Abstract | BACKGROUND: METHODS: RESULTS: The Jak2-specific inhibitor AG490 decreased Stat1 and Stat3 phosphorylations and promoted HKC apoptosis induced by ATP depletion/recovery. CONCLUSIONS: Our results have demonstrated that Jak2 inhibition participated in the ATP depletion-induced apoptosis of HKCs, which might be a potential target for prevention and treatment of ARF.
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Authors | Jianzhong Wang, Chun Ouyang, Xiangmei Chen, Bo Fu, Yang Lu, Quan Hong |
Journal | Journal of nephrology
(J Nephrol)
2008 Nov-Dec
Vol. 21
Issue 6
Pg. 919-23
ISSN: 1121-8428 [Print] Italy |
PMID | 19034877
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Enzyme Inhibitors
- STAT1 Transcription Factor
- STAT1 protein, human
- STAT3 Transcription Factor
- STAT3 protein, human
- Tyrphostins
- alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide
- Adenosine Triphosphate
- Janus Kinase 2
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Topics |
- Adenosine Triphosphate
(metabolism)
- Apoptosis
(drug effects)
- Blotting, Western
- Cells, Cultured
- Enzyme Inhibitors
(pharmacology)
- Epithelial Cells
(drug effects, metabolism, pathology)
- Humans
- Janus Kinase 2
(antagonists & inhibitors)
- Kidney Tubules, Proximal
(metabolism, pathology)
- STAT1 Transcription Factor
(drug effects, metabolism)
- STAT3 Transcription Factor
(drug effects, metabolism)
- Tyrphostins
(pharmacology)
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