ArticleCommunications biology2022
Generation of transgenic mice expressing a FRET biosensor, SMART, that responds to necroptosis.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Non-necroptotic MLKL function damages mitochondria and promotes hematopoietic stem cell aging.Nature communications · 2026Article
- Visualization of RIM-BP2's crane-like function in neuronal vesicle transport using FRET.Communications biology · 2025Article
- Mapping where and when necroptotic cell death occurs in disease.Cell death and differentiation · 2024Article
- Necroptosis and Its Involvement in Various Diseases.Advances in experimental medicine and biology · 2024Article
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Authors and funding
13 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is a regulated form of cell death involved in various pathological conditions, including ischemic reperfusion injuries, virus infections, and drug-induced tissue injuries. However, it is not fully understood when and where necroptosis occurs in vivo. We previously generated a Forster resonance energy transfer (FRET) biosensor, termed SMART (the sensor for MLKL activation by RIPK3 based on FRET), which monitors conformational changes of MLKL along with progression of necroptosis in human and murine cell lines in vitro. Here, we generate transgenic (Tg) mice that express the SMART biosensor in various tissues. The FRET ratio is increased in necroptosis, but not apoptosis or pyroptosis, in primary cells. Moreover, the FRET signals are elevated in renal tubular cells of cisplatin-treated SMART Tg mice compared to untreated SMART Tg mice. Together, SMART Tg mice may provide a valuable tool for monitoring necroptosis in different types of cells in vitro and in vivo.
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