Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Qingdong Ke"'
Autor:
Jimin Gao, Dongyun Zhang, Xun Che, Haishan Huang, Xiaoyi Mi, Qing Xia, Qingdong Ke, Chuanshu Huang, Jingxia Li, Jinyi Liu
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1833(9):2083-2091
p27 is a cyclin-dependent kinase (CDK) inhibitor that suppresses a cell's transition from G0 to S phase, therefore acting as a tumor suppressor. Our most recent studies demonstrate that upon arsenite exposure, p27 suppresses Hsp27 and Hsp70 expressio
Epidemiological studies have demonstrated that nickel, chromium, arsenic, cadmium, and beryllium compounds are human carcinogens. Most of these epidemiological studies were done retrospectively in humans occupationally exposed to compounds of these m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::3abdcd65a9ad90770d8777113ec550b2
https://doi.org/10.1016/b978-0-444-59453-2.00018-4
https://doi.org/10.1016/b978-0-444-59453-2.00018-4
Autor:
Max Costa, Qingdong Ke
Publikováno v:
Molecular Pharmacology. 70:1469-1480
Adaptation to low oxygen tension (hypoxia) in cells and tissues leads to the transcriptional induction of a series of genes that participate in angiogenesis, iron metabolism, glucose metabolism, and cell proliferation/survival. The primary factor med
Publikováno v:
Molecular and Cellular Biology. 26:3728-3737
We have previously reported that carcinogenic nickel compounds decreased global histone H4 acetylation and silenced the gpt transgene in G12 Chinese hamster cells. However, the nature of this silencing is still not clear. Here, we report that nickel
Publikováno v:
Carcinogenesis. 27:1481-1488
Although it has been well established that insoluble nickel compounds are potent carcinogens and soluble nickel compounds are less potent, the mechanisms remain unclear. Nickel compounds are weakly mutagenic, but cause epigenetic effects in cells. Pr
Autor:
Haobin Chen, Todd Davidson, Yan Yan, Chuanshu Huang, Max Costa, Thomas Kluz, Ping Zhang, Qingdong Ke
Publikováno v:
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 592:79-88
Both water soluble and insoluble nickel compounds have been implicated in the etiology of human lung and nasal cancers. Water insoluble nickel compounds have been shown to enter cells by phagocytosis and are contained in cytoplasmic vacuoles, which a
Publikováno v:
International Journal of Environmental Research and Public Health, Vol 2, Iss 1, Pp 10-13 (2005)
International Journal of Environmental Research and Public Health
International Journal of Environmental Research and Public Health; Volume 2; Issue 1; Pages: 10-13
International Journal of Environmental Research and Public Health
International Journal of Environmental Research and Public Health; Volume 2; Issue 1; Pages: 10-13
Although nickel and cobalt compounds have been known to cause induction of the transcription factor hypoxia-inducible factor 1 (HIF-1) and activation of a battery of hypoxia-inducible genes in the cell, the molecular mechanisms of this induction rema
Publikováno v:
Molecular and Cellular Biochemistry. 255:57-66
Arsenic is a metalloid compound that is widely distributed in the environment. Human exposure of this compound has been associated with increased cancer incidence. Although the exact mechanisms remain to be investigated, numerous carcinogenic pathway
In the present study, we examined the effects of CoCl(2) on multiple histone modifications at the global level. We found that in both human lung carcinoma A549 cells and human bronchial epithelial Beas-2B cells, exposure to CoCl(2) (>/=200 muM) for 2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3ccaadfa6d416f9a8b0ef4af486c615a
https://europepmc.org/articles/PMC2704281/
https://europepmc.org/articles/PMC2704281/
Publikováno v:
Carcinogenesis. 29(6)
Nickel (Ni) is a known carcinogen, although the mechanism of its carcinogenicity is not clear. Here, we provide evidence that Ni can induce phosphorylation of histone H3 at its serine 10 residue in a c-jun N-terminal kinase (JNK)/stress-activated pro