Cell Signaling Technology

Phospho-MYPT1 (Thr853) Antibody

#4563 · $150

100
Citing papers
10.3k
Combined citations
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Research areas

Neuroscience and Neuropharmacology Research12Retinal Development and Disorders11Cell death mechanisms and regulation9Neuroinflammation and Neurodegeneration Mechanisms8PI3K/AKT/mTOR signaling in cancer6Melanoma and MAPK Pathways5Receptor Mechanisms and Signaling5Adipose Tissue and Metabolism4

Papers citing this product

1
Glioma cancer stem cells induce immunosuppressive macrophages/microglia
Neuro-Oncology·2010·708 cit.·DOI
2
IL-18 Production Downstream of the Nlrp3 Inflammasome Confers Protection against Colorectal Tumor Formation
The Journal of Immunology·2010·414 cit.·DOI
3
Activation of Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase in Hippocampal Circuitry Is Required for Consolidation and Reconsolidation of Recognition Memory
Journal of Neuroscience·2003·361 cit.·DOI
4
A Wnt-producing niche drives proliferative potential and progression in lung adenocarcinoma
Nature·2017·348 cit.·DOI
5
PLX4032, a selective BRAF <sup>V600E</sup> kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF <sup>WT</sup> melanoma cells
Pigment Cell & Melanoma Research·2010·322 cit.·DOI
6
The Scaffold Protein Homer1b/c Links Metabotropic Glutamate Receptor 5 to Extracellular Signal-Regulated Protein Kinase Cascades in Neurons
Journal of Neuroscience·2005·243 cit.·DOI
7
The Nuclear Kinase Mitogen- and Stress-Activated Protein Kinase 1 Regulates Hippocampal Chromatin Remodeling in Memory Formation
Journal of Neuroscience·2007·234 cit.·DOI
8
The Epithelial-Mesenchymal Transition (EMT) Regulatory Factor SLUG (SNAI2) Is a Downstream Target of SPARC and AKT in Promoting Melanoma Cell Invasion
PLoS ONE·2012·223 cit.·DOI
9
β-Amyloid Peptide at Sublethal Concentrations Downregulates Brain-Derived Neurotrophic Factor Functions in Cultured Cortical Neurons
Journal of Neuroscience·2004·220 cit.·DOI
10
Phosphatidylinositol 3-Kinase Regulates the Induction of Long-Term Potentiation through Extracellular Signal-Related Kinase-Independent Mechanisms
Journal of Neuroscience·2003·214 cit.·DOI