Cell Signaling Technology

Cyclin B1 (V152) Mouse Monoclonal Antibody (Alexa Fluor® 488 Conjugate)

#4112 · $465

65
Evidence Score · Well-Established
Used by 478 independent labs across 509 papers. How we score this →
100
Citing papers
10.6k
Combined citations
Supplier page Find this product

Research areas

Ubiquitin and proteasome pathways10Neurogenesis and neuroplasticity mechanisms9Glycosylation and Glycoproteins Research7Adipose Tissue and Metabolism7NF-κB Signaling Pathways7Cancer Cells and Metastasis6Telomeres, Telomerase, and Senescence6Proteoglycans and glycosaminoglycans research6

Papers citing this product

1
Macronuclear Genome Sequence of the Ciliate Tetrahymena thermophila, a Model Eukaryote
PLoS Biology·2006·798 cit.·DOI
2
MiR-26b, Upregulated in Alzheimer's Disease, Activates Cell Cycle Entry, Tau-Phosphorylation, and Apoptosis in Postmitotic Neurons
Journal of Neuroscience·2013·291 cit.·DOI
3
Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin
Aging·2012·280 cit.·DOI
4
The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway
Aging·2010·274 cit.·DOI
5
Characterization of a novel cell line established from a patient with Herceptin-resistant breast cancer
Molecular Cancer Therapeutics·2004·269 cit.·DOI
6
Oxidative stress disrupts oligodendrocyte maturation
Journal of Neuroscience Research·2009·239 cit.·DOI
7
Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts
Nature Communications·2014·209 cit.·DOI
8
The db/db Mouse: A Useful Model for the Study of Diabetic Retinal Neurodegeneration
PLoS ONE·2014·203 cit.·DOI
9
3,3′-Diindolylmethane (DIM) induces a G1 cell cycle arrest in human breast cancer cells that is accompanied by Sp1-mediated activation of p21WAF1/CIP1 expression
Carcinogenesis·2002·187 cit.·DOI
10
The ubiquitin E3 ligase TRAF6 exacerbates pathological cardiac hypertrophy via TAK1-dependent signalling
Nature Communications·2016·182 cit.·DOI

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