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Article ; Online: How to kill an ERKsome target: PROTACs deliver the deathblow.

Potts, Malia B

Cell chemical biology

2022 Volume 29, Issue 11, Page(s) 1569–1571

Abstract: In this issue of Cell Chemical Biology, You et al. demonstrate that selective degradation of ERK5 exhibits neither anti-proliferative nor anti-inflammatory activities previously attributed to ERK5 inactivation. This settles a longstanding debate in the ... ...

Abstract	In this issue of Cell Chemical Biology, You et al. demonstrate that selective degradation of ERK5 exhibits neither anti-proliferative nor anti-inflammatory activities previously attributed to ERK5 inactivation. This settles a longstanding debate in the field and highlights the power of PROTACs to investigate non-enzymatic activities of target proteins.
MeSH term(s)	Proteolysis ; Proteins/metabolism
Chemical Substances	Proteins
Language	English
Publishing date	2022-11-16
Publishing country	United States
Document type	Journal Article ; Comment
ISSN	2451-9448
ISSN (online)	2451-9448
DOI	10.1016/j.chembiol.2022.11.002
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Article ; Online: FANCL supports Parkin-mediated mitophagy in a ubiquitin ligase-independent manner.

Beesetti, Swarna / Sirasanagandla, Shyam / Sakurada, Sadie Miki / Pruett-Miller, Shondra M / Sumpter, Rhea / Levine, Beth / Potts, Malia B

Biochimica et biophysica acta. Molecular basis of disease

2022 Volume 1868, Issue 9, Page(s) 166453

Abstract: Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome. The FA proteins have functions in genome maintenance and in the cytoplasmic process of selective autophagy, beyond their canonical roles of repairing DNA interstrand cross- ... ...

Abstract	Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome. The FA proteins have functions in genome maintenance and in the cytoplasmic process of selective autophagy, beyond their canonical roles of repairing DNA interstrand cross-links. FA core complex proteins FANCC, FANCF, FANCL, FANCA, FANCD2, BRCA1 and BRCA2, which previously had no known direct functions outside the nucleus, have recently been implicated in mitophagy. Although mutations in FANCL account for only a very small number of cases in FA families, it plays a key role in the FA pathophysiology and might drive carcinogenesis. Here, we demonstrate that FANCL protein is present in mitochondria in the control and Oligomycin and Antimycin (OA)-treated cells and its ubiquitin ligase activity is not required for its localization to mitochondria. CRISPR/Cas9-mediated knockout of FANCL in HeLa cells overexpressing parkin results in increased sensitivity to mitochondrial stress and defective clearing of damaged mitochondria upon OA treatment. This defect was reversed by the reintroduction of either wild-type FANCL or FANCL(C307A), a mutant lacking ubiquitin ligase activity. To summarize, FANCL protects from mitochondrial stress and supports Parkin-mediated mitophagy in a ubiquitin ligase-independent manner.
MeSH term(s)	Fanconi Anemia/genetics ; Fanconi Anemia/metabolism ; Fanconi Anemia Complementation Group L Protein ; Fanconi Anemia Complementation Group Proteins/genetics ; Fanconi Anemia Complementation Group Proteins/metabolism ; HeLa Cells ; Humans ; Mitophagy ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Fanconi Anemia Complementation Group Proteins ; Ubiquitin ; FANCL protein, human (EC 2.3.2.27) ; Fanconi Anemia Complementation Group L Protein (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-05-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2022.166453
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Article: SRMS correlated with immune infiltration and lung cancer: Allusion for COVID-19

Swarna, Beesetti / Wang, Yong-Dong / Potts, Malia B.

Clinical Cancer Research

Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #840342
Database	COVID19

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Article ; Online: Cell lineage and cell death: Caenorhabditis elegans and cancer research.

Potts, Malia B / Cameron, Scott

Nature reviews. Cancer

2010 Volume 11, Issue 1, Page(s) 50–58

Abstract: Cancer is a complex disease in which cells have circumvented normal restraints on tissue growth and have acquired complex abnormalities in their genomes, posing a considerable challenge to identifying the pathways and mechanisms that drive fundamental ... ...

Abstract	Cancer is a complex disease in which cells have circumvented normal restraints on tissue growth and have acquired complex abnormalities in their genomes, posing a considerable challenge to identifying the pathways and mechanisms that drive fundamental aspects of the malignant phenotype. Genetic analyses of the normal development of the nematode Caenorhabditis elegans have revealed evolutionarily conserved mechanisms through which individual cells establish their fates, and how they make and execute the decision to survive or undergo programmed cell death. The pathways identified through these studies have mammalian counterparts that are co-opted by malignant cells. Effective cancer drugs now target some of these pathways, and more are likely to be discovered.
MeSH term(s)	Animals ; Biomedical Research ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Death ; Cell Lineage ; Disease Models, Animal ; Medical Oncology
Chemical Substances	Caenorhabditis elegans Proteins
Language	English
Publishing date	2010-12-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc2984
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: FUSION-Guided Hypothesis Development Leads to the Identification of N⁶,N⁶-Dimethyladenosine, a Marine-Derived AKT Pathway Inhibitor.

