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Book ; Online ; Thesis: Charakterisierung der molekularen Mechanismen des Adipokins-Adiponectin bei der nicht-alkoholischen Steatohepatitis (NASH)

Wanninger, Josef [Verfasser]

2011

Author's details	vorgelegt von Josef Wanninger
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	German
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: Chemerin Is Induced in Non-Alcoholic Fatty Liver Disease and Hepatitis B-Related Hepatocellular Carcinoma.

Haberl, Elisabeth M / Feder, Susanne / Pohl, Rebekka / Rein-Fischboeck, Lisa / Dürholz, Kerstin / Eichelberger, Laura / Wanninger, Josef / Weiss, Thomas S / Buechler, Christa

Cancers

2020 Volume 12, Issue 10

Abstract: Chemerin is protective in experimental models of hepatocellular carcinoma (HCC). Noteworthy, chemerin mRNA and protein were reduced in HCC tissues of Asian patients with mostly hepatitis B disease etiology. The current study nevertheless showed that ... ...

Abstract	Chemerin is protective in experimental models of hepatocellular carcinoma (HCC). Noteworthy, chemerin mRNA and protein were reduced in HCC tissues of Asian patients with mostly hepatitis B disease etiology. The current study nevertheless showed that chemerin protein was induced in tumor tissues of European HCC patients with non-alcoholic fatty liver disease (NAFLD) and patients with unclear disease etiology. A similar regulation was observed in hepatitis B virus (HBV), but not in hepatitis C virus (HCV), related HCC. The apparent discrepancy between the regulation of chemerin in HBV-HCC obtained from our study and recent reports led us to use the chemerin antibodies applied in the previous assays. These antibodies could not equally detect different chemerin isoforms, which were overexpressed in HepG2 cells. Higher chemerin protein in HCC was nevertheless confirmed by the use of all antibodies. Chemerin protein was low in Huh7 and PLC/PRF/5 cells whereas HepG2 and Hep3B cells had chemerin protein similar as primary human hepatocytes. Besides, the anti-tumor effects of retinoids in hepatocyte cell lines did not enclose upregulation of chemerin, which was initially discovered as a tazarotene induced protein in the skin. Finally, protein levels of the chemerin receptor, chemokine-like receptor 1 (CMKLR1), declined in non-viral, and tended to be lower in HBV-HCC tissues suggesting reduced chemerin activity in the tumors. To sum up, our work showed an opposite regulation of chemerin and CMKLR1 in NAFLD and HBV associated HCC. In HCV-HCC neither chemerin nor its receptor were changed in the tumor tissues. Current findings do not support a critical role of total chemerin protein levels in HCC of non-viral and viral etiology. Accordingly, tumor-localized chemerin protein was not associated with tumor-node-metastasis classification.
Language	English
Publishing date	2020-10-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12102967
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Article ; Online: Hepatocyte expressed chemerin-156 does not protect from experimental non-alcoholic steatohepatitis.

Pohl, Rebekka / Eichelberger, Laura / Feder, Susanne / Haberl, Elisabeth M / Rein-Fischboeck, Lisa / McMullen, Nichole / Sinal, Christopher J / Bruckmann, Astrid / Weiss, Thomas S / Beck, Michael / Höring, Marcus / Krautbauer, Sabrina / Liebisch, Gerhard / Wiest, Reiner / Wanninger, Josef / Buechler, Christa

Molecular and cellular biochemistry

2022 Volume 477, Issue 8, Page(s) 2059–2071

Abstract: Non-alcoholic steatohepatitis (NASH) is a rapidly growing liver disease. The chemoattractant chemerin is abundant in hepatocytes, and hepatocyte expressed prochemerin protected from NASH. Prochemerin is inactive and different active isoforms have been ... ...

