ArticleCell death and differentiation2013
Genetic disruption of Abl nuclear import reduces renal apoptosis in a mouse model of cisplatin-induced nephrotoxicity.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential.Frontiers in pharmacology · 2023Review
- c-Abl kinase regulates neutrophil extracellular trap formation and lung injury in abdominal sepsis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Lansoprazole promotes cisplatin-induced acute kidney injury via enhancing tubular necroptosis.Journal of cellular and molecular medicine · 2021Article
- Exogenous spermidine ameliorates tubular necrosis during cisplatin nephrotoxicity.Anatomy & cell biology · 2018Article
- Extracellular vesicles transfer nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander effects.Molecular biology of the cell · 2018Article
- Dexmedetomidine protects against cisplatin-induced acute kidney injury in mice through regulating apoptosis and inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Beneficial Effects ofJournal of the American Society of Nephrology : JASN · 2017Article
- DNA damage response in nephrotoxic and ischemic kidney injury.Toxicology and applied pharmacology · 2016Review
- Amelioration of cisplatin-induced acute kidney injury by recombinant neutrophil gelatinase-associated lipocalin.Renal failure · 2016Article
- Autophagy in acute kidney injury.Kidney international · 2016Review
- DNA damage response in cisplatin-induced nephrotoxicity.Archives of toxicology · 2015Review
- A Role for Tubular Necroptosis in Cisplatin-Induced AKI.Journal of the American Society of Nephrology : JASN · 2015Article
- The kinase ABL phosphorylates the microprocessor subunit DGCR8 to stimulate primary microRNA processing in response to DNA damage.Science signaling · 2015Article
- Detection of dietary plant-based small RNAs in animals.Cell research · 2015Article
- The capable ABL: what is its biological function?Molecular and cellular biology · 2014Review
- Pathophysiology of cisplatin-induced acute kidney injury.BioMed research international · 2014Review
- Article
- EnABLing microprocessor for apoptosis.Molecular & cellular oncologyArticle
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3 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage activates nuclear Abl tyrosine kinase to stimulate intrinsic apoptosis in cancer cell lines and mouse embryonic stem cells. To examine the in vivo function of nuclear Abl in apoptosis, we generated Abl-μNLS (μ, mutated in nuclear localization signals) mice. We show here that cisplatin-induced apoptosis is defective in the renal proximal tubule cells (RPTC) from the Abl(μ/μ) mice. When injected with cisplatin, we found similar levels of platinum in the Abl(+/+) and the Abl(μ/μ) kidneys, as well as similar initial inductions of p53 and PUMAα expression. However, the accumulation of p53 and PUMAα could not be sustained in the Abl(μ/μ) kidneys, leading to reductions in renal apoptosis and tubule damage. Co-treatment of cisplatin with the Abl kinase inhibitor, imatinib, reduced the accumulation of p53 and PUMAα in the Abl(+/+) but not in the Abl(μ/μ) kidneys. The residual apoptosis in the Abl(μ/μ) mice was not further reduced in the Abl(μ/μ); p53(-/-) double-mutant mice, suggesting that nuclear Abl and p53 are epistatic to each other in this apoptosis response. Although apoptosis and tubule damage were reduced, cisplatin-induced increases in phospho-Stat-1 and blood urea nitrogen were similar between the Abl(+/+) and the Abl(μ/μ) kidneys, indicating that RPTC apoptosis is not the only factor in cisplatin-induced nephrotoxicity. These results provide in vivo evidence for the pro-apoptotic function of Abl, and show that its nuclear localization and tyrosine kinase activity are both required for the sustained expression of p53 and PUMAα in cisplatin-induced renal apoptosis.
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