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Article ; Online: Hypoxia Promotes Mitochondrial Complex I Abundance via HIF-1α in Complex III and Complex IV Eficient Cells.

Saldana-Caboverde, Amy / Nissanka, Nadee / Garcia, Sofia / Lombès, Anne / Diaz, Francisca

2020 Volume 9, Issue 10

Abstract: Murine fibroblasts deficient in mitochondria respiratory complexes III (CIII) and IV (CIV) produced by either the ablation ... ...

Abstract	Murine fibroblasts deficient in mitochondria respiratory complexes III (CIII) and IV (CIV) produced by either the ablation of
MeSH term(s)	Alkyl and Aryl Transferases/genetics ; Alkyl and Aryl Transferases/metabolism ; Animals ; Cell Hypoxia/genetics ; Cell Line ; Cytochrome-c Oxidase Deficiency/metabolism ; Doxycycline/pharmacology ; Electron Transport Complex I/metabolism ; Electron Transport Complex III/deficiency ; Electron Transport Complex III/genetics ; Electron Transport Complex III/metabolism ; Electron Transport Complex IV/genetics ; Electron Transport Complex IV/metabolism ; Fibroblasts/metabolism ; Gene Knockout Techniques ; Gene Silencing ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mitochondria/metabolism ; RNA, Small Interfering ; Reactive Oxygen Species/metabolism
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; Membrane Proteins ; RNA, Small Interfering ; Reactive Oxygen Species ; Rieske iron-sulfur protein ; COX10 protein, human (EC 1.9.3.1) ; Electron Transport Complex IV (EC 1.9.3.1) ; Alkyl and Aryl Transferases (EC 2.5.-) ; Electron Transport Complex I (EC 7.1.1.2) ; Electron Transport Complex III (EC 7.1.1.8) ; Doxycycline (N12000U13O)
Language	English
Publishing date	2020-09-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9102197
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Organization of Mitochondrial Supercomplexes is Modulated by Oxidative Stress In Vivo in Mouse Models of Mitochondrial Encephalopathy.

Anwar, Mir R / Saldana-Caboverde, Amy / Garcia, Sofia / Diaz, Francisca

International journal of molecular sciences

2018 Volume 19, Issue 6

Abstract: We examine the effect of oxidative stress on the stability of mitochondrial respiratory complexes and their association into supercomplexes (SCs) in the neuron-specific Rieske iron sulfur protein (RISP) and COX10 knockout (KO) mice. Previously we ... ...

Abstract	We examine the effect of oxidative stress on the stability of mitochondrial respiratory complexes and their association into supercomplexes (SCs) in the neuron-specific Rieske iron sulfur protein (RISP) and COX10 knockout (KO) mice. Previously we reported that these two models display different grades of oxidative stress in distinct brain regions. Using blue native gel electrophoresis, we observed a redistribution of the architecture of SCs in KO mice. Brain regions with moderate levels of oxidative stress (cingulate cortex of both COX10 and RISP KO and hippocampus of the RISP KO) showed a significant increase in the levels of high molecular weight (HMW) SCs. High levels of oxidative stress in the piriform cortex of the RISP KO negatively impacted the stability of CI, CIII and SCs. Treatment of the RISP KO with the mitochondrial targeted antioxidant mitoTEMPO preserved the stability of respiratory complexes and formation of SCs in the piriform cortex and increased the levels of glutathione peroxidase. These results suggest that mild to moderate levels of oxidative stress can modulate SCs into a more favorable architecture of HMW SCs to cope with rising levels of free radicals and cover the energetic needs.
MeSH term(s)	Alkyl and Aryl Transferases/genetics ; Animals ; Brain/metabolism ; Brain/pathology ; Disease Models, Animal ; Electron Transport Complex III/genetics ; Female ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Encephalomyopathies/metabolism ; Mitochondrial Encephalomyopathies/pathology ; Oxidative Stress
Chemical Substances	Membrane Proteins ; Rieske iron-sulfur protein ; Electron Transport Complex III (EC 1.10.2.2) ; Alkyl and Aryl Transferases (EC 2.5.-) ; COX10 protein, mouse (EC 2.5.1.-)
Language	English
Publishing date	2018-05-26
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/ijms19061582
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Article ; Online: Enhanced glycolysis and GSK3 inactivation promote brain metabolic adaptations following neuronal mitochondrial stress.

