Target intelligence / Profile preview

Peptidylprolyl isomerase A pseudogene 53 (PPIAP53)

Target
PPIAP53
Molecular classification
Pseudogene, processed pseudogene, noncoding RNA
01

Overview

Peptidylprolyl isomerase A pseudogene 53 (PPIAP53) is classified as a processed pseudogene within the human genome[1][7]. Like other pseudogenes, PPIAP53 is believed to be a noncoding sequence derived from the parental PPIA gene (Peptidylprolyl isomerase A), which encodes the enzyme cyclophilin A. Unlike its parental gene, PPIAP53 does not encode a functional protein and is not currently associated with any known biological function, disease role, or therapeutic intervention. Pseudogenes in general can sometimes regulate their parental gene or participate in gene regulatory networks, typically by acting as long noncoding RNAs or microRNA sponges, but there is no evidence that PPIAP53 performs such roles[5].\n \nThere are other PPIA pseudogenes such as PPIAP22 with described regulatory functions in cancer, but these findings do not apply to PPIAP53[2][4]. As such, PPIAP53 is not considered a therapeutic target, nor does it have any known alias, interacting drug, biomarker utility, or safety concerns[1][7].\n\nNote: If you are seeking information about the functional parental PPIA gene (Peptidylprolyl isomerase A, also known as Cyclophilin A), it is a well-characterized enzyme involved in protein folding and immune modulation, but this is distinct from the noncoding pseudogene PPIAP53[6].

02

Biological functions

Possible regulatory functions as noncoding RNA, but there are no specific reported functions for PPIAP53 itself in the literature or curated databases.In general, pseudogenes may regulate their parental genes through mechanisms such as serving as competing endogenous RNA (ceRNA) or producing small interfering RNAs. This has not been demonstrated for PPIAP53 specifically.
03

Disease associations

None known for PPIAP53.There is evidence that other peptidylprolyl isomerase A pseudogenes, such as PPIAP22, may be involved in cancer through regulatory effects on PPIA expression, but this is not documented for PPIAP53.

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