LIVIVO - Search results -

Search results

Result 1 - 10 of total 57

Search options

Article: A Researcher at an AREA Grant-Eligible Institution.

Tuma, Pamela L

Cellular and molecular gastroenterology and hepatology

2016 Volume 2, Issue 3, Page(s) 260–262

Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Editorial
ISSN	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2016.03.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Micromechanical Study of Hyperacetylated Nucleosomes Using Single Molecule Transverse Magnetic Tweezers.

Gaire, Santosh / Fabian, Roberto L / Adhikari, Raghabendra / Tuma, Pamela L / Pegg, Ian L / Sarkar, Abhijit

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: Nucleosomes are stable complexes of DNA and histone proteins that are essential for the proper functioning of the genome. These structures must be unwrapped and disassembled for processes such as gene expression, replication, and repair. Histone post- ... ...

Abstract	Nucleosomes are stable complexes of DNA and histone proteins that are essential for the proper functioning of the genome. These structures must be unwrapped and disassembled for processes such as gene expression, replication, and repair. Histone post-translational modifications (PTMs) are known to play a significant role in regulating the structural changes of nucleosomes. However, the underlying mechanisms by which these modifications function remain unclear. In this study, we report the results of single molecule micromanipulation experiments on DNA-protein complexes composed of hyperacetylated histone proteins using transverse magnetic tweezers. The experiments were conducted by pre-extending
MeSH term(s)	Nucleosomes ; Histones/metabolism ; DNA/chemistry ; Nanotechnology ; Magnetic Phenomena
Chemical Substances	Nucleosomes ; Histones ; DNA (9007-49-2)
Language	English
Publishing date	2023-03-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076188
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Alcohol-induced tubulin post-translational modifications directly alter hepatic protein trafficking.

Adhikari, Raghabendra / Mitra, Ramyajit / Bennett, Robert G / McVicker, Benita L / Tuma, Pamela L

Hepatology communications

2023 Volume 7, Issue 4

Abstract: Background: Chronic ethanol exposure leads to enhanced protein acetylation and acetaldehyde adduction. Of the multitude of proteins that are modified on ethanol administration, tubulin is among the best studied. However, an open question is whether ... ...

Abstract	Background: Chronic ethanol exposure leads to enhanced protein acetylation and acetaldehyde adduction. Of the multitude of proteins that are modified on ethanol administration, tubulin is among the best studied. However, an open question is whether these modifications are observed in patient samples. Both modifications have also been implicated in promoting alcohol-induced defects in protein trafficking, but whether they do so directly is also unanswered. Methods and results: We first confirmed that tubulin was hyperacetylated and acetaldehyde-adducted in the livers from ethanol-exposed individuals to a similar extent as observed in the livers from ethanol-fed animals and hepatic cells. Livers from individuals with nonalcohol-associated fatty liver showed modest increases in tubulin acetylation, whereas nonalcohol-associated fibrotic human and mouse livers showed virtually no tubulin modifications. We also asked whether tubulin acetylation or acetaldehyde adduction can directly explain the known alcohol-induced defects in protein trafficking. Acetylation was induced by overexpressing the α-tubulin-specific acetyltransferase, αTAT1, whereas adduction was induced by directly adding acetaldehyde to cells. Both αTAT1 overexpression and acetaldehyde treatment significantly impaired plus-end (secretion) and minus-end (transcytosis)-directed microtubule-dependent trafficking and clathrin-mediated endocytosis. Each modification led to similar levels of impairment as observed in ethanol-treated cells. The levels of impairment by either modification showed no dose dependence or no additive effects suggesting that substoichiometric tubulin modifications lead to altered protein trafficking and that lysines are not selectively modified. Conclusions: These results not only confirm that enhanced tubulin acetylation is observed in human livers but that it is most relevant to alcohol-induced injury. Because these tubulin modifications are associated with altered protein trafficking that alters proper hepatic function, we propose that changing the cellular acetylation levels or scavenging free aldehydes are feasible strategies for treating alcohol-associated liver disease.
MeSH term(s)	Mice ; Animals ; Humans ; Tubulin/metabolism ; Ethanol/pharmacology ; Liver Diseases, Alcoholic/metabolism ; Acetaldehyde/metabolism ; Protein Processing, Post-Translational ; Protein Transport
Chemical Substances	Tubulin ; Ethanol (3K9958V90M) ; Acetaldehyde (GO1N1ZPR3B)
Language	English
Publishing date	2023-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1097/HC9.0000000000000103
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Micromechanical Study of Hyperacetylated Nucleosomes Using Single Molecule Transverse Magnetic Tweezers

