Cell Signaling Technology

SignalSilence® c-Myc siRNA I

#6341 · $381

100
Citing papers
7.5k
Combined citations
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Research areas

Cardiac Fibrosis and Remodeling11Protein Kinase Regulation and GTPase Signaling7GDF15 and Related Biomarkers7Alzheimer's disease research and treatments6Cancer Immunotherapy and Biomarkers5Growth Hormone and Insulin-like Growth Factors5Neuroinflammation and Neurodegeneration Mechanisms5Cancer-related Molecular Pathways4

Papers citing this product

1
Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy
Journal of Clinical Investigation·2007·303 cit.·DOI
2
Naturally occurring mitochondrial-derived peptides are age-dependent regulators of apoptosis, insulin sensitivity, and inflammatory markers
Aging·2016·283 cit.·DOI
3
An FHL1-containing complex within the cardiomyocyte sarcomere mediates hypertrophic biomechanical stress responses in mice
Journal of Clinical Investigation·2008·250 cit.·DOI
4
Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy
Journal of Clinical Investigation·2003·235 cit.·DOI
5
MEK-ERK pathway modulation ameliorates disease phenotypes in a mouse model of Noonan syndrome associated with the Raf1L613V mutation
Journal of Clinical Investigation·2011·232 cit.·DOI
6
IFN-γ Promotes Complement Expression and Attenuates Amyloid Plaque Deposition in Amyloid β Precursor Protein Transgenic Mice
The Journal of Immunology·2010·227 cit.·DOI
7
HDAC inhibitors elicit metabolic reprogramming by targeting super-enhancers in glioblastoma models
Journal of Clinical Investigation·2020·204 cit.·DOI
8
Receptor Tyrosine Kinase EphB4 Is a Survival Factor in Breast Cancer
American Journal Of Pathology·2006·190 cit.·DOI
9
Expression of PD-L1 and presence of CD8-positive T cells in pre-treatment specimens of locally advanced cervical cancer
Modern Pathology·2017·188 cit.·DOI
10
Cardiac-specific disruption of the c-raf-1 gene induces cardiac dysfunction and apoptosis
Journal of Clinical Investigation·2004·186 cit.·DOI