Please use this identifier to cite or link to this item:
|Title:||Inhibitory effect of kinetin riboside in human heptamoa, HepG2|
Wan Hong Yong, J.
Ngin Tan, S.
Shi Ong, E.
|Source:||Cheong, J., Goh, D., Wan Hong Yong, J., Ngin Tan, S., Shi Ong, E. (2009). Inhibitory effect of kinetin riboside in human heptamoa, HepG2. Molecular BioSystems 5 (1) : 91-98. ScholarBank@NUS Repository. https://doi.org/10.1039/b712807j|
|Abstract:||Cytokinins ribosides such as kinetin riboside are a class of plant hormone that were first identified as factors that promote cell division and have since been implicated in many other aspects of plant growth and development. From the data obtained from cell cycle analysis with flow cytometry, the in vitro growth inhibition of human heptamoa, HepG2 cells with kinetin riboside was mediated by causing G2/M cell cycle arrest and cell death. At the same time, treatment with various doses of kinetin riboside in HepG2 cells did not result in a population of cells positive for the active caspase 3. Differentially expressed proteins in the mitochondria of HepG2 cells with cell death induced by kinetin riboside were investigated. Without the use of stable isotope labeling, the proposed method using LC/MSMS provided a rapid approach to study the differentially expressed proteins in the mitochondria due to the cell death induced by kinetin riboside in HepG2 cells. The ability of kinetin riboside to induce cell death and attenuate G1 to S transition is probably a consequence of its ability to interfere with several components in the mitochondria. Hence, it was proposed that the cell death caused by kinetin riboside in HepG2 cells affected a network of proteins involved in cell death and electron transport. © The Royal Society of Chemistry.|
|Source Title:||Molecular BioSystems|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Jan 16, 2018
WEB OF SCIENCETM
checked on Dec 13, 2017
checked on Jan 13, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.