Santosh Gaire / Roberto L. Fabian / Raghabendra Adhikari / Pamela L. Tuma / Ian L. Pegg / Abhijit Sarkar

International Journal of Molecular Sciences, Vol 24, Iss 6188, p

2023 Volume 6188

Abstract	Nucleosomes are stable complexes of DNA and histone proteins that are essential for the proper functioning of the genome. These structures must be unwrapped and disassembled for processes such as gene expression, replication, and repair. Histone post-translational modifications (PTMs) are known to play a significant role in regulating the structural changes of nucleosomes. However, the underlying mechanisms by which these modifications function remain unclear. In this study, we report the results of single molecule micromanipulation experiments on DNA–protein complexes composed of hyperacetylated histone proteins using transverse magnetic tweezers. The experiments were conducted by pre-extending λ -DNA with a force less than 4 <semantics> pN </semantics> before introducing hyperacetylated histones into the sample chamber. The DNA shortened as the histones formed complexes with it and the nucleosome arrays were then exposed to increasing tension, resulting in quantized changes in the DNA’s extension with step sizes of (integral multiples of) ~50 <semantics> nm </semantics> . We also compared results of experiments using PTM histones and native histones with data collected for both types of histones for the same force ranges (2–80 <semantics> pN </semantics> ) and loading rates. Our data show that hyperacetylated nucleosomes require an unbinding force of around ~2.5 <semantics> pN </semantics> , which is similar to that required for native histones. Moreover, we identified clear differences between the step-size distributions of native and hyperacetylated histones and found that in contrast to tethers reconstituted with native histones, the majority of nucleosomes in tethers compacted with hyperacetylated histones underwent disassembly at forces significantly lower than 6 <semantics> pN </semantics> .
Keywords	single molecule micromanipulation techniques ; transverse magnetic tweezers ; horizontal magnetic tweezers ; proteins ; DNA–protein complexes ; DNA–histone interactions ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	612
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: The GTP-bound and Sumoylated Form of the rab17 Small Molecular Weight GTPase Selectively Binds Syntaxin 2 in Polarized Hepatic WIF-B Cells.

Striz, Anneliese C / Tuma, Pamela L

The Journal of biological chemistry

2016 Volume 291, Issue 18, Page(s) 9721–9732

Abstract: A major focus for our laboratory is identifying the molecules and mechanisms that regulate polarized apical protein sorting in hepatocytes, the major epithelial cells of the liver. These trafficking pathways are regulated, in part, by small molecular ... ...

Abstract	A major focus for our laboratory is identifying the molecules and mechanisms that regulate polarized apical protein sorting in hepatocytes, the major epithelial cells of the liver. These trafficking pathways are regulated, in part, by small molecular weight rab GTPases. We chose to investigate rab17, whose expression is restricted to polarized epithelial cells, is enriched in liver, and has been implicated in regulating basolateral to apical transcytosis. To initiate our studies, we generated three recombinant adenoviruses expressing wild type, constitutively active (GTP bound), or dominant-negative (GDP bound) rab17. Immunoblotting revealed rab17 immunoreactive species at 25 kDa (the predicted rab17 molecular mass) and 40 kDa. We determined that mono-sumoylation of the 25-kDa rab17 is responsible for the shift in molecular mass, and that rab17 prenylation is required for sumoylation. We further determined that sumoylation selectively promotes interactions with syntaxin 2 (but not syntaxins 3 or 4) and that these interactions are nucleotide dependent. Furthermore, a K68R-mutated rab17 led to the redistribution of syntaxin 2 and 5' nucleotidase from the apical membrane to subapical puncta, whereas multidrug resistance protein 2 distributions were not changed. Together these data are consistent with the proposed role of rab17 in vesicle fusion with the apical plasma membrane and further implicate sumoylation as an important mediator of protein-protein interactions. The selectivity in syntaxin binding and apical protein redistribution further suggests that rab17 and syntaxin 2 mediate fusion of transcytotic vesicles at the apical surface.
MeSH term(s)	Amino Acid Substitution ; Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Cell Line ; Liver/cytology ; Liver/immunology ; Mice ; Mutation, Missense ; Sumoylation/genetics ; Sumoylation/immunology ; Syntaxin 1/genetics ; Syntaxin 1/immunology ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/immunology
Chemical Substances	Syntaxin 1 ; Rab17 protein, mouse (EC 3.6.1.-) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2016-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M116.723353
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.108: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The Altered Hepatic Tubulin Code in Alcoholic Liver Disease.

