECIN in the treatment of community-acquired pneumonia requiring hospitalization (the CAP1 trial).
Cubist also announced today a complete re-analysis of the data from the CAP1 study.
Thus far in 2002, we presented positive human data on OCTX and announced mixed results from the CAP1 trial.