Cell Signaling Technology

Drosophila ICE (drICE) Antibody

#13085 · $317

69
Citing papers
2.2k
Combined citations
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Research areas

Telomeres, Telomerase, and Senescence13PI3K/AKT/mTOR signaling in cancer5RNA Research and Splicing4Muscle Physiology and Disorders4RNA and protein synthesis mechanisms4Autophagy in Disease and Therapy4DNA Repair Mechanisms4Genomics, phytochemicals, and oxidative stress4

Papers citing this product

1
Inhibition of PI3K/AKT and MAPK/ERK pathways causes activation of FOXO transcription factor, leading to cell cycle arrest and apoptosis in pancreatic cancer
Journal of Molecular Signaling·2010·374 cit.·DOI
2
Distinct functional significance of Akt and mTOR constitutive activation in mantle cell lymphoma
Blood·2008·147 cit.·DOI
3
Cardiac-Specific IGF-1 Expression Attenuates Dilated Cardiomyopathy in Tropomodulin-Overexpressing Transgenic Mice
Circulation Research·2002·147 cit.·DOI
4
Recruitment of the RNA Helicase RHAU to Stress Granules via a Unique RNA-binding Domain
Journal of Biological Chemistry·2008·115 cit.·DOI
5
Telomerase Mediates the Cell Survival-Promoting Actions of Brain-Derived Neurotrophic Factor and Secreted Amyloid Precursor Protein in Developing Hippocampal Neurons
Journal of Neuroscience·2002·104 cit.·DOI
6
Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling
Cell·2024·97 cit.·DOI
7
ATR-dependent phosphorylation of FANCA on serine 1449 after DNA damage is important for FA pathway function
Blood·2008·88 cit.·DOI
8
Prostaglandin E2 receptor <scp>EP</scp>4 as the common target on cancer cells and macrophages to abolish angiogenesis, lymphangiogenesis, metastasis, and stem‐like cell functions
Cancer Science·2014·86 cit.·DOI
9
Chronic Jet Lag Simulation Decreases Hippocampal Neurogenesis and Enhances Depressive Behaviors and Cognitive Deficits in Adult Male Rats
Frontiers in Behavioral Neuroscience·2020·68 cit.·DOI
10
CDK1 dependent phosphorylation of hTERT contributes to cancer progression
Nature Communications·2020·63 cit.·DOI