Groebner, Jennifer L / Tuma, Pamela L

Biomolecules

2015 Volume 5, Issue 3, Page(s) 2140–2159

Abstract: The molecular mechanisms that lead to the progression of alcoholic liver disease have been actively examined for decades. Because the hepatic microtubule cytoskeleton supports innumerable cellular processes, it has been the focus of many such mechanistic ...

Abstract	The molecular mechanisms that lead to the progression of alcoholic liver disease have been actively examined for decades. Because the hepatic microtubule cytoskeleton supports innumerable cellular processes, it has been the focus of many such mechanistic studies. It has long been appreciated that α-tubulin is a major target for modification by highly reactive ethanol metabolites and reactive oxygen species. It is also now apparent that alcohol exposure induces post-translational modifications that are part of the natural repertoire, mainly acetylation. In this review, the modifications of the "tubulin code" are described as well as those adducts by ethanol metabolites. The potential cellular consequences of microtubule modification are described with a focus on alcohol-induced defects in protein trafficking and enhanced steatosis. Possible mechanisms that can explain hepatic dysfunction are described and how this relates to the onset of liver injury is discussed. Finally, we propose that agents that alter the cellular acetylation state may represent a novel therapeutic strategy for treating liver disease.
MeSH term(s)	Animals ; Humans ; Liver Diseases, Alcoholic/metabolism ; Microtubules/metabolism ; Protein Processing, Post-Translational ; Tubulin/metabolism
Chemical Substances	Tubulin
Language	English
Publishing date	2015-09-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom5032140
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A Serine/Threonine Kinase 16-Based Phospho-Proteomics Screen Identifies WD Repeat Protein-1 As A Regulator Of Constitutive Secretion.

López-Coral, Alfonso / Striz, Anneliese C / Tuma, Pamela L

Scientific reports

2018 Volume 8, Issue 1, Page(s) 13049

Abstract: The plasma membrane of polarized hepatocytes is functionally divided into two domains: the apical and basolateral. Our focus is to define the molecular basis of polarized protein sorting of newly-synthesized membrane and secretory proteins in WIF-B cells, ...

Abstract	The plasma membrane of polarized hepatocytes is functionally divided into two domains: the apical and basolateral. Our focus is to define the molecular basis of polarized protein sorting of newly-synthesized membrane and secretory proteins in WIF-B cells, an excellent model system for polarized hepatocytes. We determined that MAL2 (myelin and lymphocyte protein 2) and its binding partner, serine/threonine kinase 16 (STK16) regulate basolateral constitutive secretion. Because STK16 is a constitutively active kinase, we reasoned that constitutively phosphorylated substrates must participate in constitutive secretion. To identify either STK16 substrates or other proteins that regulate constitutive secretion, we took a proteomics approach. Post-nuclear supernatants from cells expressing wild type or a kinase-dead (E202A) STK16 were separated on 2D gels and immunoblotted with antibodies against phospho-serine/threonine residues. Sixteen spots were identified from E202A-expressing cells that reproducibly displayed decreased immunoreactivity. From these spots, 28 proteins were identified as possible STK16 substrates. Out of these 28 possible substrates, 25% of them encode predicted STK16 phosphorylation consensus sites, with WD repeat containing protein-1 (WDR1) encoding two such sites. Based on this finding and on the finding that actin remodeling is required for hepatic secretion, we further confirmed that WDR1 is a phosphoprotein that regulates secretion.
MeSH term(s)	Animals ; Cell Line ; Electrophoresis, Gel, Two-Dimensional ; Hepatocytes/metabolism ; Humans ; Immunoblotting ; Microfilament Proteins/metabolism ; Myelin and Lymphocyte-Associated Proteolipid Proteins/metabolism ; Phosphoproteins/analysis ; Protein Transport ; Protein-Serine-Threonine Kinases/metabolism ; Proteome/analysis ; Rats ; Transcription Factors/metabolism
Chemical Substances	MAL2 protein, human ; Microfilament Proteins ; Myelin and Lymphocyte-Associated Proteolipid Proteins ; Phosphoproteins ; Proteome ; Transcription Factors ; WDR1 protein, human ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; STK16 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2018-08-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-31426-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: MAL2-Induced Actin-Based Protrusion Formation is Anti-Oncogenic in Hepatocellular Carcinoma.

