Cell Signaling Technology

Sox17 (D1T8M) Rabbit Monoclonal Antibody (BSA and Azide Free)

#20584 · $865

89
Citing papers
1.8k
Combined citations
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Research areas

RNA modifications and cancer13Cancer-related molecular mechanisms research10Epigenetics and DNA Methylation8Cancer, Hypoxia, and Metabolism6Circular RNAs in diseases6Fibroblast Growth Factor Research5interferon and immune responses5Ubiquitin and proteasome pathways5

Papers citing this product

1
Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein–Induced Angiogenesis
Molecular Pharmacology·2018·134 cit.·DOI
2
Human Keratinocytes Release ATP and Utilize Three Mechanisms for Nucleotide Interconversion at the Cell Surface
Journal of Biological Chemistry·2005·129 cit.·DOI
3
Cancer-associated fibroblast-secreted IGFBP7 promotes gastric cancer by enhancing tumor associated macrophage infiltration via FGF2/FGFR1/PI3K/AKT axis
Cell Death Discovery·2023·118 cit.·DOI
4
Chromatin dysregulation and DNA methylation at transcription start sites associated with transcriptional repression in cancers
Nature Communications·2019·109 cit.·DOI
5
Integrative genomics analysis reveals the multilevel dysregulation and oncogenic characteristics of TEAD4 in gastric cancer
Carcinogenesis·2013·105 cit.·DOI
6
Pleiotropic requirements for human TDP-43 in the regulation of cell and organelle homeostasis
Life Science Alliance·2019·75 cit.·DOI
7
Protease-activated receptor 2 (PAR-2) antagonist AZ3451 as a novel therapeutic agent for osteoarthritis
Aging·2019·65 cit.·DOI
8
Mutual reinforcement of inflammation and carcinogenesis by the Helicobacter pylori CagA oncoprotein
Scientific Reports·2015·60 cit.·DOI
9
Formononetin inhibits colon carcinoma cell growth and invasion by microRNA‑149‑mediated EphB3 downregulation and inhibition of PI3K/AKT and STAT3 signaling pathways
Molecular Medicine Reports·2018·56 cit.·DOI
10
CMTM6 overexpression confers trastuzumab resistance in HER2-positive breast cancer
Molecular Cancer·2023·50 cit.·DOI

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