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Showing 1 to 10 of 10 entries
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TNFα in liver fibrosis.

Current pathobiology reports

Yang YM, Seki E.
PMID: 26726307
Curr Pathobiol Rep. 2015 Dec;3(4):253-261. doi: 10.1007/s40139-015-0093-z. Epub 2015 Sep 30.

Hepatocyte death, inflammation, and liver fibrosis are the hallmarks of chronic liver disease. Tumor necrosis factor-α (TNFα) is an inflammatory cytokine involved in liver inflammation and sustained liver inflammation leads to liver fibrosis. TNFα exerts inflammation, proliferation, and apoptosis....

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Yang YM, Seki E. TNFα in liver fibrosis. Curr Pathobiol Rep. 2015;3(4):253-261doi: 10.1007/s40139-015-0093-z.
Yang, Y. M., & Seki, E. (2015). TNFα in liver fibrosis. Current pathobiology reports, 3(4), 253-261. https://doi.org/10.1007/s40139-015-0093-z
Yang, Yoon Mee, and Seki, Ekihiro. "TNFα in liver fibrosis." Current pathobiology reports vol. 3,4 (2015): 253-261. doi: https://doi.org/10.1007/s40139-015-0093-z
Yang YM, Seki E. TNFα in liver fibrosis. Curr Pathobiol Rep. 2015 Dec;3(4):253-261. doi: 10.1007/s40139-015-0093-z. Epub 2015 Sep 30. PMID: 26726307; PMCID: PMC4693602.
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TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis.

Molecular & cellular oncology

Seki E.
PMID: 26709386
Mol Cell Oncol. 2014;1(4). doi: 10.4161/23723548.2014.968507. Epub 2014 Dec 31.

In addition to regulating the activation of nuclear factor (NF)-κB and c-Jun N-terminal kinase (JNK), TGF-β activated kinase 1 (TAK1) also upregulates the activation of AMP-activated protein kinase (AMPK) and autophagy. In the liver, TAK1-mediated autophagy plays a role...

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Seki E. TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis. Mol Cell Oncol. 2014;1(4)doi: 10.4161/23723548.2014.968507.
Seki, E. (2014). TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis. Molecular & cellular oncology, 1(4), . https://doi.org/10.4161/23723548.2014.968507
Seki, Ekihiro. "TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis." Molecular & cellular oncology vol. 1,4 (2014). doi: https://doi.org/10.4161/23723548.2014.968507
Seki E. TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis. Mol Cell Oncol. 2014;1(4). doi: 10.4161/23723548.2014.968507. Epub 2014 Dec 31. PMID: 26709386; PMCID: PMC4687902.
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The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis.

Gastroenterology

Roh YS, Loomba R, Seki E.
PMID: 25451657
Gastroenterology. 2015 Jan;148(1):252-4. doi: 10.1053/j.gastro.2014.11.014. Epub 2014 Nov 18.

No abstract available.

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Roh YS, Loomba R, Seki E. The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis. Gastroenterology. 2014;148(1):252-4doi: 10.1053/j.gastro.2014.11.014.
Roh, Y. S., Loomba, R., & Seki, E. (2015). The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis. Gastroenterology, 148(1), 252-4. https://doi.org/10.1053/j.gastro.2014.11.014
Roh, Yoon-Seok, et al. "The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis." Gastroenterology vol. 148,1 (2015): 252-4. doi: https://doi.org/10.1053/j.gastro.2014.11.014
Roh YS, Loomba R, Seki E. The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis. Gastroenterology. 2015 Jan;148(1):252-4. doi: 10.1053/j.gastro.2014.11.014. Epub 2014 Nov 18. PMID: 25451657; PMCID: PMC4718074.
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Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase.

Hepatology research : the official journal of the Japan Society of Hepatology

Brenner DA, Seki E, Taura K, Kisseleva T, Deminicis S, Iwaisako K, Inokuchi S, Schnabl B, Oesterreicher CH, Paik YH, Miura K, Kodama Y.
PMID: 21711427
Hepatol Res. 2011 Jul;41(7):683-6. doi: 10.1111/j.1872-034X.2011.00814.x.

Non-alcoholic steatohepatitis (NASH) represents the progression of hepatic steatosis to streatohepatitis, fibrosis and cirrhosis. Three signaling pathways have been associated with this progression; Toll-like receptors, reactive oxygen species and Jun N-terminal kinase. This review will describe how activation of...

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Brenner DA, Seki E, Taura K, et al. Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase. Hepatol Res. 2011;41(7):683-6doi: 10.1111/j.1872-034X.2011.00814.x.
Brenner, D. A., Seki, E., Taura, K., Kisseleva, T., Deminicis, S., Iwaisako, K., Inokuchi, S., Schnabl, B., Oesterreicher, C. H., Paik, Y. H., Miura, K., & Kodama, Y. (2011). Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase. Hepatology research : the official journal of the Japan Society of Hepatology, 41(7), 683-6. https://doi.org/10.1111/j.1872-034X.2011.00814.x
Brenner, David A, et al. "Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase." Hepatology research : the official journal of the Japan Society of Hepatology vol. 41,7 (2011): 683-6. doi: https://doi.org/10.1111/j.1872-034X.2011.00814.x
Brenner DA, Seki E, Taura K, Kisseleva T, Deminicis S, Iwaisako K, Inokuchi S, Schnabl B, Oesterreicher CH, Paik YH, Miura K, Kodama Y. Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase. Hepatol Res. 2011 Jul;41(7):683-6. doi: 10.1111/j.1872-034X.2011.00814.x. PMID: 21711427; PMCID: PMC3341613.
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Alcoholic liver disease: A current molecular and clinical perspective.

