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Article: The Chemical Biology of NO that Regulates Oncogenic Signaling and Metabolism: NOS2 and Its Role in Inflammatory Disease.

Miranda, Katrina M / Ridnour, Lisa A / Cheng, Robert Y S / Wink, David A / Thomas, Douglas D

2023 Volume 28, Issue 1, Page(s) 27–45

Abstract: Nitric oxide (NO) and the enzyme that synthesizes it, nitric oxide synthase 2 (NOS2), have emerged as key players in inflammation and cancer. Expression of NOS2 in tumors has been correlated both with positive outcomes and with poor prognoses. The ... ...

Abstract	Nitric oxide (NO) and the enzyme that synthesizes it, nitric oxide synthase 2 (NOS2), have emerged as key players in inflammation and cancer. Expression of NOS2 in tumors has been correlated both with positive outcomes and with poor prognoses. The chemistry of NO is the major determinate to the biological outcome and the concentration of NO, which can range over five orders of magnitude, is critical in determining which pathways are activated. It is the activation of specific oncogenic and immunological mechanisms that shape the outcome. The kinetics of specific reactions determine the mechanisms of action. In this review, the relevant reactions of NO and related species are discussed with respect to these oncogenic and immunological signals.
MeSH term(s)	Humans ; Neoplasms/genetics ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Signal Transduction
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; NOS2 protein, human (EC 1.14.13.39)
Language	English
Publishing date	2023-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036388-9
ISSN	0893-9675
ISSN	0893-9675
DOI	10.1615/CritRevOncog.2023047302
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2587: Show issues

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Article ; Online: Chronic Exposure to Nitric Oxide Induces P53 Mutations and Malignant-like Features in Human Breast Epithelial Cells.

Cheng, Robert Y S / Burkett, Sandra / Ambs, Stefan / Moody, Terry / Wink, David A / Ridnour, Lisa A

Biomolecules

2023 Volume 13, Issue 2

Abstract: The small endogenous signaling molecule nitric oxide (NO) has been linked with chronic inflammation and cancer. The effects of NO are both concentration and temporally dependent; under some conditions, NO protects against damage caused by reactive oxygen ...

Abstract	The small endogenous signaling molecule nitric oxide (NO) has been linked with chronic inflammation and cancer. The effects of NO are both concentration and temporally dependent; under some conditions, NO protects against damage caused by reactive oxygen species and activates P53 signaling. During chronic inflammation, NO causes DNA damage and inhibits repair proteins. To extend our understanding of the roles of NO during carcinogenesis, we investigated the possible effects of chronic NO exposure on MCF10A breast epithelial cells, as defined by changes in cellular morphology, chromosome/genomic stability, RNA, and protein expression, and altered cell phenotypes. Human MCF10A cells were maintained in varying doses of the NO donor DETANO for three weeks. Distinct patterns of genomic modifications in TP53 and KRAS target genes were detected in NO-treated cells when compared to background mutations. In addition, quantitative real-time PCR demonstrated an increase in the expression of cancer stem cell (CSC) marker CD44 after prolonged exposure to 300 μM DETANO. While similar changes in cell morphology were found in cells exposed to 300-500 μM DETANO, cells cultured in 100 μM DETANO exhibited enhanced motility. In addition, 100 μM NO-treated cells proliferated in serum-free media and selected clonal populations and pooled cells formed colonies in soft agar that were clustered and disorganized. These findings show that chronic exposure to NO generates altered breast epithelial cell phenotypes with malignant characteristics.
MeSH term(s)	Humans ; Female ; Nitric Oxide/metabolism ; Tumor Suppressor Protein p53/metabolism ; Epithelial Cells/metabolism ; Mutation ; Inflammation/metabolism ; Breast Neoplasms/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-02-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13020311
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Article ; Online: Targeting Nitric Oxide: Say NO to Metastasis.

Reddy, Tejaswini P / Glynn, Sharon A / Billiar, Timothy R / Wink, David A / Chang, Jenny C

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 29, Issue 10, Page(s) 1855–1868

Abstract: Utilizing targeted therapies capable of reducing cancer metastasis, targeting chemoresistant and self-renewing cancer stem cells, and augmenting the efficacy of systemic chemo/radiotherapies is vital to minimize cancer-associated mortality. Targeting ... ...

Abstract	Utilizing targeted therapies capable of reducing cancer metastasis, targeting chemoresistant and self-renewing cancer stem cells, and augmenting the efficacy of systemic chemo/radiotherapies is vital to minimize cancer-associated mortality. Targeting nitric oxide synthase (NOS), a protein within the tumor microenvironment, has gained interest as a promising therapeutic strategy to reduce metastatic capacity and augment the efficacy of chemo/radiotherapies in various solid malignancies. Our review highlights the influence of nitric oxide (NO) in tumor progression and cancer metastasis, as well as promising preclinical studies that evaluated NOS inhibitors as anticancer therapies. Lastly, we highlight the prospects and outstanding challenges of using NOS inhibitors in the clinical setting.
MeSH term(s)	Humans ; Nitric Oxide/metabolism ; Neoplasms/drug therapy ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Tumor Microenvironment
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2022-12-15
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-2791
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Zs.A 4223: Show issues

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Article ; Online: NOS2 as an Emergent Player in Progression of Cancer.