López-Coral, Alfonso / Del Vecchio, Gianna-Jade / Chahine, Joeffrey J / Kallakury, Bhaskar V / Tuma, Pamela L

Cancers

2020 Volume 12, Issue 2

Abstract: Recent studies report that the polarity gene myelin and lymphocyte protein 2 (MAL2), is overexpressed in multiple human carcinomas largely at the transcript level. Because chromosome 8q24 amplification (where MAL2 resides) is associated with ... ...

Abstract	Recent studies report that the polarity gene myelin and lymphocyte protein 2 (MAL2), is overexpressed in multiple human carcinomas largely at the transcript level. Because chromosome 8q24 amplification (where MAL2 resides) is associated with hepatocellular- and cholangio-carcinomas, we examined MAL2 protein expression in these human carcinoma lesions and adjacent benign tissue using immunohistochemistry. For comparison, we analyzed renal cell carcinomas that are not associated with chromosome 8q24 amplification. Surprisingly, we found that MAL2 protein levels were decreased in the malignant tissues compared to benign in all three carcinomas, suggesting MAL2 expression may be anti-oncogenic. Consistent with this conclusion, we determined that endogenously overexpressed MAL2 in HCC-derived Hep3B cells or exogenously expressed MAL2 in hepatoma-derived Clone 9 cells (that lack endogenous MAL2) promoted actin-based protrusion formation with a reciprocal decrease in invadopodia. MAL2 overexpression also led to decreased cell migration, invasion and proliferation (to a more modest extent) while loss of MAL2 expression reversed the phenotypes. Mutational analysis revealed that a putative Ena/VASP homology 1 recognition site confers the MAL2-phenotype suggesting its role in tumor suppression involves actin remodeling. To reconcile decreased MAL2 protein expression in human carcinomas and its anti-oncogenic phenotypes with increased transcript levels, we propose a transcriptional regulatory model for MAL2 transient overexpression.
Language	English
Publishing date	2020-02-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12020422
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Alcohol-induced microtubule acetylation leads to the accumulation of large, immobile lipid droplets.

Groebner, Jennifer L / Girón-Bravo, Marlene T / Rothberg, Mia L / Adhikari, Raghabendra / Tuma, Dean J / Tuma, Pamela L

American journal of physiology. Gastrointestinal and liver physiology

2019 Volume 317, Issue 4, Page(s) G373–G386

Abstract: Although steatosis (fatty liver) is a clinically well-described early stage of alcoholic liver disease, surprisingly little is known about how it promotes hepatotoxicity. We have shown that ethanol consumption leads to microtubule hyperacetylation that ... ...