Garcia, Sofia / Saldana-Caboverde, Amy / Anwar, Mir / Raval, Ami Pravinkant / Nissanka, Nadee / Pinto, Milena / Moraes, Carlos Torres / Diaz, Francisca

Human molecular genetics

2021 Volume 31, Issue 5, Page(s) 692–704

Abstract: We analyzed early brain metabolic adaptations in response to mitochondrial dysfunction in a mouse model of mitochondrial encephalopathy with complex IV deficiency [neuron-specific COX10 knockout (KO)]. In this mouse model, the onset of the mitochondrial ... ...

Abstract	We analyzed early brain metabolic adaptations in response to mitochondrial dysfunction in a mouse model of mitochondrial encephalopathy with complex IV deficiency [neuron-specific COX10 knockout (KO)]. In this mouse model, the onset of the mitochondrial defect did not coincide with immediate cell death, suggesting early adaptive metabolic responses to compensate for the energetic deficit. Metabolomic analysis in the KO mice revealed increased levels of glycolytic and pentose phosphate pathway intermediates, amino acids and lysolipids. Glycolysis was modulated by enhanced activity of glycolytic enzymes, and not by their overexpression, suggesting the importance of post-translational modifications in the adaptive response. Glycogen synthase kinase 3 inactivation was the most upstream regulation identified, implying that it is a key event in this adaptive mechanism. Because neurons are thought not to rely on glycolysis for adenosine triphosphate production in normal conditions, our results indicate that neurons still maintain their ability to upregulate this pathway when under mitochondrial respiration stress.
MeSH term(s)	Alkyl and Aryl Transferases/metabolism ; Animals ; Brain/metabolism ; Glycogen Synthase Kinase 3/metabolism ; Glycolysis/genetics ; Membrane Proteins/metabolism ; Mice ; Mitochondria/genetics ; Mitochondria/metabolism ; Neurons/metabolism
Chemical Substances	Membrane Proteins ; Alkyl and Aryl Transferases (EC 2.5.-) ; COX10 protein, mouse (EC 2.5.1.-) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2021-09-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddab282
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Article ; Online: Hypoxia Promotes Mitochondrial Complex I Abundance via HIF-1α in Complex III and Complex IV Eficient Cells

Amy Saldana-Caboverde / Nadee Nissanka / Sofia Garcia / Anne Lombès / Francisca Diaz

Cells, Vol 9, Iss 2197, p

2020 Volume 2197

Abstract: Murine fibroblasts deficient in mitochondria respiratory complexes III (CIII) and IV (CIV) produced by either the ablation of Uqcrfs1 (encoding for Rieske iron sulfur protein, RISP) or Cox10 (encoding for protoheme IX farnesyltransferase, COX10) genes, ... ...

Abstract	Murine fibroblasts deficient in mitochondria respiratory complexes III (CIII) and IV (CIV) produced by either the ablation of Uqcrfs1 (encoding for Rieske iron sulfur protein, RISP) or Cox10 (encoding for protoheme IX farnesyltransferase, COX10) genes, respectively, showed a pleiotropic effect in complex I (CI). Exposure to 1–5% oxygen increased the levels of CI in both RISP and COX10 KO fibroblasts. De novo assembly of the respiratory complexes occurred at a faster rate and to higher levels in 1% oxygen compared to normoxia in both RISP and COX10 KO fibroblasts. Hypoxia did not affect the levels of assembly of CIII in the COX10 KO fibroblasts nor abrogated the genetic defect impairing CIV assembly. Mitochondrial signaling involving reactive oxygen species (ROS) has been implicated as necessary for HIF-1α stabilization in hypoxia. We did not observe increased ROS production in hypoxia. Exposure to low oxygen levels stabilized HIF-1α and increased CI levels in RISP and COX10 KO fibroblasts. Knockdown of HIF-1α during hypoxic conditions abrogated the beneficial effect of hypoxia on the stability/assembly of CI. These findings demonstrate that oxygen and HIF-1α regulate the assembly of respiratory complexes.
Keywords	mitochondrial respiratory supercomplexes ; oxidative phosphorylation ; hypoxia ; complex I ; complex III ; complex IV ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Roles of endothelin signaling in melanocyte development and melanoma.

Saldana-Caboverde, Amy / Kos, Lidia

Pigment cell & melanoma research

2010 Volume 23, Issue 2, Page(s) 160–170

Abstract: Endothelin (Edn) signaling via the G-coupled, Edn receptor type B (Ednrb) is essential for the development of melanocytes from the neural crest (NC) and has been associated with melanoma progression. Edn3 plays varying roles during melanocyte development, ...