Abstract	Non-alcoholic steatohepatitis (NASH) is a rapidly growing liver disease. The chemoattractant chemerin is abundant in hepatocytes, and hepatocyte expressed prochemerin protected from NASH. Prochemerin is inactive and different active isoforms have been described. Here, the effect of hepatocyte expressed muChem-156, a highly active murine chemerin isoform, was studied in the methionine-choline deficient dietary model of NASH. Mice overexpressing muChem-156 had higher hepatic chemerin protein. Serum chemerin levels and the capability of serum to activate the chemerin receptors was unchanged showing that the liver did not release active chemerin. Notably, activation of the chemerin receptors by hepatic vein blood did not increase in parallel to total chemerin protein in patients with liver cirrhosis. In experimental NASH, muChem-156 had no effect on liver lipids. Accordingly, overexpression of active chemerin in hepatocytes or treatment of hepatocytes with recombinant chemerin did not affect cellular triglyceride and cholesterol levels. Importantly, overexpression of muChem-156 in the murine liver did not change the hepatic expression of inflammatory and profibrotic genes. The downstream targets of chemerin such as p38 kinase were neither activated in the liver of muChem-156 producing mice nor in HepG2, Huh7 and Hepa1-6 cells overexpressing this isoform. Recombinant chemerin had no effect on global gene expression of primary human hepatocytes and hepatic stellate cells within 24 h of incubation. Phosphorylation of p38 kinase was, however, increased upon short-time incubation of HepG2 cells with chemerin. These findings show that muChem-156 overexpression in hepatocytes does not protect from liver steatosis and inflammation.
MeSH term(s)	Animals ; Chemokines ; Disease Models, Animal ; Hepatic Stellate Cells/metabolism ; Hepatocytes/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Liver/metabolism ; Mice ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Protein Isoforms/metabolism
Chemical Substances	Chemokines ; Intercellular Signaling Peptides and Proteins ; Protein Isoforms ; RARRES2 protein, human ; chemerin protein, mouse
Language	English
Publishing date	2022-04-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-022-04430-3
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Article ; Online: Adiponectin, a key adipokine in obesity related liver diseases.

Buechler, Christa / Wanninger, Josef / Neumeier, Markus

World journal of gastroenterology

2011 Volume 17, Issue 23, Page(s) 2801–2811

Abstract: Non-alcoholic fatty liver disease (NAFLD) comprising hepatic steatosis, non-alcoholic steatohepatitis (NASH), and progressive liver fibrosis is considered the most common liver disease in western countries. Fatty liver is more prevalent in overweight ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) comprising hepatic steatosis, non-alcoholic steatohepatitis (NASH), and progressive liver fibrosis is considered the most common liver disease in western countries. Fatty liver is more prevalent in overweight than normal-weight people and liver fat positively correlates with hepatic insulin resistance. Hepatic steatosis is regarded as a benign stage of NAFLD but may progress to NASH in a subgroup of patients. Besides liver biopsy no diagnostic tools to identify patients with NASH are available, and no effective treatment has been established. Visceral obesity is a main risk factor for NAFLD and inappropriate storage of triglycerides in adipocytes and higher concentrations of free fatty acids may add to increased hepatic lipid storage, insulin resistance, and progressive liver damage. Most of the adipose tissue-derived proteins are elevated in obesity and may contribute to systemic inflammation and liver damage. Adiponectin is highly abundant in human serum but its levels are reduced in obesity and are even lower in patients with hepatic steatosis or NASH. Adiponectin antagonizes excess lipid storage in the liver and protects from inflammation and fibrosis. This review aims to give a short survey on NAFLD and the hepatoprotective effects of adiponectin.
MeSH term(s)	Adiponectin/metabolism ; Adipose Tissue/metabolism ; Animals ; Apoptosis/physiology ; Diet ; Exercise ; Fatty Liver/epidemiology ; Fatty Liver/etiology ; Fatty Liver/pathology ; Fatty Liver/physiopathology ; Fibrosis ; Humans ; Non-alcoholic Fatty Liver Disease ; Obesity/complications ; Receptors, Adiponectin/metabolism
Chemical Substances	Adiponectin ; Receptors, Adiponectin
Language	English
Publishing date	2011-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v17.i23.2801
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Article ; Online: Adiponectin receptor binding proteins--recent advances in elucidating adiponectin signalling pathways.

Buechler, Christa / Wanninger, Josef / Neumeier, Markus

FEBS letters

2010 Volume 584, Issue 20, Page(s) 4280–4286

Abstract: Adiponectin whose systemic levels are reduced in obesity-related diseases ameliorates insulin sensitivity and regulates biological processes like apoptosis, proliferation, migration and inflammation. Adiponectin binds to adiponectin receptors, AdipoR1 ... ...

