ABCB6 p.Gly12Val
| Predicted by SNAP2: | A: N (72%), C: N (57%), D: N (78%), E: N (82%), F: N (53%), H: N (61%), I: N (82%), K: N (72%), L: N (61%), M: N (66%), N: N (78%), P: N (53%), Q: N (78%), R: N (61%), S: N (93%), T: N (87%), V: N (87%), W: D (75%), Y: N (57%), |
| Predicted by PROVEAN: | A: N, C: N, D: N, E: N, F: N, H: N, I: N, K: N, L: N, M: N, N: N, P: N, Q: N, R: N, S: N, T: N, V: N, W: N, Y: N, |
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[hide] Gene expression profiling of adenosine triphosphat... Pancreas. 2009 Jan;38(1):85-93. Lo M, Tsao MS, Hedley D, Ling V
Gene expression profiling of adenosine triphosphate-binding cassette transporters in response to K-ras activation and hypoxia in human pancreatic cancer cell cultures.
Pancreas. 2009 Jan;38(1):85-93., [PMID:19117087]
Abstract [show]
OBJECTIVES: Pancreatic cancer (PC) is hypoxic and highly resistant to conventional chemotherapy. We sought to determine whether K-ras oncogene and/or hypoxia can induce expression of drug resistance-promoting adenosine triphosphate-binding cassette (ABC) transporters in human PC cell lines. METHODS: Immortalized near-normal human pancreatic ductal epithelial(HPDE) cells, HPDE cells expressing K-rasG12V oncogene, and PCcell lines (MIA PaCa-2, PANC-1, BxPC-3) were subjected to hypoxia and examined for messenger RNA expression of 48 ABC transporters. RESULTS: Mutant K-ras activation and/or hypoxia of HPDE cells led to induction of various ABC transporters. In the case of PC cell lines, no clear correlation was found between expression of constitutively active K-ras and global ABC transporter expression. Moreover, hypoxic treatment of PC cell lines had different effects on ABC transporter expression.Importantly, PC cell lines did not express the multidrug resistance 1 ABC transporter, a major mechanism of drug resistance. However, multi drug resistance 1 expression in the cells was up-regulated in response to continuous exposure to low doses of vincristine, indicating that drug resistance could be induced. CONCLUSIONS: Expression of K-ras oncogene and hypoxia, as well as exposure to drugs, can contribute to drug resistance in PC cells.
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No. Sentence Comment
129 The K-ras point mutation G12V, which results in a constitutively active K-ras protein, is present in over 90% of PC and occurs at a very early stage of cancer development.24Y26 Immortalized HPDE cells stably transfected with the K-rasG12V oncogene are weakly tumorigenic and exhibit gene expression changes that closely resemble those observed in pancreatic ductal adenocarcinomas.15 Specifically, microarray expression profiling studies identified 584 genes whose expression levels were specifically up-regulated by the K-ras oncogene, of which 42 have been reported previously as differentially overexpressed in PC cell lines or primary tumors.15 However, none of the 42 genes mentioned in this report were from the ABC transporter family.15 It is also unknown whether any of the remaining 542 genes might be from the ABC transporter family.
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ABCB6 p.Gly12Val 19117087:129:25
status: NEW