Cell Signaling Technology

Phospho-Rb (Ser780) (D59B7) Rabbit Monoclonal Antibody

#8180 · western blot · $169,415

66
Evidence Score · Well-Established
Used by 313 independent labs across 334 papers. How we score this →
100
Citing papers
6.6k
Combined citations
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Research areas

Advanced Breast Cancer Therapies11Cancer, Lipids, and Metabolism11Cancer-related Molecular Pathways11MicroRNA in disease regulation9Cancer, Hypoxia, and Metabolism8Cancer-related molecular mechanisms research8Immune Cell Function and Interaction7Circular RNAs in diseases6

Papers citing this product

1
Toll‐like receptors control autophagy
The EMBO Journal·2008·727 cit.·DOI
2
<i>De novo</i> Lipogenesis Protects Cancer Cells from Free Radicals and Chemotherapeutics by Promoting Membrane Lipid Saturation
Cancer Research·2010·714 cit.·DOI
3
Acquired CDK6 amplification promotes breast cancer resistance to CDK4/6 inhibitors and loss of ER signaling and dependence
Oncogene·2016·430 cit.·DOI
4
Glutaredoxin Exerts an Antiapoptotic Effect by Regulating the Redox State of Akt
Journal of Biological Chemistry·2003·314 cit.·DOI
5
MARCO, TLR2, and CD14 Are Required for Macrophage Cytokine Responses to Mycobacterial Trehalose Dimycolate and Mycobacterium tuberculosis
PLoS Pathogens·2009·307 cit.·DOI
6
Inhibition of StearoylCoA Desaturase Activity Blocks Cell Cycle Progression and Induces Programmed Cell Death in Lung Cancer Cells
PLoS ONE·2010·191 cit.·DOI
7
Naive and memory human B cells have distinct requirements for STAT3 activation to differentiate into antibody-secreting plasma cells
The Journal of Experimental Medicine·2013·184 cit.·DOI
8
Bacterial persistence increases as environmental fitness decreases
Microbial Biotechnology·2012·174 cit.·DOI
9
PD-0332991, a CDK4/6 Inhibitor, Significantly Prolongs Survival in a Genetically Engineered Mouse Model of Brainstem Glioma
PLoS ONE·2013·163 cit.·DOI
10
Inhibition of Acetyl-CoA Carboxylase 1 (ACC1) and 2 (ACC2) Reduces Proliferation and De Novo Lipogenesis of EGFRvIII Human Glioblastoma Cells
PLoS ONE·2017·112 cit.·DOI

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