Liver research

Ohashi K, Pimienta M, Seki E.
PMID: 31214376
Liver Res. 2018 Dec;2(4):161-172. doi: 10.1016/j.livres.2018.11.002. Epub 2018 Dec 12.

Heavy alcohol use is the cause of alcoholic liver disease (ALD). The ALD spectrum ranges from alcoholic steatosis to steatohepatitis, fibrosis, and cirrhosis. In Western countries, approximately 50% of cirrhosis-related deaths are due to alcohol use. While alcoholic cirrhosis...

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Ohashi K, Pimienta M, Seki E. Alcoholic liver disease: A current molecular and clinical perspective. Liver Res. 2018;2(4):161-172doi: 10.1016/j.livres.2018.11.002.
Ohashi, K., Pimienta, M., & Seki, E. (2018). Alcoholic liver disease: A current molecular and clinical perspective. Liver research, 2(4), 161-172. https://doi.org/10.1016/j.livres.2018.11.002
Ohashi, Koichiro, et al. "Alcoholic liver disease: A current molecular and clinical perspective." Liver research vol. 2,4 (2018): 161-172. doi: https://doi.org/10.1016/j.livres.2018.11.002
Ohashi K, Pimienta M, Seki E. Alcoholic liver disease: A current molecular and clinical perspective. Liver Res. 2018 Dec;2(4):161-172. doi: 10.1016/j.livres.2018.11.002. Epub 2018 Dec 12. PMID: 31214376; PMCID: PMC6581514.
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Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms.

Frontiers in physiology

Yang L, Seki E.
PMID: 22661952
Front Physiol. 2012 May 22;3:138. doi: 10.3389/fphys.2012.00138. eCollection 2012.

Toll-like receptors (TLRs) are pattern recognition receptors that distinguish conserved microbial products, also known as pathogen-associated molecular patterns (PAMPs), from host molecules. Liver is the first filter organ between the gastrointestinal tracts and the rest of the body through...

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Yang L, Seki E. Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms. Front Physiol. 2012;3:138doi: 10.3389/fphys.2012.00138.
Yang, L., & Seki, E. (2012). Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms. Frontiers in physiology, 3138. https://doi.org/10.3389/fphys.2012.00138
Yang, Ling, and Seki, Ekihiro. "Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms." Frontiers in physiology vol. 3 (2012): 138. doi: https://doi.org/10.3389/fphys.2012.00138
Yang L, Seki E. Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms. Front Physiol. 2012 May 22;3:138. doi: 10.3389/fphys.2012.00138. eCollection 2012. PMID: 22661952; PMCID: PMC3357552.
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TRIF Differentially Regulates Hepatic Steatosis and Inflammation/Fibrosis in Mice.

Cellular and molecular gastroenterology and hepatology

Yang L, Miura K, Zhang B, Matsushita H, Yang YM, Liang S, Song J, Roh YS, Seki E.
PMID: 28462384
Cell Mol Gastroenterol Hepatol. 2017 Jan 17;3(3):469-483. doi: 10.1016/j.jcmgh.2016.12.004. eCollection 2017 May.

BACKGROUND & AIMS: Toll-like receptor 4 (TLR4) signaling is activated through 2 adaptor proteins: MyD88 and TIR-domain containing adaptor-inducing interferon-β (TRIF). TLR4 and MyD88 are crucial in nonalcoholic steatohepatitis (NASH) and fibrosis. However, the role of TRIF in TLR4-mediated...

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Yang L, Miura K, Zhang B, et al. TRIF Differentially Regulates Hepatic Steatosis and Inflammation/Fibrosis in Mice. Cell Mol Gastroenterol Hepatol. 2017;3(3):469-483doi: 10.1016/j.jcmgh.2016.12.004.
Yang, L., Miura, K., Zhang, B., Matsushita, H., Yang, Y. M., Liang, S., Song, J., Roh, Y. S., & Seki, E. (2017). TRIF Differentially Regulates Hepatic Steatosis and Inflammation/Fibrosis in Mice. Cellular and molecular gastroenterology and hepatology, 3(3), 469-483. https://doi.org/10.1016/j.jcmgh.2016.12.004
Yang, Ling, et al. "TRIF Differentially Regulates Hepatic Steatosis and Inflammation/Fibrosis in Mice." Cellular and molecular gastroenterology and hepatology vol. 3,3 (2017): 469-483. doi: https://doi.org/10.1016/j.jcmgh.2016.12.004
Yang L, Miura K, Zhang B, Matsushita H, Yang YM, Liang S, Song J, Roh YS, Seki E. TRIF Differentially Regulates Hepatic Steatosis and Inflammation/Fibrosis in Mice. Cell Mol Gastroenterol Hepatol. 2017 Jan 17;3(3):469-483. doi: 10.1016/j.jcmgh.2016.12.004. eCollection 2017 May. PMID: 28462384; PMCID: PMC5403956.
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Toll-like receptor signaling in liver regeneration, fibrosis and carcinogenesis.