Abstract	Endothelin (Edn) signaling via the G-coupled, Edn receptor type B (Ednrb) is essential for the development of melanocytes from the neural crest (NC) and has been associated with melanoma progression. Edn3 plays varying roles during melanocyte development, promoting the proliferation and self-renewal of NC-derived multi- and bi-potential precursors as well as the survival, proliferation, differentiation and migration of committed melanocyte precursors. Melanocyte differentiation is achieved via the interaction of Ednrb and Kit signaling, with Ednrb being specifically required in the final differentiation step, rather than in the initial specification of melanocytic fate. Ednrb has also been implicated in the de-differentiation of mature melanocytes, a process that takes place during the malignant transformation of these cells. Ednrb was found to be upregulated in melanoma metastases and was shown to alter tumor-host interactions leading to melanoma progression. Antagonists to this receptor were shown to inhibit melanoma cell growth and increase the apoptotic rate of these cells, and to lead to disease stabilization in melanoma patients. Thus, Edn signaling inhibition may prove useful in the treatment of certain types of melanoma.
MeSH term(s)	Animals ; Endothelins/metabolism ; Humans ; Melanocytes/cytology ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/metabolism ; Melanoma/pathology ; Signal Transduction
Chemical Substances	Endothelins
Language	English
Publishing date	2010-02-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/j.1755-148X.2010.00678.x
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Article ; Online: The Organization of Mitochondrial Supercomplexes is Modulated by Oxidative Stress In Vivo in Mouse Models of Mitochondrial Encephalopathy

Mir R. Anwar / Amy Saldana-Caboverde / Sofia Garcia / Francisca Diaz

International Journal of Molecular Sciences, Vol 19, Iss 6, p

2018 Volume 1582

Abstract	We examine the effect of oxidative stress on the stability of mitochondrial respiratory complexes and their association into supercomplexes (SCs) in the neuron-specific Rieske iron sulfur protein (RISP) and COX10 knockout (KO) mice. Previously we reported that these two models display different grades of oxidative stress in distinct brain regions. Using blue native gel electrophoresis, we observed a redistribution of the architecture of SCs in KO mice. Brain regions with moderate levels of oxidative stress (cingulate cortex of both COX10 and RISP KO and hippocampus of the RISP KO) showed a significant increase in the levels of high molecular weight (HMW) SCs. High levels of oxidative stress in the piriform cortex of the RISP KO negatively impacted the stability of CI, CIII and SCs. Treatment of the RISP KO with the mitochondrial targeted antioxidant mitoTEMPO preserved the stability of respiratory complexes and formation of SCs in the piriform cortex and increased the levels of glutathione peroxidase. These results suggest that mild to moderate levels of oxidative stress can modulate SCs into a more favorable architecture of HMW SCs to cope with rising levels of free radicals and cover the energetic needs.
Keywords	mitochondrial supercomplexes ; oxidative phosphorylation ; antioxidants ; COX10 ; Rieske iron sulfur protein ; complex III ; complex IV ; blue native gel electrophoresis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	500
Language	English
Publishing date	2018-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The transcription factors Ets1 and Sox10 interact during murine melanocyte development.

Saldana-Caboverde, Amy / Perera, Erasmo M / Watkins-Chow, Dawn E / Hansen, Nancy F / Vemulapalli, Meghana / Mullikin, James C / Pavan, William J / Kos, Lidia

Developmental biology

2015 Volume 407, Issue 2, Page(s) 300–312

Abstract: Melanocytes, the pigment-producing cells, arise from multipotent neural crest (NC) cells during embryogenesis. Many genes required for melanocyte development were identified using mouse pigmentation mutants. The variable spotting mouse pigmentation ... ...

