ArticleCell death and differentiation2012
cIAP1 and cIAP2 limit macrophage necroptosis by inhibiting Rip1 and Rip3 activation.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
92 citing papers in PubMed, 144 citations in OpenAlex.
- TheInternational journal of molecular sciences · 2021Trial
- HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH.bioRxiv : the preprint server for biology · 2026Article
- Review
- A RANKLBone research · 2026Article
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction.Nature cardiovascular research · 2026Article
- IL-1β Controls Proliferation, Apoptosis, and Necroptosis Through the PI3K/AKT/Src/NF-κB Pathway in Leukaemic Lymphoblasts.Biomedicines · 2025Article
- SPOP mediates apoptosis and protects against necroptosis by regulating ubiquitination of RIPK1 and RIPK3.JCI insight · 2025Article
- Genes Associated with Apoptosis in an Experimental Breast Cancer Model.International journal of molecular sciences · 2025Article
- Molecular mechanisms of immune cell death in immunosenescence.Cell death and differentiation · 2025Review
- Exploring necroptosis: mechanistic analysis and antitumor potential of nanomaterials.Cell death discovery · 2025Review
- Necroptosis-based glioblastoma prognostic subtypes: implications for TME remodeling and therapy response.Annals of medicine · 2024Article
- The study of the mechanism of non-coding RNA regulation of programmed cell death in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024Review
- Die Hard: Necroptosis and its Impact on Age-Dependent Neuroinflammatory Diseases.Frontiers in cell death · 2024Article
- The dance of macrophage death: the interplay between the inevitable and the microenvironment.Frontiers in immunology · 2024Review
- Bioinformatics analysis of necroptosis‑related lncRNAs and immune infiltration, and prediction of the prognosis of patients with esophageal carcinoma.Experimental and therapeutic medicine · 2023Article
- Article
- The Many Faces of MLKL, the Executor of Necroptosis.International journal of molecular sciences · 2023Review
- A biochemical necroptosis model explains cell-type-specific responses to cell death cues.Biophysical journal · 2023Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular inhibitor of apoptosis proteins (cIAPs) have emerged as important anti-cell death mediators, particularly in cancer. Although they are known to be expressed in immune tissue, their specific immune function remains unclear. We observed that degradation of cIAPs with SMAC mimetic (SM) results in death of primary bone-marrow-derived macrophages. SM-induced death of macrophages occurred by programmed necrosis (necroptosis), which was dependent on TNF receptor expression. Consistent with necroptosis, SM-induced death of macrophages was abrogated by inhibition of receptor interacting protein 1 (Rip1) kinase signaling or by receptor interacting protein 3 (Rip3) knockdown. SM-induced necroptosis was also dependent on inhibition of SM-induced apoptosis due to the expression of the endogenous caspase inhibitor, xIAP. We found that cIAPs limit Rip3, and to a lesser extent Rip1, expression via post-transcriptional mechanisms, leading to inhibition of the Rip1-Rip3 death complex (necrosome). Reduced cIAP activity in vivo, via SM treatment or specific knockout of either cIAP, resulted in elevated macrophage cell death and compromised control of an intracellular bacterium, Listeria monocytogenes. These results show that cIAPs have an important role in limiting programmed necrosis of macrophages, which facilitates effective control of a pathogen.
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What OpenQuestion holds
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.