Abstract	Adiponectin whose systemic levels are reduced in obesity-related diseases ameliorates insulin sensitivity and regulates biological processes like apoptosis, proliferation, migration and inflammation. Adiponectin binds to adiponectin receptors, AdipoR1 and AdipoR2, which are ubiquitously expressed. Clathrin-dependent endocytosis of AdipoR1 and adiponectin has been demonstrated to modulate adiponectin bioactivity. Recently, APPL1 has been identified as an AdipoR1 and AdipoR2 binding protein. Furthermore, activated protein kinase C1, endoplasmic reticulum protein 46 and protein kinase CK2β subunit form a complex with AdipoR1. This review summarizes recent studies exploiting heterologous expression of adiponectin receptors in yeast, and the type and function of the recently described adiponectin receptor associated proteins.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Adiponectin/metabolism ; Animals ; Endocytosis ; Humans ; Models, Biological ; Protein Binding ; Receptors, Adiponectin/metabolism ; Signal Transduction
Chemical Substances	ADIPOR1 protein, human ; ADIPOR2 protein, human ; APPL1 protein, human ; Adaptor Proteins, Signal Transducing ; Adiponectin ; Receptors, Adiponectin
Language	English
Publishing date	2010-10-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2010.09.035
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Article ; Online: Adiponectin, a key adipokine in obesity related liver diseases

Christa Buechler / Josef Wanninger / Markus Neumeier

World Journal of Gastroenterology, Vol 17, Iss 23, Pp 2801-

2011 Volume 2811

Abstract	Non-alcoholic fatty liver disease (NAFLD) comprising hepatic steatosis, non-alcoholic steatohepatitis (NASH), and progressive liver fibrosis is considered the most common liver disease in western countries. Fatty liver is more prevalent in overweight than normal-weight people and liver fat positively correlates with hepatic insulin resistance. Hepatic steatosis is regarded as a benign stage of NAFLD but may progress to NASH in a subgroup of patients. Besides liver biopsy no diagnostic tools to identify patients with NASH are available, and no effective treatment has been established. Visceral obesity is a main risk factor for NAFLD and inappropriate storage of triglycerides in adipocytes and higher concentrations of free fatty acids may add to increased hepatic lipid storage, insulin resistance, and progressive liver damage. Most of the adipose tissue-derived proteins are elevated in obesity and may contribute to systemic inflammation and liver damage. Adiponectin is highly abundant in human serum but its levels are reduced in obesity and are even lower in patients with hepatic steatosis or NASH. Adiponectin antagonizes excess lipid storage in the liver and protects from inflammation and fibrosis. This review aims to give a short survey on NAFLD and the hepatoprotective effects of adiponectin.
Keywords	Hepatic steatosis ; Non-alcoholic steatohepatitis ; Adiponectin ; Obesity ; Adipose tissue ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Baishideng Publishing Group Co., Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Lipidomic analysis of the liver identifies changes of major and minor lipid species in adiponectin deficient mice

Wanninger, Josef / Liebisch, Gerhard / Schmitz, Gerd / Bauer, Sabrina / Eisinger, Kristina / Neumeier, Markus / Ouchi, Noriyuki / Walsh, Kenneth / Buechler, Christa

Experimental and molecular pathology. 2013 Apr., v. 94, no. 2

2013

Abstract: Adiponectin protects from hepatic fat storage but adiponectin deficient mice (APN−/−) fed a standard chow do not develop liver steatosis. This indicates that other pathways might be activated to compensate for adiponectin deficiency. An unbiased and ... ...

Abstract	Adiponectin protects from hepatic fat storage but adiponectin deficient mice (APN−/−) fed a standard chow do not develop liver steatosis. This indicates that other pathways might be activated to compensate for adiponectin deficiency. An unbiased and comprehensive screen was performed to identify hepatic alterations of lipid classes in these mice. APN−/− mice had decreased hepatic cholesteryl esters while active SREBP2 and systemic total cholesterol were not altered. Upregulation of cytochromes for bile acid synthesis suggests enhanced biliary cholesterol excretion. Analysis of 37 individual fatty acid species showed reduced stearate whereas total fatty acids were not altered. Total amount of triglycerides and phospholipids were equally abundant. A selective increase of monounsaturated phosphatidylcholine and phosphatidylethanolamine which positively correlate with hepatic and systemic triglycerides with the latter being elevated in APN−/− mice, was identified. Stearoyl-CoA desaturase 1 (SCD1) is involved in the synthesis of monounsaturated fatty acids and despite higher mRNA expression enzyme activity was not enhanced. Glucosylceramide postulated to contribute to liver damage was decreased. This study demonstrates that adiponectin deficiency is associated with hepatic changes in lipid classes in mice fed a standard chow which may protect from liver steatosis.
Keywords	adiponectin ; bile acids ; cholesterol ; cholesteryl esters ; cytochromes ; enzyme activity ; excretion ; fatty acid composition ; fatty liver ; gene expression ; liver ; messenger RNA ; mice ; monounsaturated fatty acids ; phosphatidylcholines ; phosphatidylethanolamines ; stearic acid ; stearoyl-CoA desaturase ; triacylglycerols
Language	English
Dates of publication	2013-04
Size	p. 412-417.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	207655-x
ISSN	1096-0945 ; 0014-4800
ISSN (online)	1096-0945
ISSN	0014-4800
DOI	10.1016/j.yexmp.2012.03.008
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Article ; Online: Annexin A6 protein is downregulated in human hepatocellular carcinoma.

