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1.
Figure 3

Figure 3. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

Induction of hMLH1 protein expression after 5-azacytidine (AzaC) treatment. The Western analysis was performed as described in Materials and Methods. U, Cells untreated; T, cells treated with 5-azacytidine.

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.
2.
Figure 2

Figure 2. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

Analysis of methylation status of the hMLH1 promoter. Shown is the product resulting from PCR amplification of the hMLH1 promoter region before or after digestion. U, Undigested; H, digested with HpaII; M, digested with MspI. The methylation status (+, methylated; −, unmethylated) of the hMLH1 promoter is designated below each sample.

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.
3.
Figure 6

Figure 6. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

Allele-specific analysis of hMLH1 expression after 5-azacytidine treatment in Vaco 5 and Vaco 6. (A) Reverse transcription–PCR analysis of hMLH1 expression in Vaco5 and Vaco432 before (+) and after (−) treatment with 5-azacytidine (AzaC). (B) DNA sequences of hMLH1 cDNAs from Vaco5 and Vaco432 amplified by reverse transcription–PCR after treatment with 5-azacytidine. The arrow points to a coding region polymorphism at codon 219 (ATC to GTC).

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.
4.
Figure 1

Figure 1. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

hMLH1 protein expression in MSI cancers. Shown is a Western blot of hMLH1 protein expression. The presence (+) or absence (−) of MSI and the status of the coding region of the hMLH1 gene (wt, wild type; mut, mutant) are denoted below each lane. The Western analysis was performed as described in Materials and Methods.

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.
5.
Figure 4

Figure 4. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

Time course of hMLH1 protein expression after 5-azacytidine treatment. AN3CA cells were treated with 5-azacytidine as detailed in Materials and Methods. An untreated sample (day 0), a sample immediately after 5-azacytidine treatment (day 8), and samples 1 week (day 15) and 2 weeks (day 21) after 5-azacytidine treatment were collected for Western analysis to evaluate production of hMLH1 protein.

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.
6.
Figure 5

Figure 5. From: Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers.

Reversible expression of hMLH1 protein in single-cell clones treated with 5-azacytidine. Western analysis of hMLH1 protein expression was performed as described in Materials and Methods and is shown for AN3CA cells untreated (U) or on day 8 of treatment with 5-azacytidine (T). As described in Materials and Methods, subclones 1, 2, and 3 were established from the day 8 treated AN3CA cell population immediately after washout of the drug and were analyzed for continued hMLH1 expression when they had reached confluence. The same three subclones were then retreated with 5-azacytidine and again analyzed (treated subclones). Subclones 1 and 3 are representative normal-growth-rate subclones; whereas subclone 2 is representative of the group of slow-growth-rate subclones.

Martina L. Veigl, et al. Proc Natl Acad Sci U S A. 1998 July 21;95(15):8698-8702.

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