Cell Signaling Technology

ERCC1 Antibody

#3885 · western blot · $317

64
Evidence Score · Well-Established
Used by 298 independent labs across 318 papers. How we score this →
100
Citing papers
14.5k
Combined citations
Supplier page Find this product

Research areas

Epigenetics and DNA Methylation9Acute Myeloid Leukemia Research9MicroRNA in disease regulation7Chronic Myeloid Leukemia Treatments7SARS-CoV-2 and COVID-19 Research6Parkinson's Disease Mechanisms and Treatments6Autophagy in Disease and Therapy5Histone Deacetylase Inhibitors Research5

Papers citing this product

1
Loss of furin cleavage site attenuates SARS-CoV-2 pathogenesis
Nature·2021·781 cit.·DOI
2
AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)
Blood·2009·641 cit.·DOI
3
Severe Acute Respiratory Syndrome Coronavirus 2 from Patient with Coronavirus Disease, United States
Emerging infectious diseases·2020·628 cit.·DOI
4
Exosome engineering for efficient intracellular delivery of soluble proteins using optically reversible protein–protein interaction module
Nature Communications·2016·574 cit.·DOI
5
Hepatic triglyceride accumulation via endoplasmic reticulum stress-induced SREBP-1 activation is regulated by ceramide synthases
Experimental & Molecular Medicine·2019·474 cit.·DOI
6
Expression profile of class I histone deacetylases in human cancer tissues
Oncology Reports·2007·341 cit.·DOI
7
Mutant FLT3: A Direct Target of Sorafenib in Acute Myelogenous Leukemia
JNCI Journal of the National Cancer Institute·2008·338 cit.·DOI
8
Human αA- and αB-crystallins bind to Bax and Bcl-XS to sequester their translocation during staurosporine-induced apoptosis
Cell Death and Differentiation·2004·332 cit.·DOI
9
Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML
Blood·2008·305 cit.·DOI
10
Resveratrol Inhibits Breast Cancer Stem-Like Cells and Induces Autophagy via Suppressing Wnt/β-Catenin Signaling Pathway
PLoS ONE·2014·286 cit.·DOI

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