NIK-mediated reactivation of SIX2 enhanced the CSC-like traits of hepatocellular carcinoma cells through suppressing ubiquitin-proteasome system.

Daren L, Dan Y, Jinhong W, Chao L

DOI: 10.1002/tox.23892
Published: 2024 Feb
Container: Environmental toxicology
Publisher: Not recorded
Open access: unknown

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Cite this work

BibTeX

@article{allodium:10.1002/tox.23892,
  title = {NIK-mediated reactivation of SIX2 enhanced the CSC-like traits of hepatocellular carcinoma cells through suppressing ubiquitin-proteasome system.},
  author = {Daren L and Dan Y and Jinhong W and Chao L},
  year = {2024},
  journal = {Environmental toxicology},
  doi = {10.1002/tox.23892},
  url = {https://doi.org/10.1002/tox.23892}
}

RIS

TY  - JOUR
TI  - NIK-mediated reactivation of SIX2 enhanced the CSC-like traits of hepatocellular carcinoma cells through suppressing ubiquitin-proteasome system.
AU  - Daren L
AU  - Dan Y
AU  - Jinhong W
AU  - Chao L
PY  - 2024
JO  - Environmental toxicology
DO  - 10.1002/tox.23892
UR  - https://doi.org/10.1002/tox.23892
ER  -

APA

L, D., Y, D., W, J., & L, C. (2024). NIK-mediated reactivation of SIX2 enhanced the CSC-like traits of hepatocellular carcinoma cells through suppressing ubiquitin-proteasome system.. Environmental toxicology. https://doi.org/10.1002/tox.23892

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pubmed · retrieved 2026-09-24T23:27:18.573Z