Thomas, Douglas D / Wink, David A

Antioxidants & redox signaling

2017 Volume 26, Issue 17, Page(s) 963–965

Abstract: Although the inducible form of nitric oxide synthase (NOS2) was initially shown to be a major player as an antitumor component of the immune response, more recent data have shown that NOS2 expression in cancer cells often predicts poor outcome. Unlike ... ...

Abstract	Although the inducible form of nitric oxide synthase (NOS2) was initially shown to be a major player as an antitumor component of the immune response, more recent data have shown that NOS2 expression in cancer cells often predicts poor outcome. Unlike growth factors associated with a single oncogenic pathway, nitric oxide (NO) has a ubiquitous nature wherein it simultaneously mediates major oncogenic pathways from Akt/PI3K and RAS/ERK to HIF1a and TGFb. These interactive loops perpetuate oncogenic mechanism that leads to increased cancer stemness, proliferation metastasis, chemoresistance, angiogenesis, and immunosuppression. Examination of a wide variety of patient tumors demonstrates that NOS2 expression is >50% for most cancers. In many cases, elevated NOS2 has been shown to predict poor outcome in cancer such as ER- breast cancer, glioma, melanoma, cervical, liver, ovarian, and pancreatic. Taken together, NOS2 may be one of the most powerful biomarker and predictors of poor prognosis and an ideal target for cancer therapy. Antioxid. Redox Signal. 26, 963-965.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Neoplasm Metastasis ; Neoplasms/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Prognosis ; Signal Transduction ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; Nitric Oxide (31C4KY9ESH) ; NOS2 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2017--10
Publishing country	United States
Document type	Editorial ; Introductory Journal Article
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2016.6835
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Zs.A 5488: Show issues

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Article: HNO Protects the Myocardium against Reperfusion Injury, Inhibiting the mPTP Opening via PKCε Activation.

Mancardi, Daniele / Pagliaro, Pasquale / Ridnour, Lisa A / Tocchetti, Carlo G / Miranda, Katrina / Juhaszova, Magdalena / Sollott, Steven J / Wink, David A / Paolocci, Nazareno

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 2

Abstract: Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide ( ... ...

Abstract	Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO
Language	English
Publishing date	2022-02-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11020382
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Article ; Online: Nitric Oxide and Cancer: When to Give and When to Take Away?

Miranda, Katrina M / Ridnour, Lisa A / McGinity, Christopher L / Bhattacharyya, Dana / Wink, David A

Inorganic chemistry

2021 Volume 60, Issue 21, Page(s) 15941–15947

Abstract: The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, ... ...

Abstract	The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment. In this Viewpoint, the current understanding of the concentration, spatial, and temporal dependence of responses to NO is correlated with potential treatment and prevention technologies and strategies.
MeSH term(s)	Nitric Oxide
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2021-10-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1484438-2
ISSN	1520-510X ; 0020-1669
ISSN (online)	1520-510X
ISSN	0020-1669
DOI	10.1021/acs.inorgchem.1c02434
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Article ; Online: International Committee on Systematics of Prokaryotes: subcommittee on the taxonomy of Myxobacteria (Myxococcota). Minutes of the closed online meeting, 21 September 2022.

Hahnke, Richard L / Müller, Rolf / Whitworth, David / Wink, Joachim / Garcia, Ronald

International journal of systematic and evolutionary microbiology

2023 Volume 73, Issue 5

MeSH term(s)	Myxococcales ; Phylogeny ; DNA, Bacterial/genetics ; RNA, Ribosomal, 16S/genetics ; Sequence Analysis, DNA ; Bacterial Typing Techniques ; Base Composition ; Fatty Acids/chemistry ; Bacteria
Chemical Substances	DNA, Bacterial ; RNA, Ribosomal, 16S ; Fatty Acids
Language	English
Publishing date	2023-05-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2002336-4
ISSN	1466-5034 ; 1466-5026
ISSN (online)	1466-5034
ISSN	1466-5026
DOI	10.1099/ijsem.0.005846
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Zs.A 409: Show issues

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Article ; Online: An in vitro tumorigenesis model based on live-cell-generated oxygen and nutrient gradients.

Gilmore, Anne C / Flaherty, Sarah J / Somasundaram, Veena / Scheiblin, David A / Lockett, Stephen J / Wink, David A / Heinz, William F

Communications biology

2021 Volume 4, Issue 1, Page(s) 477

Abstract: The tumor microenvironment (TME) is multi-cellular, spatially heterogenous, and contains cell-generated gradients of soluble molecules. Current cell-based model systems lack this complexity or are difficult to interrogate microscopically. We present a 2D ...

