Cell Signaling Technology

PathScan® Phospho-Akt2 (Ser474) Sandwich ELISA Kit

#7932 · $661

100
Citing papers
4.5k
Combined citations
Supplier page Find this product

Research areas

Neuroscience and Neuropharmacology Research7Cancer-related molecular mechanisms research6Receptor Mechanisms and Signaling5Epigenetics and DNA Methylation5Cancer Cells and Metastasis5Neurofibromatosis and Schwannoma Cases5Neuroinflammation and Neurodegeneration Mechanisms5Cancer-related Molecular Pathways4

Papers citing this product

1
Tissue Distribution of 5-Hydroxymethylcytosine and Search for Active Demethylation Intermediates
PLoS ONE·2010·856 cit.·DOI
2
Activation of Raf/MEK/ERK/cPLA2 Signaling Pathway Is Essential for Chlamydial Acquisition of Host Glycerophospholipids
Journal of Biological Chemistry·2004·154 cit.·DOI
3
GTPase Activity and Neuronal Toxicity of Parkinson's Disease–Associated LRRK2 Is Regulated by ArfGAP1
PLoS Genetics·2012·138 cit.·DOI
4
Low-intensity pulsed ultrasound activates the phosphatidylinositol 3 kinase/Akt pathway and stimulates the growth of chondrocytes in three-dimensional cultures: a basic science study
Arthritis Research & Therapy·2008·134 cit.·DOI
5
Gut dysbiosis induces the development of mastitis through a reduction in host anti-inflammatory enzyme activity by endotoxemia
Microbiome·2022·134 cit.·DOI
6
Synapse Loss in Cortex of Agrin-Deficient Mice after Genetic Rescue of Perinatal Death
Journal of Neuroscience·2007·116 cit.·DOI
7
miR-655 Is an EMT-Suppressive MicroRNA Targeting ZEB1 and TGFBR2
PLoS ONE·2013·115 cit.·DOI
8
DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells
Molecular Cancer·2014·109 cit.·DOI
9
Yin Yang 1 Plays an Essential Role in Breast Cancer and Negatively Regulates p27
American Journal Of Pathology·2012·101 cit.·DOI
10
DNA damage-induced ephrin-B2 reverse signaling promotes chemoresistance and drives EMT in colorectal carcinoma harboring mutant p53
Cell Death and Differentiation·2015·99 cit.·DOI

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