Cell Signaling Technology

p47phox Antibody

#4312 · $317

100
Citing papers
12.6k
Combined citations
Supplier page Find this product

Research areas

Cell death mechanisms and regulation11Inflammasome and immune disorders9Adipose Tissue and Metabolism7Peroxisome Proliferator-Activated Receptors7PI3K/AKT/mTOR signaling in cancer6Immune cells in cancer6Immunotherapy and Immune Responses6Cancer-related Molecular Pathways5

Papers citing this product

1
<scp>GSDMD</scp> membrane pore formation constitutes the mechanism of pyroptotic cell death
The EMBO Journal·2016·1.1k cit.·DOI
2
Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke
Cell Death and Disease·2013·490 cit.·DOI
3
Phosphatidylinositol 3-Kinase Activates ERK in Primary Sensory Neurons and Mediates Inflammatory Heat Hyperalgesia through TRPV1 Sensitization
Journal of Neuroscience·2004·415 cit.·DOI
4
Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis
Nature Communications·2017·342 cit.·DOI
5
Blood-brain-barrier spheroids as an in vitro screening platform for brain-penetrating agents
Nature Communications·2017·332 cit.·DOI
6
Increased Malonyl-CoA Levels in Muscle From Obese and Type 2 Diabetic Subjects Lead to Decreased Fatty Acid Oxidation and Increased Lipogenesis; Thiazolidinedione Treatment Reverses These Defects
Diabetes·2006·281 cit.·DOI
7
Hypoxia and defective apoptosis drive genomic instability and tumorigenesis
Genes & Development·2004·277 cit.·DOI
8
Quercetin prevents hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing autophagy via the TGF-β1/Smads and PI3K/Akt pathways
Scientific Reports·2017·267 cit.·DOI
9
Quercetin and Allopurinol Ameliorate Kidney Injury in STZ-Treated Rats with Regulation of Renal NLRP3 Inflammasome Activation and Lipid Accumulation
PLoS ONE·2012·231 cit.·DOI
10
Dendritic Cell (DC)-Specific Targeting Reveals Stat3 as a Negative Regulator of DC Function
The Journal of Immunology·2010·220 cit.·DOI

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