ArticleProceedings of the National Academy of Sciences of the United States of America1997
Activation of hPAK65 by caspase cleavage induces some of the morphological and biochemical changes of apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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
54 citing papers in PubMed, 189 citations in OpenAlex.
- Regulation of Cancer Metastasis by PAK2.International journal of molecular sciences · 2024Review
- Dose-dependent effects of silver nanoparticles on cell death modes in mouse blastocysts induced via endoplasmic reticulum stress and mitochondrial apoptosis.Toxicology research · 2024Article
- Role of activated p21-activated kinase 2 in methylmercury-induced embryotoxic effects on mouse blastocysts.Toxicology research · 2023Article
- Role of caspase-3-cleaved/activated PAK2 in brusatol-triggered apoptosis of human lung cancer A549 cells.Toxicology research · 2022Article
- Group I p21-activated kinases in leukemia cell adhesion to fibronectin.Cell adhesion & migration · 2021Article
- Article
- Apoptotic Bodies: Mechanism of Formation, Isolation and Functional Relevance.Sub-cellular biochemistry · 2021Article
- ROCK1 but not LIMK1 or PAK2 is a key regulator of apoptotic membrane blebbing and cell disassembly.Cell death and differentiation · 2020Article
- PAK1, PAK1Δ15, and PAK2: similarities, differences and mutual interactions.Scientific reports · 2019Article
- Disassembly of dying cells in diverse organisms.Cellular and molecular life sciences : CMLS · 2019Review
- TRPC1 expression and function inhibit ER stress and cell death in salivary gland cells.FASEB bioAdvances · 2019Article
- Plasma membrane changes during programmed cell deaths.Cell research · 2018Review
- Evolution of caspase-mediated cell death and differentiation: twins separated at birth.Cell death and differentiation · 2017Review
- Dual Site Phosphorylation of Caspase-7 by PAK2 Blocks Apoptotic Activity by Two Distinct Mechanisms.Structure (London, England : 1993) · 2017Article
- The p21-activated kinase, PAK2, is important in the activation of numerous pancreatic acinar cell signaling cascades and in the onset of early pancreatitis events.Biochimica et biophysica acta · 2016Article
- A bead-based cleavage method for large-scale identification of protease substrates.Scientific reports · 2016Article
- Prostasin may contribute to chemoresistance, repress cancer cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.Cell death & disease · 2014Article
- Group I PAK inhibitor IPA-3 induces cell death and affects cell adhesivity to fibronectin in human hematopoietic cells.PloS one · 2014Article
- Distinct roles for Ste20-like kinase SLK in muscle function and regeneration.Skeletal muscle · 2013Article
- N-terminal cleavage of the mitochondrial fusion GTPase OPA1 occurs via a caspase-independent mechanism in cerebellar granule neurons exposed to oxidative or nitrosative stress.Brain research · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is a highly regulated form of cell death, characterized by distinctive features such as cellular shrinkage and nuclear condensation. We demonstrate here that proteolytic activation of hPAK65, a p21-activated kinase, induces morphological changes and elicits apoptosis. hPAK65 is cleaved both in vitro and in vivo by caspases at a single site between the N-terminal regulatory p21-binding domain and the C-terminal kinase domain. The C-terminal cleavage product becomes activated, with a kinetic profile that parallels caspase activation during apoptosis. This C-terminal hPAK65 fragment also activates the c-Jun N-terminal kinase pathway in vivo. Microinjection or transfection of this truncated hPAK65 causes striking alterations in cellular and nuclear morphology, which subsequently promotes apoptosis in both CHO and Hela cells. Conversely, apoptosis is delayed in cells expressing a dominant-negative form of hPAK65. These findings provide a direct evidence that the activated form of hPAK65 generated by caspase cleavage is a proapoptotic effector that mediates morphological and biochemical changes seen in apoptosis.
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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.