Cell Signaling Technology

SignalSilence® GSK-3 alpha/beta siRNA

#6301 · $381

100
Citing papers
6.5k
Combined citations
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Research areas

Neuroinflammation and Neurodegeneration Mechanisms11Neurogenesis and neuroplasticity mechanisms5Autophagy in Disease and Therapy5Curcumin's Biomedical Applications5Immune Response and Inflammation5MicroRNA in disease regulation5Cell death mechanisms and regulation5interferon and immune responses5

Papers citing this product

1
Trimethylamine N-oxide in atherogenesis: impairing endothelial self-repair capacity and enhancing monocyte adhesion
Bioscience Reports·2017·263 cit.·DOI
2
Antiangiogenic treatment with Sunitinib ameliorates inflammatory infiltrate, fibrosis, and portal pressure in cirrhotic rats
Hepatology·2007·261 cit.·DOI
3
Early glycolytic reprogramming controls microglial inflammatory activation
Journal of Neuroinflammation·2021·254 cit.·DOI
4
Tumor suppressor activity of the ERK/MAPK pathway by promoting selective protein degradation
Genes & Development·2013·190 cit.·DOI
5
Interleukin-1β Decreases Expression of the Epithelial Sodium Channel α-Subunit in Alveolar Epithelial Cells via a p38 MAPK-dependent Signaling Pathway
Journal of Biological Chemistry·2005·168 cit.·DOI
6
Peroxiredoxin 2 activates microglia by interacting with Toll-like receptor 4 after subarachnoid hemorrhage
Journal of Neuroinflammation·2018·155 cit.·DOI
7
Transforming Growth Factor-β1 Decreases Expression of the Epithelial Sodium Channel αENaC and Alveolar Epithelial Vectorial Sodium and Fluid Transport via an ERK1/2-dependent Mechanism
Journal of Biological Chemistry·2003·150 cit.·DOI
8
Tangeretin Alleviates Cisplatin-Induced Acute Hepatic Injury in Rats: Targeting MAPKs and Apoptosis
PLoS ONE·2016·132 cit.·DOI
9
Rescue of platinum-damaged oocytes from programmed cell death through inactivation of the p53 family signaling network
Cell Death and Differentiation·2013·129 cit.·DOI
10
FOXM1 is a critical driver of lung fibroblast activation and fibrogenesis
Journal of Clinical Investigation·2018·128 cit.·DOI