Vaden, Rachel M / Oswald, Nathaniel W / Potts, Malia B / MacMillan, John B / White, Michael A

Marine drugs

2017 Volume 15, Issue 3

Abstract: Chemicals found in nature have evolved over geological time scales to productively interact with biological molecules, and thus represent an effective resource for pharmaceutical development. Marine-derived bacteria are rich sources of chemically diverse, ...

Abstract	Chemicals found in nature have evolved over geological time scales to productively interact with biological molecules, and thus represent an effective resource for pharmaceutical development. Marine-derived bacteria are rich sources of chemically diverse, bioactive secondary metabolites, but harnessing this diversity for biomedical benefit is limited by challenges associated with natural product purification and determination of biochemical mechanism. Using Functional Signature Ontology (FUSION), we report the parallel isolation and characterization of a marine-derived natural product,
MeSH term(s)	Aquatic Organisms/chemistry ; Bacteria/chemistry ; Biological Ontologies ; Biological Products/chemistry ; Biological Products/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Cell Line, Tumor ; Humans ; Lung Neoplasms/drug therapy ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects
Chemical Substances	Biological Products ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2017-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2175190-0
ISSN	1660-3397 ; 1660-3397
ISSN (online)	1660-3397
ISSN	1660-3397
DOI	10.3390/md15030075
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Article ; Online: The nonreceptor tyrosine kinase SRMS inhibits autophagy and promotes tumor growth by phosphorylating the scaffolding protein FKBP51.

Park, Jung Mi / Yang, Seung Wook / Zhuang, Wei / Bera, Asim K / Liu, Yan / Gurbani, Deepak / von Hoyningen-Huene, Sergei J / Sakurada, Sadie Miki / Gan, Haiyun / Pruett-Miller, Shondra M / Westover, Kenneth D / Potts, Malia B

PLoS biology

2021 Volume 19, Issue 6, Page(s) e3001281

Abstract: Nutrient-responsive protein kinases control the balance between anabolic growth and catabolic processes such as autophagy. Aberrant regulation of these kinases is a major cause of human disease. We report here that the vertebrate nonreceptor tyrosine ... ...

Abstract	Nutrient-responsive protein kinases control the balance between anabolic growth and catabolic processes such as autophagy. Aberrant regulation of these kinases is a major cause of human disease. We report here that the vertebrate nonreceptor tyrosine kinase Src-related kinase lacking C-terminal regulatory tyrosine and N-terminal myristylation sites (SRMS) inhibits autophagy and promotes growth in a nutrient-responsive manner. Under nutrient-replete conditions, SRMS phosphorylates the PHLPP scaffold FK506-binding protein 51 (FKBP51), disrupts the FKBP51-PHLPP complex, and promotes FKBP51 degradation through the ubiquitin-proteasome pathway. This prevents PHLPP-mediated dephosphorylation of AKT, causing sustained AKT activation that promotes growth and inhibits autophagy. SRMS is amplified and overexpressed in human cancers where it drives unrestrained AKT signaling in a kinase-dependent manner. SRMS kinase inhibition activates autophagy, inhibits cancer growth, and can be accomplished using the FDA-approved tyrosine kinase inhibitor ibrutinib. This illuminates SRMS as a targetable vulnerability in human cancers and as a new target for pharmacological induction of autophagy in vertebrates.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/pharmacology ; Animals ; Autophagy/drug effects ; Beclin-1/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cellular Senescence/drug effects ; Enzyme Activation/drug effects ; Mice ; Neoplasms/metabolism ; Neoplasms/pathology ; Nuclear Proteins/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation/drug effects ; Phosphotyrosine/metabolism ; Piperidines/pharmacology ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Tacrolimus Binding Proteins/metabolism ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/metabolism
Chemical Substances	Beclin-1 ; Nuclear Proteins ; Piperidines ; ibrutinib (1X70OSD4VX) ; Phosphotyrosine (21820-51-9) ; SRMS protein, human (EC 2.7.1.-) ; src-Family Kinases (EC 2.7.10.2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PHLPP1 protein, human (EC 3.1.3.16) ; Phosphoprotein Phosphatases (EC 3.1.3.16) ; Tacrolimus Binding Proteins (EC 5.2.1.-) ; tacrolimus binding protein 5 (EC 5.2.1.8) ; Adenine (JAC85A2161)
Language	English
Publishing date	2021-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3001281
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Article: Studies of Jatrogossone A as a Reactive Oxygen Species Inducer in Cancer Cellular Models

Ling, Taotao / Bollinger, John / Budhraja, Amit / Craig, Jane / Lang, Walter H / Maier, Julie / Marsico, Travis D / Opferman, Joseph / Potts, Malia B / Rivas, Fatima

Journal of natural products. 2019 May 14, v. 82, no. 5

2019

Abstract: Natural products continue to provide a platform to study biological systems. A bioguided study of cancer cell models led us to a new member of the jatrophane natural products from Jatropha gossypiifolia, which was independently identified and ... ...

