Cell Signaling Technology

Cyclin A2 (E9Q5G) Rabbit Monoclonal Antibody (BSA and Azide Free)

#18676 · $865

39
Citing papers
2.2k
Combined citations
Supplier page Find this product

Research areas

Parkinson's Disease Mechanisms and Treatments12Wound Healing and Treatments5Neurological diseases and metabolism5Nuclear Receptors and Signaling4Genomics and Chromatin Dynamics3Fungal and yeast genetics research3Plant Gene Expression Analysis3Cellular transport and secretion3

Papers citing this product

1
14-3-3 binding to LRRK2 is disrupted by multiple Parkinson's disease-associated mutations and regulates cytoplasmic localization
Biochemical Journal·2010·402 cit.·DOI
2
Enhanced Striatal Dopamine Transmission and Motor Performance with LRRK2 Overexpression in Mice Is Eliminated by Familial Parkinson's Disease Mutation G2019S
Journal of Neuroscience·2010·344 cit.·DOI
3
Mutant LRRK2 Toxicity in Neurons Depends on LRRK2 Levels and Synuclein But Not Kinase Activity or Inclusion Bodies
Journal of Neuroscience·2014·140 cit.·DOI
4
GTPase Activity and Neuronal Toxicity of Parkinson's Disease–Associated LRRK2 Is Regulated by ArfGAP1
PLoS Genetics·2012·138 cit.·DOI
5
LRRK2 Transport Is Regulated by Its Novel Interacting Partner Rab32
PLoS ONE·2014·97 cit.·DOI
6
Lupeol, a Pentacyclic Triterpene, Promotes Migration, Wound Closure, and Contractile Effect In Vitro: Possible Involvement of PI3K/Akt and p38/ERK/MAPK Pathways
Molecules·2018·93 cit.·DOI
7
Regulation of LRRK2 Stability by the E3 Ubiquitin Ligase CHIP
PLoS ONE·2009·91 cit.·DOI
8
Interleukin-6 stimulates Akt and p38 MAPK phosphorylation and fibroblast migration in non-diabetic but not diabetic mice
PLoS ONE·2017·82 cit.·DOI
9
Fibroblast Growth Factor-2 Is a Downstream Mediator of Phosphatidylinositol 3-Kinase-Akt Signaling in 14,15-Epoxyeicosatrienoic Acid-induced Angiogenesis
Journal of Biological Chemistry·2005·79 cit.·DOI
10
Overexpression of Parkin Ameliorates Dopaminergic Neurodegeneration Induced by 1- Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice
PLoS ONE·2012·78 cit.·DOI

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