A5052078201- Folate and B Vitamins Research
- RNA modifications and cancer
- Cancer Research and Treatments
- Epigenetics and DNA Methylation
- Cancer, Lipids, and Metabolism
- Chromosomal and Genetic Variations
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- Cancer-related gene regulation
- Reproductive biology and impacts on aquatic species
- Fish Biology and Ecology Studies
- Cancer-related molecular mechanisms research
- Animal Genetics and Reproduction
- Fish Ecology and Management Studies
- Aquaculture Nutrition and Growth
- Marine Bivalve and Aquaculture Studies
- Genomics and Phylogenetic Studies
- Marine and fisheries research
Hunan Normal University
2021-2024
Children's Nutrition Research Center at Baylor College of Medicine
2024
Computer Algorithms for Medicine
2020
RELX Group (United States)
2020
Center for Special Minimally Invasive and Robotic Surgery
2015-2019
European Foundation for the Study of Chronic Liver Failure
2016
Canon (Japan)
2016
Chinese Academy of Fishery Sciences
2010-2012
The extent to which non-genetic environmental factors, such as diet, contribute carcinogenesis has been long debated. One potential mechanism for the effects of factors is through epigenetic modifications that affect gene expression without changing underlying DNA sequence. However, functional cooperation between dietary and cancer-causing regulation largely unknown. Here, we use a mouse model age-dependent p16 epimutation, in activity directly controlled by promoter methylation. We show...
<p>Supplementary Table S3 shows 25 differentially expressed metabolites in serum induced by dietary supplementation.</p>
<p>Supplementary Table S2 shows 78 differentially expressed metabolites in liver induced by dietary supplementation.</p>
<div>Abstract<p>The extent to which non-genetic environmental factors, such as diet, contribute carcinogenesis has been long debated. One potential mechanism for the effects of factors is through epigenetic modifications that affect gene expression without changing underlying DNA sequence. However, functional cooperation between dietary and cancer-causing regulation largely unknown. Here, we use a mouse model age-dependent <i>p16</i> epimutation, in activity directly...
<p>Supplementary Table S1 shows comparison of diets between current and previous studies.</p>
<p>Supplementary Table S4 shows 18 differentially expressed metabolites in tumor samples induced by dietary supplementation.</p>
<p>Supplementary Table S3 shows 25 differentially expressed metabolites in serum induced by dietary supplementation.</p>
<p>Supplementary Figure S2 shows an enhanced 1C metabolic pathway that contributes to tumor growth in response dietary methyl donor supplementation.</p>
<p>Supplementary Figure S4 shows scRNA-seq analysis which reveals the immune landscape of colon tumors from supplemented mice.</p>
<p>Supplementary Figure S3 shows dietary methyl donor supplementation markedly increases tumor cell proliferation and immune infiltration.</p>
<p>Supplementary Table S1 shows comparison of diets between current and previous studies.</p>
<p>Supplementary Figure S1 shows that colon tumors from mice fed with control diet had significantly smaller size.</p>
<p>Supplementary Figure S3 shows dietary methyl donor supplementation markedly increases tumor cell proliferation and immune infiltration.</p>
<div>Abstract<p>The extent to which non-genetic environmental factors, such as diet, contribute carcinogenesis has been long debated. One potential mechanism for the effects of factors is through epigenetic modifications that affect gene expression without changing underlying DNA sequence. However, functional cooperation between dietary and cancer-causing regulation largely unknown. Here, we use a mouse model age-dependent <i>p16</i> epimutation, in activity directly...
<p>Supplementary Figure S4 shows scRNA-seq analysis which reveals the immune landscape of colon tumors from supplemented mice.</p>
<p>Supplementary Figure S1 shows that colon tumors from mice fed with control diet had significantly smaller size.</p>
<p>Supplementary Figure S2 shows an enhanced 1C metabolic pathway that contributes to tumor growth in response dietary methyl donor supplementation.</p>
<p>Supplementary Table S4 shows 18 differentially expressed metabolites in tumor samples induced by dietary supplementation.</p>
<p>Supplementary Table S2 shows 78 differentially expressed metabolites in liver induced by dietary supplementation.</p>
Introduction In the Dongting water system, Carassius auratus (Crucian carp) complex is characterized by coexistence of diploid forms (2n=100, 2nCC) and polyploidy forms. The (2nCC) triploid C.auratus (3n=150, 3nCC) had same fertility levels, reaching sexual maturity at one year. Methods nucleotide sequence, gene expression, methylation, immunofluorescence gonadotropin releasing hormone 2( Gnrh2 ), Gonadotropin beta( Gthβ Gonadotropin-releasing receptor( Gthr ) genes pivotal...
Abstract Background: In the Dongting water system, Carassius auratus (Crucian carp) complex is characterized by coexistence of diploid forms (2n=100, 2nCC) and polyploid forms. The (2nCC) triploid C. (3n=150, 3nCC) had same fertility levels, reaching sexual maturity at one year. Results: nucleotide sequence, gene expression, methylation, immunofluorescence gonadotropin releasing hormone 2( Gnrh2 ), Gonadotropin beta( Gthβ ) , Gonadotropin-releasing receptor( Gthr genes pivotal...