PAX-Interacting Protein 1 (PTIP) Promotes Apoptosis
PAX-interacting protein 1 (PTIP/PAXIP1) was discovered and initially characterized over three decades ago as a 1,056 amino acid-containing protein with six tandem BReast cancer C-Terminal (BRCT) repeats. PTIP functions broadly to catalyze histone methylation in DNA damage repair and within the hematopoietic lineage, to promote immunoglobulin variable region (variable, diversity, joining [VDJ]) and class switch recombination (CSR). In this report, we show that a fraction of PTIP is actively transported from the nucleus to mitochondria resulting in their aggregation, release of cytochrome c into the cytoplasm and cellular apoptosis. Deletion of an N-terminal glutamine-rich region (QR), mutation of a conserved threonine within BRCT3 and truncation of the C-terminal BRCT5 domain each significantly reduced apoptosis as well as its previously documented G<sub>2</sub>/M cell cycle function. This is the first report to identify a mitochondrial-based apoptotic mechanism employed by the PTIP transcription factor.
Authors
- Kangsan Kim (ORCID: https://orcid.org/0000-0002-5283-8644)
- Y. Jessie Zhang
- Haley O. Tucker
- Danyang Yu
- Ching-Jung Huang
- Chuan Li
- Hyein
Institutions
- New York University Shanghai (CN)
- Advanced Institute of Convergence Technology (KR)
- Ajou University (KR)
- The University of Texas at Austin (US)
Publication Details
- Journal
- Journal of Cellular Signaling
- Published
- 2025-11-29
- DOI
- https://doi.org/10.33696/signaling.6.142
- Citations
- 1
- Primary Topic
- PI3K/AKT/mTOR signaling in cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.81