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TP53 regulated inhibitor of apoptosis 1 pseudogene 1 (TRIAP1P1)

Target
TRIAP1P1
Molecular classification
Other (Pseudogene)
01

Overview

TP53 regulated inhibitor of apoptosis 1 pseudogene 1 (TRIAP1P1) is classified as a **pseudogene**, meaning it is a non-functional copy of a gene—in this case, related to the TP53-regulated inhibitor of apoptosis 1 (TRIAP1) gene. Pseudogenes do not code for functional proteins but can sometimes be transcribed into noncoding RNAs that may regulate their protein-coding paralogs by serving as microRNA decoys or through antisense regulation. Although some pseudogenes impact gene expression or disease phenotypes, there is no direct evidence that TRIAP1P1 acts as a therapeutic target, receptor, enzyme, or biomarker, nor is it considered a druggable target. The confusion may arise from the similarity of the name to the actual functional gene, **TRIAP1**, which is regulated by TP53 and does play a role in apoptosis and cancer biology; *however, TRIAP1P1 is a pseudogene* and not a direct mediator of these functions. **Key clarification:** TRIAP1P1 is frequently included in gene databases as a noncoding pseudogene. The actual functional target is **TP53 regulated inhibitor of apoptosis 1** (TRIAP1, not TRIAP1P1). If you are looking for a valid therapeutic target in the p53-apoptosis pathway, refer to TRIAP1 or other direct effectors as summarized in Reactome and the literature on p53 targets. **Summary:** TRIAP1P1/bA748L13.4 is a non-functional pseudogene, not a direct molecular target. For structured data, mark it as incorrect for use as a therapeutic target, and do not conflate it with the functional, apoptosis-regulating TRIAP1 gene.

Other names
bA748L13.4C10orf135
02

Mechanism of action

None

03

Biological functions

None known for the pseudogene directly; in general, pseudogenes can participate in regulation of gene expression as noncoding RNAs, microRNA decoys, antisense regulators, etc.
04

Disease associations

Other; no direct evidence links TRIAP1P1 to a specific disease, but dysregulation of pseudogenes can contribute to cancer biology

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