Abstract	Natural products continue to provide a platform to study biological systems. A bioguided study of cancer cell models led us to a new member of the jatrophane natural products from Jatropha gossypiifolia, which was independently identified and characterized as jatrogossone A (1). Purification and structure elucidation was performed by column chromatography and high-performance liquid chromatography–mass spectrometry and NMR techniques, and the structure was confirmed via X-ray crystallography. The unique molecular scaffold of jatrogossone A prompted an evaluation of its mode of action. Cytotoxicity assays demonstrated that jatrogossone A displays selective antiproliferative activity against cancer cell models in the low micromolar range with a therapeutic window. Jatrogossone A (1) affects mitochondrial membrane potential (ΔΨm) in a time- and dose-dependent manner. This natural product induces radical oxygen species (ROS) selectively in cancer cellular models, with minimal ROS induction in noncancerous cells. Compound 1 induces ROS in the mitochondria, as determined by colocalization studies, and it induces mitophagy. It promotes also in vitro cell death by causing cell arrest at the G2/M stage, caspase (3/7) activation, and PARP-1 cleavage. The combined findings provide a potential mechanism by which 1 relies on upregulation of mitochondrial ROS to potentiate cytotoxic effects through intracellular signaling.
Keywords	caspases ; cytotoxicity ; dose response ; high performance liquid chromatography ; Jatropha gossypiifolia ; mass spectrometry ; mechanism of action ; membrane potential ; mitochondria ; mitochondrial membrane ; mitophagy ; models ; neoplasm cells ; neoplasms ; nuclear magnetic resonance spectroscopy ; oxygen ; reactive oxygen species ; therapeutics ; toxicity testing ; X-ray diffraction
Language	English
Dates of publication	2019-0514
Size	p. 1301-1311.
Publishing place	American Chemical Society and American Society of Pharmacognosy
Document type	Article
ZDB-ID	304325-3
ISSN	1520-6025 ; 0163-3864
ISSN (online)	1520-6025
ISSN	0163-3864
DOI	10.1021/acs.jnatprod.8b01087
Database	NAL-Catalogue (AGRICOLA)

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Article: MEKK3-MEK5-ERK5 signaling promotes mitochondrial degradation.

Craig, Jane E / Miller, Joseph N / Rayavarapu, Raju R / Hong, Zhenya / Bulut, Gamze B / Zhuang, Wei / Sakurada, Sadie Miki / Temirov, Jamshid / Low, Jonathan A / Chen, Taosheng / Pruett-Miller, Shondra M / Huang, Lily Jun-Shen / Potts, Malia B

Cell death discovery

2020 Volume 6, Page(s) 107

Abstract: Mitochondria are vital organelles that coordinate cellular energy homeostasis and have important roles in cell death. Therefore, the removal of damaged or excessive mitochondria is critical for maintaining proper cellular function. The PINK1-Parkin ... ...

Abstract	Mitochondria are vital organelles that coordinate cellular energy homeostasis and have important roles in cell death. Therefore, the removal of damaged or excessive mitochondria is critical for maintaining proper cellular function. The PINK1-Parkin pathway removes acutely damaged mitochondria through a well-characterized mitophagy pathway, but basal mitochondrial turnover occurs via distinct and less well-understood mechanisms. Here we report that the MEKK3-MEK5-ERK5 kinase cascade is required for mitochondrial degradation in the absence of exogenous damage. We demonstrate that genetic or pharmacological inhibition of the MEKK3-MEK5-ERK5 pathway increases mitochondrial content by reducing lysosome-mediated degradation of mitochondria under basal conditions. We show that the MEKK3-MEK5-ERK5 pathway plays a selective role in basal mitochondrial degradation but is not required for non-selective bulk autophagy, damage-induced mitophagy, or restraint of mitochondrial biogenesis. This illuminates the MEKK3-MEK5-ERK5 pathway as a positive regulator of mitochondrial degradation that acts independently of exogenous mitochondrial stressors.
Language	English
Publishing date	2020-10-20
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-020-00342-7
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Article ; Online: Trithorax, Hox, and TALE-class homeodomain proteins ensure cell survival through repression of the BH3-only gene egl-1.

