Prx4 (Jafrac2, DPx-4156, CG1274; Q9V3Q4) notes

Identity check

UniProt Q9V3Q4 gene synonyms include DPx-4156, Jafrac2 and dPrx4 (CG1274, FBgn0040308): Prx4 is the protein called Jafrac2 by Tenev et al. 2002, so PMID:12356728 does concern this gene.
Typical 2-Cys peroxiredoxin (AhpC/Prx1 subfamily) with a 1-17 signal peptide (UniProt FT SIGNAL 1..17); mature chain begins at Ala18 ("AKPE..."), matching an N-terminal IAP-binding motif.

2-Cys Prx with thioredoxin-dependent peroxidase activity PMID:11677042; one family member secreted PMID:11677042.
IAP antagonist claim [PMID:12356728 "We have identified the thioredoxin peroxidase Jafrac2 as an IAP-interacting protein in Drosophila cells that harbours a conserved N-terminal IAP-binding motif"; "In healthy cells, Jafrac2 resides in the endoplasmic reticulum but is rapidly released into the cytosol following induction of apoptosis"; "Jafrac2 displaces Dronc from DIAP1 by competing with Dronc for the binding of DIAP1"].
In vivo physiology PMID:23271054; overexpression causes redistribution and apoptosis PMID:23271054; JAK/STAT PMID:23271054; stress-induced secretion PMID:23271054.
Hyperoxidation of 2-Cys Prxs PMID:33920774.

Evidence: a single primary study (Tenev et al. 2002) with co-IP/binding to DIAP1 BIR2, competition with Dronc, motif-mutant (N-terminal Ala) loss of DIAP1 binding and of eye-ablation activity, and genetic suppression by reduced dronc dosage (per abstract and falcon deep research summary of the full text). The 2013 study refers to "the known proapoptotic effects of the cytosolic form of dPrx4" and observed apoptosis on strong overexpression, but did not independently test DIAP1 binding.
Limits: all death-promoting evidence is gain-of-function (overexpression/ectopic expression) or in cultured cells; no loss-of-function study shows Prx4 is required for developmental or stress-induced apoptosis; the full text is not in the local cache. The claim is therefore plausible and curator-annotated, but is a single-lab, overexpression-based finding.
Conclusion: the IAP-antagonist activity is kept as a non-core, conditional (stress-released cytosolic pool) role; Prx4's core function is ER-luminal thioredoxin-dependent peroxide reduction. Its membership in an RHG/apoptosome caspase-activation module should be treated as peripheral and flagged as resting on one study.

Obsolete thioredoxin peroxidase activity IBA -> thioredoxin-dependent peroxiredoxin activity.
Determination of adult lifespan (IEA): knockdown had no longevity effect -> over-annotated.