Abstract	The tumor microenvironment (TME) is multi-cellular, spatially heterogenous, and contains cell-generated gradients of soluble molecules. Current cell-based model systems lack this complexity or are difficult to interrogate microscopically. We present a 2D live-cell chamber that approximates the TME and demonstrate that breast cancer cells and macrophages generate hypoxic and nutrient gradients, self-organize, and have spatially varying phenotypes along the gradients, leading to new insights into tumorigenesis.
MeSH term(s)	Animals ; Breast Neoplasms/physiopathology ; Carcinogenesis ; Cell Culture Techniques ; Macrophages/physiology ; Mice ; Tumor Cells, Cultured/physiology ; Tumor Microenvironment
Language	English
Publishing date	2021-04-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-021-01954-0
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Article ; Online: New nitrosyl ruthenium complexes with combined activities for multiple cardiovascular disorders.

Gouveia Júnior, Florêncio Sousa / Silveira, João Alison de Moraes / Holanda, Thais Muratori / Marinho, Aline Diogo / Ridnour, Lisa A / Wink, David A / de Siqueira, Rodrigo José Bezerra / Monteiro, Helena Serra Azul / Sousa, Eduardo Henrique Silva de / Lopes, Luiz Gonzaga de França

Dalton transactions (Cambridge, England : 2003)

2023 Volume 52, Issue 16, Page(s) 5176–5191

Abstract: Nitrosyl ruthenium complexes are promising platforms for nitric oxide (NO) and nitroxyl (HNO) release, which exert their therapeutic application. In this context, we developed two polypyridinic compounds with the general ... ...

Abstract	Nitrosyl ruthenium complexes are promising platforms for nitric oxide (NO) and nitroxyl (HNO) release, which exert their therapeutic application. In this context, we developed two polypyridinic compounds with the general formula
MeSH term(s)	Animals ; Rats ; Coordination Complexes ; Nitric Oxide/chemistry ; Nitrogen Oxides/chemistry ; Ruthenium/chemistry ; Sulfhydryl Compounds/chemistry ; Cardiovascular Diseases
Chemical Substances	Coordination Complexes ; Nitric Oxide (31C4KY9ESH) ; Nitrogen Oxides ; nitroxyl (GFQ4MMS07W) ; Ruthenium (7UI0TKC3U5) ; Sulfhydryl Compounds
Language	English
Publishing date	2023-04-25
Publishing country	England
Document type	Journal Article
ZDB-ID	1472887-4
ISSN	1477-9234 ; 1364-5447 ; 0300-9246 ; 1477-9226
ISSN (online)	1477-9234 ; 1364-5447
ISSN	0300-9246 ; 1477-9226
DOI	10.1039/d3dt00059a
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Article ; Online: Pyruvate dehydrogenase operates as an intramolecular nitroxyl generator during macrophage metabolic reprogramming.

Palmieri, Erika M / Holewinski, Ronald / McGinity, Christopher L / Pierri, Ciro L / Maio, Nunziata / Weiss, Jonathan M / Tragni, Vincenzo / Miranda, Katrina M / Rouault, Tracey A / Andresson, Thorkell / Wink, David A / McVicar, Daniel W

Nature communications

2023 Volume 14, Issue 1, Page(s) 5114

Abstract: M1 macrophages enter a glycolytic state when endogenous nitric oxide (NO) reprograms mitochondrial metabolism by limiting aconitase 2 and pyruvate dehydrogenase (PDH) activity. Here, we provide evidence that NO targets the PDH complex by using lipoate to ...

Abstract	M1 macrophages enter a glycolytic state when endogenous nitric oxide (NO) reprograms mitochondrial metabolism by limiting aconitase 2 and pyruvate dehydrogenase (PDH) activity. Here, we provide evidence that NO targets the PDH complex by using lipoate to generate nitroxyl (HNO). PDH E2-associated lipoate is modified in NO-rich macrophages while the PDH E3 enzyme, also known as dihydrolipoamide dehydrogenase (DLD), is irreversibly inhibited. Mechanistically, we show that lipoate facilitates NO-mediated production of HNO, which interacts with thiols forming irreversible modifications including sulfinamide. In addition, we reveal a macrophage signature of proteins with reduction-resistant modifications, including in DLD, and identify potential HNO targets. Consistently, DLD enzyme is modified in an HNO-dependent manner at Cys
MeSH term(s)	Nitrogen Oxides ; Nitric Oxide ; Macrophages ; Pyruvate Dehydrogenase Complex ; Oxidoreductases ; Pyruvates
Chemical Substances	nitroxyl (GFQ4MMS07W) ; Nitrogen Oxides ; Nitric Oxide (31C4KY9ESH) ; Pyruvate Dehydrogenase Complex ; Oxidoreductases (EC 1.-) ; Pyruvates
Language	English
Publishing date	2023-08-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-40738-4
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