Hepatology research : the official journal of the Japan Society of Hepatology

Seki E, Park E, Fujimoto J.
PMID: 21696522
Hepatol Res. 2011 Jul;41(7):597-610. doi: 10.1111/j.1872-034X.2011.00822.x. Epub 2011 Jun 22.

Toll-like receptors (TLR) are the germline-coded pattern recognition receptors that sense microbial products. This signaling orchestrates complex signaling pathways that induce expression of inflammatory genes for host defense against invading microorganisms. Recent studies illustrate the role of TLR on...

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Seki E, Park E, Fujimoto J. Toll-like receptor signaling in liver regeneration, fibrosis and carcinogenesis. Hepatol Res. 2011;41(7):597-610doi: 10.1111/j.1872-034X.2011.00822.x.
Seki, E., Park, E., & Fujimoto, J. (2011). Toll-like receptor signaling in liver regeneration, fibrosis and carcinogenesis. Hepatology research : the official journal of the Japan Society of Hepatology, 41(7), 597-610. https://doi.org/10.1111/j.1872-034X.2011.00822.x
Seki, Ekihiro, et al. "Toll-like receptor signaling in liver regeneration, fibrosis and carcinogenesis." Hepatology research : the official journal of the Japan Society of Hepatology vol. 41,7 (2011): 597-610. doi: https://doi.org/10.1111/j.1872-034X.2011.00822.x
Seki E, Park E, Fujimoto J. Toll-like receptor signaling in liver regeneration, fibrosis and carcinogenesis. Hepatol Res. 2011 Jul;41(7):597-610. doi: 10.1111/j.1872-034X.2011.00822.x. Epub 2011 Jun 22. PMID: 21696522; PMCID: PMC3754784.
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Toll-like receptor signaling in liver diseases.

Gastroenterology research and practice

Szabo G, Billiar TR, Machida K, Crispe IN, Seki E.
PMID: 21789039
Gastroenterol Res Pract. 2010;2010:971270. doi: 10.1155/2010/971270. Epub 2011 May 05.

No abstract available.

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Szabo G, Billiar TR, Machida K, et al. Toll-like receptor signaling in liver diseases. Gastroenterol Res Pract. 2011;2010:971270doi: 10.1155/2010/971270.
Szabo, G., Billiar, T. R., Machida, K., Crispe, I. N., & Seki, E. (2010). Toll-like receptor signaling in liver diseases. Gastroenterology research and practice, 2010971270. https://doi.org/10.1155/2010/971270
Szabo, Gyongyi, et al. "Toll-like receptor signaling in liver diseases." Gastroenterology research and practice vol. 2010 (2010): 971270. doi: https://doi.org/10.1155/2010/971270
Szabo G, Billiar TR, Machida K, Crispe IN, Seki E. Toll-like receptor signaling in liver diseases. Gastroenterol Res Pract. 2010;2010:971270. doi: 10.1155/2010/971270. Epub 2011 May 05. PMID: 21789039; PMCID: PMC3123973.
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Role of toll-like receptors and their downstream molecules in the development of nonalcoholic Fatty liver disease.

Gastroenterology research and practice

Miura K, Seki E, Ohnishi H, Brenner DA.
PMID: 21274430
Gastroenterol Res Pract. 2010;2010:362847. doi: 10.1155/2010/362847. Epub 2011 Jan 17.

Activation of innate immunity is associated with the development of liver disease, including non-alcoholic fatty liver disease (NAFLD). In the innate immune system, Toll-like receptors (TLRs) are sensors that recognize bacterial and viral components such as lipopolysaccharide, bacterial DNA,...

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Miura K, Seki E, Ohnishi H, et al. Role of toll-like receptors and their downstream molecules in the development of nonalcoholic Fatty liver disease. Gastroenterol Res Pract. 2011;2010:362847doi: 10.1155/2010/362847.
Miura, K., Seki, E., Ohnishi, H., & Brenner, D. A. (2010). Role of toll-like receptors and their downstream molecules in the development of nonalcoholic Fatty liver disease. Gastroenterology research and practice, 2010362847. https://doi.org/10.1155/2010/362847
Miura, Kouichi, et al. "Role of toll-like receptors and their downstream molecules in the development of nonalcoholic Fatty liver disease." Gastroenterology research and practice vol. 2010 (2010): 362847. doi: https://doi.org/10.1155/2010/362847
Miura K, Seki E, Ohnishi H, Brenner DA. Role of toll-like receptors and their downstream molecules in the development of nonalcoholic Fatty liver disease. Gastroenterol Res Pract. 2010;2010:362847. doi: 10.1155/2010/362847. Epub 2011 Jan 17. PMID: 21274430; PMCID: PMC3026974.
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Showing 1 to 10 of 10 entries