Cell Signaling Technology

CD27 (E6S8H) Rabbit Monoclonal Antibody

#28034 · $161

43
Citing papers
1.4k
Combined citations
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Research areas

Nerve injury and regeneration16Neurogenesis and neuroplasticity mechanisms7Axon Guidance and Neuronal Signaling7PI3K/AKT/mTOR signaling in cancer6Autophagy in Disease and Therapy6RNA Interference and Gene Delivery4Natural Compound Pharmacology Studies4Biological Activity of Diterpenoids and Biflavonoids3

Papers citing this product

1
PI3K–GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1
Nature Communications·2013·188 cit.·DOI
2
Neuroprotective effect of brain-derived neurotrophic factor mediated by autophagy through the PI3K/Akt/mTOR pathway
Molecular Medicine Reports·2013·173 cit.·DOI
3
Tissue-Type Plasminogen Activator Regulates the Neuronal Uptake of Glucose in the Ischemic Brain
Journal of Neuroscience·2012·91 cit.·DOI
4
Metformin Promotes Axon Regeneration after Spinal Cord Injury through Inhibiting Oxidative Stress and Stabilizing Microtubule
Oxidative Medicine and Cellular Longevity·2020·90 cit.·DOI
5
Atorvastatin enhances neurite outgrowth in cortical neurons in vitro via up-regulating the Akt/mTOR and Akt/GSK-3β signaling pathways
Acta Pharmacologica Sinica·2012·76 cit.·DOI
6
Neu3 Sialidase-Mediated Ganglioside Conversion Is Necessary for Axon Regeneration and Is Blocked in CNS Axons
Journal of Neuroscience·2014·63 cit.·DOI
7
Expressing Constitutively Active Rheb in Adult Neurons after a Complete Spinal Cord Injury Enhances Axonal Regeneration beyond a Chondroitinase-Treated Glial Scar
Journal of Neuroscience·2015·59 cit.·DOI
8
Rapamycin-Resistant mTOR Activity Is Required for Sensory Axon Regeneration Induced by a Conditioning Lesion
eNeuro·2016·56 cit.·DOI
9
MicroRNAs 21 and 199a-3p Regulate Axon Growth Potential through Modulation of<i>Pten</i>and<i>mTo</i>r mRNAs
eNeuro·2021·46 cit.·DOI
10
Ability of the Met Kinase Inhibitor Crizotinib and New Generation EGFR Inhibitors to Overcome Resistance to EGFR Inhibitors
PLoS ONE·2013·44 cit.·DOI

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