Potts, Malia B / Wang, David P / Cameron, Scott

Developmental biology

2009 Volume 329, Issue 2, Page(s) 374–385

Abstract: Mutations that aberrantly activate trithorax-group proteins, Hox transcription factors and TALE-class Hox cofactors promote leukemogenesis, but their target genes critical for leukemogenesis remain largely unknown. Through genetic analyses in C. elegans, ...

Abstract	Mutations that aberrantly activate trithorax-group proteins, Hox transcription factors and TALE-class Hox cofactors promote leukemogenesis, but their target genes critical for leukemogenesis remain largely unknown. Through genetic analyses in C. elegans, we find that the trithorax-group gene lin-59 and the TALE-class Hox cofactor unc-62 are required for survival of the VC motor neurons. With the goal of providing a model for how aberrantly active Hox complexes might promote leukemia, we elucidate the mechanism through which these new inhibitors of programmed cell death act: lin-59 maintains transcription of the Hox gene lin-39, while unc-62 promotes nuclear localization of the TALE-class Hox cofactor ceh-20. A LIN-39/CEH-20 complex binds the promoter of the pro-apoptotic BH3-only gene egl-1, repressing its transcription and ensuring survival of the VC neurons. In the absence of this regulatory mechanism, egl-1 is transcribed and the VC neurons die. Furthermore, ectopic expression of the Hox gene lin-39, as occurs for human Hox genes in leukemia, is sufficient to block death of some cells. This work identifies BH3-only pro-apoptotic genes as targets of Hox-mediated repression and suggests that aberrant activation of Hox networks may promote leukemia in part by inhibiting apoptosis.
MeSH term(s)	Apoptosis/genetics ; Caenorhabditis elegans Proteins/genetics ; Cell Survival/physiology ; Electrophoretic Mobility Shift Assay ; Homeodomain Proteins/genetics ; Homeodomain Proteins/physiology ; Humans ; Motor Neurons/cytology ; Mutagenesis, Site-Directed ; Repressor Proteins/genetics ; Transcription, Genetic
Chemical Substances	Caenorhabditis elegans Proteins ; EGL-1 protein, C elegans ; Homeodomain Proteins ; Repressor Proteins
Language	English
Publishing date	2009-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2009.02.022
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Article ; Online: Studies of Jatrogossone A as a Reactive Oxygen Species Inducer in Cancer Cellular Models.

Ling, Taotao / Lang, Walter H / Craig, Jane / Potts, Malia B / Budhraja, Amit / Opferman, Joseph / Bollinger, John / Maier, Julie / Marsico, Travis D / Rivas, Fatima

Journal of natural products

2019 Volume 82, Issue 5, Page(s) 1301–1311

Abstract	Natural products continue to provide a platform to study biological systems. A bioguided study of cancer cell models led us to a new member of the jatrophane natural products from Jatropha gossypiifolia, which was independently identified and characterized as jatrogossone A (1). Purification and structure elucidation was performed by column chromatography and high-performance liquid chromatography-mass spectrometry and NMR techniques, and the structure was confirmed via X-ray crystallography. The unique molecular scaffold of jatrogossone A prompted an evaluation of its mode of action. Cytotoxicity assays demonstrated that jatrogossone A displays selective antiproliferative activity against cancer cell models in the low micromolar range with a therapeutic window. Jatrogossone A (1) affects mitochondrial membrane potential (ΔΨm) in a time- and dose-dependent manner. This natural product induces radical oxygen species (ROS) selectively in cancer cellular models, with minimal ROS induction in noncancerous cells. Compound 1 induces ROS in the mitochondria, as determined by colocalization studies, and it induces mitophagy. It promotes also in vitro cell death by causing cell arrest at the G2/M stage, caspase (3/7) activation, and PARP-1 cleavage. The combined findings provide a potential mechanism by which 1 relies on upregulation of mitochondrial ROS to potentiate cytotoxic effects through intracellular signaling.
MeSH term(s)	Acetylcysteine/pharmacology ; Antineoplastic Agents, Phytogenic/chemistry ; Antineoplastic Agents, Phytogenic/pharmacology ; Antioxidants/pharmacology ; Cell Cycle Checkpoints/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Humans ; Jatropha/chemistry ; Membrane Potential, Mitochondrial/drug effects ; Mitophagy/drug effects ; Neoplasms/metabolism ; Poly (ADP-Ribose) Polymerase-1/drug effects ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Antineoplastic Agents, Phytogenic ; Antioxidants ; Reactive Oxygen Species ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2019-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	304325-3
ISSN	1520-6025 ; 0163-3864
ISSN (online)	1520-6025
ISSN	0163-3864
DOI	10.1021/acs.jnatprod.8b01087
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