Meier, Elisabeth M / Rein-Fischboeck, Lisa / Pohl, Rebekka / Wanninger, Josef / Hoy, Andrew J / Grewal, Thomas / Eisinger, Kristina / Krautbauer, Sabrina / Liebisch, Gerhard / Weiss, Thomas S / Buechler, Christa

Molecular and cellular biochemistry

2016 Volume 418, Issue 1-2, Page(s) 81–90

Abstract: Annexin A6 (AnxA6) is a lipid-binding protein highly expressed in the liver, regulating cholesterol homeostasis and signaling pathways with a role in liver physiology. Here, we analyzed whether hepatic AnxA6 levels are affected by pathological conditions ...

Abstract	Annexin A6 (AnxA6) is a lipid-binding protein highly expressed in the liver, regulating cholesterol homeostasis and signaling pathways with a role in liver physiology. Here, we analyzed whether hepatic AnxA6 levels are affected by pathological conditions that are associated with liver dysfunction and liver injury. AnxA6 levels in the fatty liver of mice fed a high-fat diet, in ob/ob and db/db animals and in human fatty liver are comparable to controls. Similarly, AnxA6 levels appear unaffected in murine nonalcoholic steatohepatitis and human liver fibrosis. Accordingly, adiponectin, lysophosphatidylcholine, palmitate, and TGFbeta, all of which have a role in liver injury, do not affect AnxA6 expression in human hepatocytes. Likewise, adiponectin and IL8 do not alter AnxA6 levels in primary human hepatic stellate cells. However, in hepatic tumors of 18 patients, AnxA6 protein levels are substantially reduced compared to nontumorous tissues. AnxA6 mRNA is even increased in the tumors suggesting that posttranscriptional mechanisms are involved herein. Lipidomic analysis shows trends toward elevated cholesteryl ester and sphingomyelin in the tumor samples, yet the ratio of tumor to nontumorous AnxA6 does not correlate with these lipids. The current study shows that AnxA6 is specifically reduced in human hepatocellular carcinoma suggesting a role of this protein in hepatocarcinogenesis.
MeSH term(s)	Annexin A6/biosynthesis ; Annexin A6/genetics ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Hep G2 Cells ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics
Chemical Substances	Annexin A6 ; Neoplasm Proteins
Language	English
Publishing date	2016-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-016-2735-9
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Article ; Online: Manganese superoxide dismutase is reduced in the liver of male but not female humans and rodents with non-alcoholic fatty liver disease.

Krautbauer, Sabrina / Eisinger, Kristina / Lupke, Madeleine / Wanninger, Josef / Ruemmele, Petra / Hader, Yvonne / Weiss, Thomas S / Buechler, Christa

Experimental and molecular pathology

2013 Volume 95, Issue 3, Page(s) 330–335

Abstract: Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. Oxidative stress is one of the pathogenic mechanisms contributing to the progression of simple fatty liver to non-alcoholic steatohepatitis (NASH). Manganese superoxide ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. Oxidative stress is one of the pathogenic mechanisms contributing to the progression of simple fatty liver to non-alcoholic steatohepatitis (NASH). Manganese superoxide dismutase (MnSOD) is a mitochondrial antioxidative enzyme and here its expression in rodent and human NAFLD has been analyzed. MnSOD is found reduced in the liver of male mice fed a high fat diet and male ob/ob mice. Female mice fed an atherogenic diet to induce NASH have MnSOD protein levels comparable to controls. In a cohort of 30 controls, 41 patients with fatty liver and 39 NASH patients, MnSOD mRNA is significantly lower in the steatotic and NASH liver. When analyzed in both genders separately reduction of MnSOD expression is only found in males. Here, MnSOD mRNA negatively correlates with steatosis grade but not with extent of fibrosis or inflammation. MnSOD is, however, not reduced in primary human hepatocytes (PHH) treated with palmitate or oleate to increase cellular triglycerides. Lipopolysaccharide, TNF, IL-6, TGFβ and leptin which are all raised in NAFLD do not affect MnSOD in PHH. Adiponectin which attenuates oxidative stress partly by increasing MnSOD in macrophages does not induce MnSOD in PHH. In summary, current data show that hepatic MnSOD is reduced in male but not female humans and rodents with NAFLD.
MeSH term(s)	Adult ; Aged ; Animals ; Apoptosis ; Blotting, Western ; Case-Control Studies ; Cell Proliferation ; Cells, Cultured ; Cohort Studies ; Fatty Liver/enzymology ; Fatty Liver/pathology ; Female ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Leptin/physiology ; Liver/cytology ; Liver/enzymology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Superoxide Dismutase/metabolism ; Young Adult
Chemical Substances	Leptin ; RNA, Messenger ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2013-12
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207655-x
ISSN	1096-0945 ; 0014-4800
ISSN (online)	1096-0945
ISSN	0014-4800
DOI	10.1016/j.yexmp.2013.10.003
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Article ; Online: Lipidomic analysis of the liver identifies changes of major and minor lipid species in adiponectin deficient mice.

