SNPs identification in swine leptin 5’ flanking region and transcriptional activity of naturally occurring promoter haplotypes

Mounting evidence suggests that the risk of developing colorectal cancer (CRC) is dramatically increased for patients with chronic inflammatory diseases. For instance, patients with Crohn's Disease (CD) or Ulcerative Colitis (UC) have a 12–20% increased risk for developing CRC. Preventive strategies utilizing nontoxic natural compounds that modulate immune responses could be successful in the suppression of inflammation-driven colorectal cancer in high-risk groups. The increase of peroxisome proliferator-activated receptor-γ(PPAR-γ) expression and its transcriptional activity has been identified as a target for anti-inflammatory efforts, and the suppression of inflammation-driven colon cancer. PPARγdown-modulates inflammation and elicits antiproliferative and proapoptotic actions in epithelial cells. All of which may decrease the risk for inflammation-induced CRC. This review will focus on the use of orally active, naturally occurring chemopreventive approaches against inflammation-induced CRC that target PPARγand therefore down-modulate inflammation.

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A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity

Cell ◽

10.1016/0092-8674(91)90504-r ◽

1991 ◽

Vol 64 (4) ◽

pp. 751-759 ◽

Cited By ~ 257

Author(s):

Yusaku Nakabeppu ◽

Daniel Nathans

Keyword(s):

Transcriptional Activity ◽

Truncated Form ◽

Naturally Occurring

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Angiopoietin-2 promoter haplotypes confer an increased risk of stroke in a Chinese Han population

Clinical Science ◽

10.1042/cs20090035 ◽

2009 ◽

Vol 117 (11) ◽

pp. 387-395 ◽

Cited By ~ 4

Author(s):

Jingzhou Chen ◽

Hui Yu ◽

Weihua Song ◽

Kai Sun ◽

Yan Song ◽

...

Keyword(s):

Transcriptional Activity ◽

Case Control Study ◽

Haemorrhagic Stroke ◽

Chinese Han ◽

Gene Encoding ◽

Important Mediator ◽

Increased Risk ◽

Angiopoietin 2 ◽

Promoter Haplotypes ◽

Control Study

Angiopoietin-2 is an important mediator of angiogenesis, and we hypothesized that genetic variants of ANGPT2 (the gene encoding angiopoietin-2) would result in abnormal angiogenesis and contribute to stroke susceptibility. To test our hypothesis, we investigated the association of variants in the promoter of ANGPT2 with stroke in a multi-centre case-control study. We found that the C allele of rs3739390 conferred a 1.42-fold risk of lacunar infarction {adjusted OR (odds ratio), 1.42 [95% CI (confidence interval), 1.08–1.87]; P=0.012} and a 2.10-fold higher transcriptional activity than did the corresponding G allele rs3739390G. The haplotype G-G-T conferred a 1.54-fold risk of atherothrombotic stroke and a 1.64-fold risk for haemorrhagic stroke, whereas the haplotype G-C-C conferred approx. a 2.0-fold risk of each subtype of stroke. In conclusion, our results indicate that haplotypes in the promoter of ANGPT2 confer a high risk of stroke in a Chinese population.

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Three Repeats of CCCCTCC on the Pyrimidine-rich Sequence in the Proximal 5′ Flanking Region are Required for Efficient Transcriptional Activity of the Human Endothelial Nitric Oxide Synthase Gene

Free Radical Research ◽

10.1080/10715160310001638029 ◽

2004 ◽

Vol 38 (1) ◽

pp. 87-95

Author(s):

Kaoru Miyahara ◽

Hideaki Kuge ◽

Yutaka Shizuta ◽

Koichi Honke

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Endothelial Nitric Oxide Synthase ◽

Transcriptional Activity ◽

Flanking Region ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

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Naturally occurring dominant-negative Stat5 suppresses transcriptional activity of estrogen receptors and induces apoptosis in T47D breast cancer cells

Oncogene ◽

10.1038/sj.onc.1206277 ◽

2003 ◽

Vol 22 (11) ◽

pp. 1638-1652 ◽

Cited By ~ 48

Author(s):

Hiroko Yamashita ◽

Hirotaka Iwase ◽

Tatsuya Toyama ◽

Yoshitaka Fujii

Keyword(s):

Breast Cancer ◽

Estrogen Receptors ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Transcriptional Activity ◽

Dominant Negative ◽

Naturally Occurring

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The role of the 5′-flanking region in the cell-specific transcription of the human von Willebrand factor gene

Biochemical Journal ◽

10.1042/bj2930641 ◽

1993 ◽

Vol 293 (3) ◽

pp. 641-648 ◽

Cited By ~ 22

Author(s):

V Ferreira ◽

Z Assouline ◽

J L Schwachtgen ◽

B R Bahnak ◽

D Meyer ◽

...

Keyword(s):

Gene Expression ◽

Thymidine Kinase ◽

Von Willebrand Factor ◽

Transcriptional Activity ◽

Cell Types ◽

Flanking Region ◽

Von Willebrand ◽

Willebrand Factor ◽

Cat Gene ◽

Cpae Cells

Transcriptional regulation of the human von Willebrand factor (vWF) gene was investigated in calf pulmonary artery endothelial (CPAE), HeLa, COS 7 and Hep G2 cells. Various lengths of flanking sequences extending up to 2123 bp 5′ of the transcription initiation site and containing 19 bp of the first exon, were linked to the bacterial chloramphenicol acetyltransferase (CAT) gene and these constructs were assayed in transient transfection assays. Sequences up to 89 bp upstream of the cap site showed transcriptional activity in all cell types. Sequences between -147 and -419 bp markedly reduced CAT activity in CPAE cells and abolished it in other cell lines. A domain from -592 to -810 bp generated low levels of expression only in CPAE cells. This transcriptional activity was repressed with constructs containing 1041 to 1240 bp upstream of the cap site. Endothelial cell-specific transcription was restored by a construct that contained 1286 bp upstream of the cap site. The additional 46 bp upstream of the negative regulatory domain were within the 5′ end of an inverse human Alu-family DNA repeat. RNAase-protection assays confirmed the correct transcriptional initiation. The sequence between -89 and -420 contained at least one negative regulatory element able to repress the CAT gene expression controlled by the heterologous thymidine kinase promoter in all cell types. A construct that included the sequence from -89 to -1286 bp increased the transcriptional activity directed by the thymidine kinase promoter only in CPAE cells. These results indicate that negative and positive elements in the 5′-flanking region interact to regulate vWF gene expression.

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