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.

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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
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article

PAX-Interacting Protein 1 (PTIP) Promotes Apoptosis

Kangsan Kim, Y. Jessie Zhang, Haley O. Tucker, Danyang Yu et al.
1 citations
Journal of Cellular Signaling
PI3K/AKT/mTOR signaling in cancer
0.81
article

PAX-Interacting Protein 1 (PTIP) Promotes Apoptosis

Kangsan Kim, Y. Jessie Zhang, Haley O. Tucker, Danyang Yu, Ching-Jung Huang, Chuan Li, Hyein
article en
1 citations

Abstract

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.

Journal of Cellular SignalingVol. 6(4)
New York University Shanghai (CN), Advanced Institute of Convergence Technology (KR), Ajou University (KR), The University of Texas at Austin (US)
Good health and well-being
Openalex Percentile: Top 20%
PI3K/AKT/mTOR signaling in cancer
0.81
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