Wanninger, Josef / Liebisch, Gerhard / Schmitz, Gerd / Bauer, Sabrina / Eisinger, Kristina / Neumeier, Markus / Ouchi, Noriyuki / Walsh, Kenneth / Buechler, Christa

Experimental and molecular pathology

2012 Volume 94, Issue 2, Page(s) 412–417

Abstract: Adiponectin protects from hepatic fat storage but adiponectin deficient mice (APN-/-) fed a standard chow do not develop liver steatosis. This indicates that other pathways might be activated to compensate for adiponectin deficiency. An unbiased and ... ...

Abstract	Adiponectin protects from hepatic fat storage but adiponectin deficient mice (APN-/-) fed a standard chow do not develop liver steatosis. This indicates that other pathways might be activated to compensate for adiponectin deficiency. An unbiased and comprehensive screen was performed to identify hepatic alterations of lipid classes in these mice. APN-/- mice had decreased hepatic cholesteryl esters while active SREBP2 and systemic total cholesterol were not altered. Upregulation of cytochromes for bile acid synthesis suggests enhanced biliary cholesterol excretion. Analysis of 37 individual fatty acid species showed reduced stearate whereas total fatty acids were not altered. Total amount of triglycerides and phospholipids were equally abundant. A selective increase of monounsaturated phosphatidylcholine and phosphatidylethanolamine which positively correlate with hepatic and systemic triglycerides with the latter being elevated in APN-/- mice, was identified. Stearoyl-CoA desaturase 1 (SCD1) is involved in the synthesis of monounsaturated fatty acids and despite higher mRNA expression enzyme activity was not enhanced. Glucosylceramide postulated to contribute to liver damage was decreased. This study demonstrates that adiponectin deficiency is associated with hepatic changes in lipid classes in mice fed a standard chow which may protect from liver steatosis.
MeSH term(s)	Adiponectin/genetics ; Adiponectin/metabolism ; Animals ; Bile Acids and Salts/metabolism ; Cholesterol/metabolism ; Cholesterol Esters/metabolism ; Cytochromes/metabolism ; Dietary Fats/administration & dosage ; Fatty Acids/metabolism ; Fatty Liver/metabolism ; Glucosylceramides/metabolism ; Lipid Metabolism ; Lipogenesis ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Phosphatidylcholines/metabolism ; Phosphatidylethanolamines/metabolism ; Phospholipids/metabolism ; Stearoyl-CoA Desaturase/genetics ; Stearoyl-CoA Desaturase/metabolism ; Sterol Regulatory Element Binding Protein 2/metabolism ; Triglycerides/metabolism ; Up-Regulation
Chemical Substances	Adiponectin ; Bile Acids and Salts ; Cholesterol Esters ; Cytochromes ; Dietary Fats ; Fatty Acids ; Glucosylceramides ; Phosphatidylcholines ; Phosphatidylethanolamines ; Phospholipids ; Srebf2 protein, mouse ; Sterol Regulatory Element Binding Protein 2 ; Triglycerides ; phosphatidylethanolamine (39382-08-6) ; Cholesterol (97C5T2UQ7J) ; Scd1 protein, mouse (EC 1.14.19.1) ; Stearoyl-CoA Desaturase (EC 1.14.19.1)
Language	English
Publishing date	2012-03-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	207655-x
ISSN	1096-0945 ; 0014-4800
ISSN (online)	1096-0945
ISSN	0014-4800
DOI	10.1016/j.yexmp.2012.03.008
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