Abstract	Although steatosis (fatty liver) is a clinically well-described early stage of alcoholic liver disease, surprisingly little is known about how it promotes hepatotoxicity. We have shown that ethanol consumption leads to microtubule hyperacetylation that can explain ethanol-induced defects in protein trafficking. Because almost all steps of the lipid droplet life cycle are microtubule dependent and because microtubule acetylation promotes adipogenesis, we examined droplet dynamics in ethanol-treated cells. In WIF-B cells treated with ethanol and/or oleic acid (a fatty acid associated with the "Western" diet), we found that ethanol dramatically increased lipid droplet numbers and led to the formation of large, peripherally located droplets. Enhanced droplet formation required alcohol dehydrogenase-mediated ethanol metabolism, and peripheral droplet distributions required intact microtubules. We also determined that ethanol-induced microtubule acetylation led to impaired droplet degradation. Live-cell imaging revealed that droplet motility was microtubule dependent and that droplets were virtually stationary in ethanol-treated cells. To determine more directly whether microtubule hyperacetylation could explain impaired droplet motility, we overexpressed the tubulin-specific acetyltransferase αTAT1 to promote microtubule acetylation in the absence of alcohol. Droplet motility was impaired in αTAT1-expressing cells but to a lesser extent than in ethanol-treated cells. However, in both cases, the large immotile droplets (but not small motile ones) colocalized with dynein and dynactin (but not kinesin), implying that altered droplet-motor microtubule interactions may explain altered dynamics. These studies further suggest that modulating cellular acetylation is a potential strategy for treating alcoholic liver disease.
MeSH term(s)	Acetylation ; Acetyltransferases/metabolism ; Alcohol Dehydrogenase/metabolism ; Cell Line ; Central Nervous System Depressants/pharmacology ; Dynactin Complex/metabolism ; Dyneins/metabolism ; Ethanol/pharmacology ; Humans ; Lipid Droplets/drug effects ; Lipid Droplets/metabolism ; Lipid Metabolism/drug effects ; Microtubule Proteins/metabolism ; Microtubules/drug effects ; Microtubules/metabolism ; Oleic Acids/pharmacology
Chemical Substances	Central Nervous System Depressants ; Dynactin Complex ; Microtubule Proteins ; Oleic Acids ; Ethanol (3K9958V90M) ; Alcohol Dehydrogenase (EC 1.1.1.1) ; Acetyltransferases (EC 2.3.1.-) ; ATAT1 protein, human (EC 2.3.1.108) ; Dyneins (EC 3.6.4.2)
Language	English
Publishing date	2019-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00026.2019
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Spermidine Prevents Ethanol and Lipopolysaccharide-Induced Hepatic Injury in Mice.

Adhikari, Raghabendra / Shah, Ruchi / Reyes-Gordillo, Karina / Arellanes-Robledo, Jaime / Cheng, Ying / Ibrahim, Joseph / Tuma, Pamela L

Molecules (Basel, Switzerland)

2021 Volume 26, Issue 6

Abstract: To date, there is no effective treatment for alcoholic liver disease, despite its prevalence world-wide. Because alcohol consumption is associated with oxidative stress-induced liver injury and pro-inflammatory responses, naturally occurring antioxidants ...

Abstract	To date, there is no effective treatment for alcoholic liver disease, despite its prevalence world-wide. Because alcohol consumption is associated with oxidative stress-induced liver injury and pro-inflammatory responses, naturally occurring antioxidants and/or anti-inflammatories may be potential therapeutics. Spermidine is an abundant, ubiquitous polyamine that has been found to display strong antioxidant and anti-inflammatory properties. To further investigate whether spermidine is an effective intervention for alcohol-induced liver disease, we examined its hepatoprotective properties using a two-hit, chronic ethanol and acute lipopolysaccharide (LPS)-induced mouse model of liver injury. We determined that spermidine administration prevented ethanol and LPS-induced increases in liver injury using plasma ALT as a readout. Furthermore, histological analysis of tissue from control and treated animals revealed that the pathology associated with ethanol and LPS treatment was prevented in mice additionally treated with spermidine. As predicted, spermidine also prevented ethanol and LPS-induced oxidative stress by decreasing the levels of both reactive oxygen species (ROS) and lipid peroxidation. We further determined that spermidine treatment prevented the nuclear translocation of nuclear factor κB (NFκB) by blocking the phosphorylation of the inhibitory protein, IκB, thereby preventing expression of pro-inflammatory cytokines. Finally, by measuring expression of known markers of hepatic stellate cell activation and monitoring collagen deposition, we observed that spermidine also prevented alcohol and LPS-induced hepatic fibrosis. Together, our results indicate that spermidine is an antioxidant thereby conferring anti-inflammatory and anti-fibrotic effects associated with alcoholic liver injury.
MeSH term(s)	Animals ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Chemical and Drug Induced Liver Injury/prevention & control ; Ethanol/toxicity ; Female ; Lipopolysaccharides/toxicity ; Liver/metabolism ; Liver/pathology ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Liver Diseases, Alcoholic/prevention & control ; Mice ; Spermidine/pharmacology
Chemical Substances	Lipopolysaccharides ; Ethanol (3K9958V90M) ; Spermidine (U87FK77H25)
Language	English
Publishing date	2021-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules26061786
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.MO 81: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito