Cell Signaling Technology

FoxK2 (E7C5H) Rabbit Monoclonal Antibody

#28712 · $161

21
Citing papers
508
Combined citations
Supplier page Find this product

Research areas

Adipose Tissue and Metabolism3Receptor Mechanisms and Signaling3Cancer, Hypoxia, and Metabolism3Mitochondrial Function and Pathology3Neuropeptides and Animal Physiology2T-cell and Retrovirus Studies2Liver Disease Diagnosis and Treatment2Beetle Biology and Toxicology Studies1

Papers citing this product

1
Telomerase reverse transcriptase promotes cancer cell proliferation by augmenting tRNA expression
Journal of Clinical Investigation·2016·136 cit.·DOI
2
ERBIN deficiency links STAT3 and TGF-β pathway defects with atopy in humans
The Journal of Experimental Medicine·2017·98 cit.·DOI
3
Wnt5a promotes cancer cell invasion and proliferation by receptor-mediated endocytosis-dependent and -independent mechanisms, respectively
Scientific Reports·2015·70 cit.·DOI
4
Erythropoietin Mitigates Diabetic Nephropathy by Restoring PINK1/Parkin-Mediated Mitophagy
Frontiers in Pharmacology·2022·36 cit.·DOI
5
Wnt5a is a TLR2/4-ligand that induces tolerance in human myeloid cells
Communications Biology·2019·34 cit.·DOI
6
Protective Effects of Rapamycin on Trabecular Meshwork Cells in Glucocorticoid-Induced Glaucoma Mice
Frontiers in Pharmacology·2020·26 cit.·DOI
7
Dihydromyricetin supplementation improves ethanol-induced lipid accumulation and inflammation
Frontiers in Nutrition·2023·21 cit.·DOI
8
Internalization and distribution of three ?<sub>1</sub>-adrenoceptor subtypes in HEK293A cells before and after agonist stimulation
Acta Pharmacologica Sinica·2007·14 cit.·DOI
9
Bicyclol Alleviates Signs of BDL-Induced Cholestasis by Regulating Bile Acids and Autophagy-Mediated HMGB1/p62/Nrf2 Pathway
Frontiers in Pharmacology·2021·12 cit.·DOI
10
Cucumber (<i>Cucumis sativus</i> L.) translationally controlled tumor protein interacts with <scp>CsRab11A</scp> and promotes activation of target of rapamycin in response to <i>Podosphaera xanthii</i>
The Plant Journal·2024·11 cit.·DOI

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