Cell Signaling Technology

Phospho-NMDA Receptor 1 (GluN1) (Ser890) Antibody

#3381 · $362

100
Citing papers
14.7k
Combined citations
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Research areas

Genomics, phytochemicals, and oxidative stress9Cancer-related Molecular Pathways7PI3K/AKT/mTOR signaling in cancer6Endoplasmic Reticulum Stress and Disease6Immune Cell Function and Interaction5Autophagy in Disease and Therapy5Cell death mechanisms and regulation5Extracellular vesicles in disease5

Papers citing this product

1
Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis
Journal of Clinical Investigation·2006·1k cit.·DOI
2
Gain-of-function human <i>STAT1</i> mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis
The Journal of Experimental Medicine·2011·797 cit.·DOI
3
Plasma cells from multiple myeloma patients express B7-H1 (PD-L1) and increase expression after stimulation with IFN-γ and TLR ligands via a MyD88-, TRAF6-, and MEK-dependent pathway
Blood·2007·575 cit.·DOI
4
Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration
Journal of Clinical Investigation·2013·532 cit.·DOI
5
Site-specific Lys-63-linked Tumor Necrosis Factor Receptor-associated Factor 6 Auto-ubiquitination Is a Critical Determinant of IκB Kinase Activation
Journal of Biological Chemistry·2006·370 cit.·DOI
6
PTEN Loss Increases PD-L1 Protein Expression and Affects the Correlation between PD-L1 Expression and Clinical Parameters in Colorectal Cancer
PLoS ONE·2013·269 cit.·DOI
7
The Cytoplasmic Deacetylase HDAC6 Is Required for Efficient Oncogenic Tumorigenesis
Cancer Research·2008·259 cit.·DOI
8
Effective delivery of large genes to the retina by dual AAV vectors
EMBO Molecular Medicine·2013·258 cit.·DOI
9
Cancer-associated fibroblast phenotypes are associated with patient outcome in non-small cell lung cancer
Cancer Cell·2024·246 cit.·DOI
10
Impaired Autolysosome Formation Correlates With Lamp-2 Depletion: Role of Apoptosis, Autophagy, and Necrosis in Pancreatitis
Gastroenterology·2009·241 cit.·DOI