ArticleMolecular and cellular biology2012
Prostate apoptosis response 4 (Par-4), a novel substrate of caspase-3 during apoptosis activation.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 71 citations in OpenAlex.
- Integrative Analysis Identifies PANoptosis-Associated Molecular Patterns and Immune Alterations in Rat Cerebral Ischemic-Reperfusion Injury.Cellular and molecular neurobiology · 2026Article
- Identification of a novel caspase cleavage motif AEAD.Virologica Sinica · 2024Article
- The Tumor Suppressor Par-4 Regulates Adipogenesis by Transcriptional Repression of PPARγ.Cells · 2024Article
- Evidence of direct interaction between cisplatin and the caspase-cleaved prostate apoptosis response-4 tumor suppressor.Protein science : a publication of the Protein Society · 2024Article
- Interaction between host cell proteins and open reading frames of porcine circovirus type 2.Journal of animal science and technology · 2023Review
- Enhancing the Conformational Stability of the cl-Par-4 Tumor Suppressor via Site-Directed Mutagenesis.Biomolecules · 2023Article
- The roles of ERIANIN in tumor and innate immunity and its' perspectives in immunotherapy.Frontiers in immunology · 2023Review
- Long non-coding RNA signatures and related signaling pathway in T-cell acute lymphoblastic leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Inhibition of Cytosolic Phospholipase A2α Induces Apoptosis in Multiple Myeloma Cells.Molecules (Basel, Switzerland) · 2021Article
- Structural Analysis of the cl-Par-4 Tumor Suppressor as a Function of Ionic Environment.Biomolecules · 2021Article
- Prostate apoptosis response-4 and tumor suppression: it's not just about apoptosis anymore.Cell death & disease · 2021Review
- Indolylkojyl methane analogue IKM5 potentially inhibits invasion of breast cancer cells via attenuation of GRP78.Breast cancer research and treatment · 2019Article
- PAR-4 overcomes chemo-resistance in breast cancer cells by antagonizing cIAP1.Scientific reports · 2019Article
- pH-Induced Folding of the Caspase-Cleaved Par-4 Tumor Suppressor: Evidence of Structure Outside of the Coiled Coil Domain.Biomolecules · 2018Article
- Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.The Journal of clinical investigation · 2018Article
- Inhibition of CRM1 activity sensitizes endometrial and ovarian cell lines to TRAIL-induced cell death.Cell communication and signaling : CCS · 2018Article
- A Naturally Generated Decoy of the Prostate Apoptosis Response-4 Protein Overcomes Therapy Resistance in Tumors.Cancer research · 2017Article
- TRIM21 is a novel regulator of Par-4 in colon and pancreatic cancer cells.Cancer biology & therapy · 2017Article
- Autophagy decreases alveolar macrophage apoptosis by attenuating endoplasmic reticulum stress and oxidative stress.Oncotarget · 2016Article
- A journey beyond apoptosis: new enigma of controlling metastasis by pro-apoptotic Par-4.Clinical & experimental metastasis · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prostate apoptosis response 4 (Par-4) is a ubiquitously expressed proapoptotic tumor suppressor protein. Here, we show for the first time, that Par-4 is a novel substrate of caspase-3 during apoptosis. We found that Par-4 is cleaved during cisplatin-induced apoptosis in human normal and cancer cell lines. Par-4 cleavage generates a C-terminal fragment of ~25 kDa, and the cleavage of Par-4 is completely inhibited by a caspase-3 inhibitor, suggesting that caspase-3 is directly involved in the cleavage of Par-4. Caspase-3-deficient MCF-7 cells do not show Par-4 cleavage in response to cisplatin treatment, and restoration of caspase-3 in MCF-7 cells produces a decrease in Par-4 levels, with the appearance of a cleaved fragment. Additionally, knockdown of Par-4 reduces caspase-3 activation and apoptosis induction. Site-directed mutagenesis reveals that Par-4 cleavage by caspase-3 occurs at an unconventional site, EEPD(131)↓G. Interestingly, overexpression of wild-type Par-4 but not the Par-4 D131A mutant sensitizes cells to cisplatin-induced apoptosis. Upon caspase-3 cleavage, the cleaved fragment of Par-4 accumulates in the nucleus and displays increased apoptotic activity. Overexpression of the cleaved fragment of Par-4 inhibits IκBα phosphorylation and blocks NF-κB nuclear translocation. We have identified a novel specific caspase-3 cleavage site in Par-4, and the cleaved fragment of Par-4 retains proapoptotic activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.