Cell Signaling Technology

EGF Receptor (D38B1) Rabbit Monoclonal Antibody (Alexa Fluor® 594 Conjugate)

#8742 · $471

100
Citing papers
5k
Combined citations
Supplier page Find this product

Research areas

Liver Disease Diagnosis and Treatment13FOXO transcription factor regulation9Cancer Cells and Metastasis8TGF-β signaling in diseases8Cancer Mechanisms and Therapy7Endoplasmic Reticulum Stress and Disease6Hepatitis C virus research5Cellular Mechanics and Interactions4

Papers citing this product

1
The hepatitis C virus core protein of genotypes 3a and 1b downregulates insulin receptor substrate 1 through genotype‐specific mechanisms†
Hepatology·2007·226 cit.·DOI
2
Dual <scp>PPAR</scp>α/γ agonist saroglitazar improves liver histopathology and biochemistry in experimental <scp>NASH</scp> models
Liver International·2017·201 cit.·DOI
3
Phosphoinositide-3 Kinase-Akt Pathway Controls Cellular Entry of Ebola Virus
PLoS Pathogens·2008·197 cit.·DOI
4
Essential Role of TRPC6 Channels in G2/M Phase Transition and Development of Human Glioma
JNCI Journal of the National Cancer Institute·2010·174 cit.·DOI
5
Genome-Wide Expression Analysis of Middle Eastern Colorectal Cancer Reveals FOXM1 as a Novel Target for Cancer Therapy
American Journal Of Pathology·2011·155 cit.·DOI
6
High Expression of H3K27me3 in Human Hepatocellular Carcinomas Correlates Closely with Vascular Invasion and Predicts Worse Prognosis in Patients
Molecular Medicine·2010·140 cit.·DOI
7
Serglycin in tumor microenvironment promotes non-small cell lung cancer aggressiveness in a CD44-dependent manner
Oncogene·2016·130 cit.·DOI
8
CDK5 is essential for TGF-β1-induced epithelial-mesenchymal transition and breast cancer progression
Scientific Reports·2013·123 cit.·DOI
9
Dietary Polyphenols Protect Against Oleic Acid-Induced Steatosis in an in Vitro Model of NAFLD by Modulating Lipid Metabolism and Improving Mitochondrial Function
Nutrients·2019·122 cit.·DOI
10
Wnt‐induced deubiquitination FoxM1 ensures nucleus β‐catenin transactivation
The EMBO Journal·2016·113 cit.·DOI

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