Cell Signaling Technology

Caspase-1 (E2Z1C) Rabbit Monoclonal Antibody

#24232 · $161

100
Citing papers
3.1k
Combined citations
Supplier page Find this product

Research areas

Inflammasome and immune disorders34Neuroinflammation and Neurodegeneration Mechanisms11Immune Response and Inflammation7Cancer, Hypoxia, and Metabolism6interferon and immune responses6Heme Oxygenase-1 and Carbon Monoxide5Gout, Hyperuricemia, Uric Acid5Mitochondrial Function and Pathology5

Papers citing this product

1
Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming
Nature Communications·2020·258 cit.·DOI
2
6-Phosphofructo-2-kinase (PFKFB3) promotes cell cycle progression and suppresses apoptosis via Cdk1-mediated phosphorylation of p27
Cell Death and Disease·2014·204 cit.·DOI
3
Conservation and divergence of vulnerability and responses to stressors between human and mouse astrocytes
Nature Communications·2021·181 cit.·DOI
4
TGR5 Regulates Macrophage Inflammation in Nonalcoholic Steatohepatitis by Modulating NLRP3 Inflammasome Activation
Frontiers in Immunology·2021·164 cit.·DOI
5
Metabolic reprogramming of alloantigen-activated T cells after hematopoietic cell transplantation
Journal of Clinical Investigation·2016·124 cit.·DOI
6
Mitochondria-targeted drugs stimulate mitophagy and abrogate colon cancer cell proliferation
Journal of Biological Chemistry·2018·122 cit.·DOI
7
ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1
Nature Communications·2021·107 cit.·DOI
8
Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages
Nature Communications·2021·101 cit.·DOI
9
TRIM21 regulates pyroptotic cell death by promoting Gasdermin D oligomerization
Cell Death and Differentiation·2021·88 cit.·DOI
10
Oxymatrine attenuates oxidized low‑density lipoprotein‑induced HUVEC injury by inhibiting NLRP3 inflammasome‑mediated pyroptosis via the activation of the SIRT1/Nrf2 signaling pathway
International Journal of Molecular Medicine·2021·84 cit.·DOI

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