Abstract	Melanocytes, the pigment-producing cells, arise from multipotent neural crest (NC) cells during embryogenesis. Many genes required for melanocyte development were identified using mouse pigmentation mutants. The variable spotting mouse pigmentation mutant arose spontaneously at the Jackson Laboratory. We identified a G-to-A nucleotide transition in exon 3 of the Ets1 gene in variable spotting, which results in a missense G102E mutation. Homozygous variable spotting mice exhibit sporadic white spotting. Similarly, mice carrying a targeted deletion of Ets1 exhibit hypopigmentation; nevertheless, the function of Ets1 in melanocyte development is unknown. The transcription factor Ets1 is widely expressed in developing organs and tissues, including the NC. In the chick, Ets1 is required for the expression of Sox10, a transcription factor critical for the development of various NC derivatives, including melanocytes. We show that Ets1 is required early for murine NC cell and melanocyte precursor survival in vivo. Given the importance of Ets1 for Sox10 expression in the chick, we investigated a potential genetic interaction between these genes by comparing the hypopigmentation phenotypes of single and double heterozygous mice. The incidence of hypopigmentation in double heterozygotes was significantly greater than in single heterozygotes. The area of hypopigmentation in double heterozygotes was significantly larger than would be expected from the addition of the areas of hypopigmentation of single heterozygotes, suggesting that Ets1 and Sox10 interact synergistically in melanocyte development. Since Sox10 is also essential for enteric ganglia development, we examined the distal colons of Ets1 null mutants and found a significant decrease in enteric innervation, which was exacerbated by Sox10 heterozygosity. At the molecular level, Ets1 was found to activate an enhancer critical for Sox10 expression in NC-derived structures. Furthermore, enhancer activation was significantly inhibited by the variable spotting mutation. Together, these results suggest that Ets1 and Sox10 interact to promote proper melanocyte and enteric ganglia development from the NC.
MeSH term(s)	Amino Acid Sequence ; Animals ; Base Sequence ; Body Patterning ; Cell Count ; Cell Line, Tumor ; Cell Lineage ; Cell Survival ; Embryo, Mammalian/metabolism ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic ; Ganglia/embryology ; Ganglia/metabolism ; Melanocytes/cytology ; Melanocytes/metabolism ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mice, Transgenic ; Molecular Sequence Data ; Mutation, Missense/genetics ; Neural Crest/cytology ; Protein Binding ; Proto-Oncogene Protein c-ets-1/chemistry ; Proto-Oncogene Protein c-ets-1/genetics ; Proto-Oncogene Protein c-ets-1/metabolism ; SOXE Transcription Factors/metabolism ; Transcriptional Activation/genetics
Chemical Substances	Ets1 protein, mouse ; Proto-Oncogene Protein c-ets-1 ; SOXE Transcription Factors ; Sox10 protein, mouse
Language	English
Publishing date	2015-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2015.04.012
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Article: The transcription factors Ets1 and Sox10 interact during murine melanocyte development

Saldana-Caboverde, Amy / Perera, Erasmo M / Watkins-Chow, Dawn E / Hansen, Nancy F / Vemulapalli, Meghana / Mullikin, James C / NISC Comparative Sequencing Program / Pavan, William J / Kos, Lidia

Elsevier Inc. Developmental biology. 2015 Nov. 15, v. 407, no. 2

2015

Abstract	Melanocytes, the pigment-producing cells, arise from multipotent neural crest (NC) cells during embryogenesis. Many genes required for melanocyte development were identified using mouse pigmentation mutants. The variable spotting mouse pigmentation mutant arose spontaneously at the Jackson Laboratory. We identified a G-to-A nucleotide transition in exon 3 of the Ets1 gene in variable spotting, which results in a missense G102E mutation. Homozygous variable spotting mice exhibit sporadic white spotting. Similarly, mice carrying a targeted deletion of Ets1 exhibit hypopigmentation; nevertheless, the function of Ets1 in melanocyte development is unknown. The transcription factor Ets1 is widely expressed in developing organs and tissues, including the NC. In the chick, Ets1 is required for the expression of Sox10, a transcription factor critical for the development of various NC derivatives, including melanocytes. We show that Ets1 is required early for murine NC cell and melanocyte precursor survival in vivo. Given the importance of Ets1 for Sox10 expression in the chick, we investigated a potential genetic interaction between these genes by comparing the hypopigmentation phenotypes of single and double heterozygous mice. The incidence of hypopigmentation in double heterozygotes was significantly greater than in single heterozygotes. The area of hypopigmentation in double heterozygotes was significantly larger than would be expected from the addition of the areas of hypopigmentation of single heterozygotes, suggesting that Ets1 and Sox10 interact synergistically in melanocyte development. Since Sox10 is also essential for enteric ganglia development, we examined the distal colons of Ets1 null mutants and found a significant decrease in enteric innervation, which was exacerbated by Sox10 heterozygosity. At the molecular level, Ets1 was found to activate an enhancer critical for Sox10 expression in NC-derived structures. Furthermore, enhancer activation was significantly inhibited by the variable spotting mutation. Together, these results suggest that Ets1 and Sox10 interact to promote proper melanocyte and enteric ganglia development from the NC.
Keywords	chicks ; embryogenesis ; exons ; ganglia ; heterozygosity ; homozygosity ; innervation ; melanocytes ; mice ; mutants ; mutation ; neural crest ; phenotype ; pigmentation ; tissues ; transcription factors
Language	English
Dates of publication	2015-1115
Size	p. 300-312.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2015.04.012
Database	NAL-Catalogue (AGRICOLA)

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