Traf5 Conditional Knockout mouse models

Traf5, the mouse ortholog of human TRAF5, encodes the closest structural relative of TRAF2, sharing a RING domain, zinc fingers, and a trimerizing TRAF domain, and it is recruited to CD27, CD30, CD40, lymphotoxin beta receptor, and TNFR2 to support NF-kB and JNK activation, in some assays acting interchangeably with TRAF2 while in others tuning IL-6 driven STAT3 signaling and helper T cell differentiation. Because its contribution is largely additive rather than unique, germline nulls are viable and fertile with only subtle defects in CD27 and CD40 driven responses, which is precisely the redundancy trap to plan for: a single Traf5 knockout will usually not report pathway dependence, and compound Traf2 Traf5 conditional genetics is required to expose shared function. RING-dead knockins separate ligase activity from scaffolding within otherwise intact receptor complexes. Fit the allele set to T cell dependent antibody responses, non-canonical NF-kB activity, or airway inflammation endpoints.

Conditional deletion of Traf5 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Traf5 floxed stock yields usable cohorts.