Cell Signaling Technology

Lamin A/C (4C11) Mouse Monoclonal Antibody

#4777 · $148

100
Citing papers
16.7k
Combined citations
Supplier page Find this product

Research areas

Cancer, Hypoxia, and Metabolism16Autophagy in Disease and Therapy13Endoplasmic Reticulum Stress and Disease7Metabolism, Diabetes, and Cancer6Immune cells in cancer6Cancer-related molecular mechanisms research5Adipose Tissue and Metabolism5Genomics, phytochemicals, and oxidative stress5

Papers citing this product

1
Molecular and pharmacological modulators of the tumor immune contexture revealed by deconvolution of RNA-seq data
Genome Medicine·2019·1.7k cit.·DOI
2
Targeting photodynamic and photothermal therapy to the endoplasmic reticulum enhances immunogenic cancer cell death
Nature Communications·2019·1.1k cit.·DOI
3
Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques
Nature Neuroscience·2022·606 cit.·DOI
4
MCOLN1 is a ROS sensor in lysosomes that regulates autophagy
Nature Communications·2016·549 cit.·DOI
5
4-Octyl itaconate inhibits aerobic glycolysis by targeting GAPDH to exert anti-inflammatory effects
Nature Communications·2019·435 cit.·DOI
6
Cancer Mutations of the Tumor Suppressor SPOP Disrupt the Formation of Active, Phase-Separated Compartments
Molecular Cell·2018·411 cit.·DOI
7
Neutralization of Transthyretin Reverses the Neuroprotective Effects of Secreted Amyloid Precursor Protein (APP) in APP<sub>Sw</sub>Mice Resulting in Tau Phosphorylation and Loss of Hippocampal Neurons: Support for the Amyloid Hypothesis
Journal of Neuroscience·2004·278 cit.·DOI
8
A functional interaction between Hippo-YAP signalling and FoxO1 mediates the oxidative stress response
Nature Communications·2014·274 cit.·DOI
9
GATA3-Driven Th2 Responses Inhibit TGF-β1–Induced FOXP3 Expression and the Formation of Regulatory T Cells
PLoS Biology·2007·267 cit.·DOI
10
Quercetin Suppresses Cyclooxygenase-2 Expression and Angiogenesis through Inactivation of P300 Signaling
PLoS ONE·2011·263 cit.·DOI

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