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Article ; Online: Sirtuin (SIRT)-1: At the crossroads of puberty and metabolism.

Aylwin, Carlos F / Lomniczi, Alejandro

Current opinion in endocrine and metabolic research

2020 Volume 14, Page(s) 65–72

Abstract: In the arcuate nucleus (ARC) of the hypothalamus reside two neuronal systems in charge of regulating feeding control and reproductive development. The melanocortin system responds to metabolic fluctuations adjusting food intake, whereas kisspeptin ... ...

Abstract	In the arcuate nucleus (ARC) of the hypothalamus reside two neuronal systems in charge of regulating feeding control and reproductive development. The melanocortin system responds to metabolic fluctuations adjusting food intake, whereas kisspeptin neurons are in charge of the excitatory control of Gonadotropin Hormone Releasing Hormone (GnRH) neurons. While it is known that the melanocortin system regulates GnRH neuronal activity, it was recently demonstrated that kisspeptin neurons not only innervate melanocortin neurons, but also play an active role in the control of metabolism. These two neuronal systems are intricately interconnected forming loops of stimulation and inhibition according to metabolic status. Furthermore, intracellular and epigenetic pathways respond to external environmental signals by changing DNA conformation and gene expression. Here we review the role of Silent mating type Information Regulation 2 homologue 1 (Sirt1), a class III NAD+ dependent protein deacetylase, in the ARC control of pubertal development and feeding behavior.
Language	English
Publishing date	2020-06-12
Publishing country	England
Document type	Journal Article
ISSN	2451-9650
ISSN (online)	2451-9650
DOI	10.1016/j.coemr.2020.06.001
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Article ; Online: Polycomb represses a gene network controlling puberty via modulation of histone demethylase Kdm6b expression.

Wright, Hollis / Aylwin, Carlos F / Toro, Carlos A / Ojeda, Sergio R / Lomniczi, Alejandro

Scientific reports

2021 Volume 11, Issue 1, Page(s) 1996

Abstract: Female puberty is subject to Polycomb Group (PcG)-dependent transcriptional repression. Kiss1, a puberty-activating gene, is a key target of this silencing mechanism. Using a gain-of-function approach and a systems biology strategy we now show that EED, ... ...

Abstract	Female puberty is subject to Polycomb Group (PcG)-dependent transcriptional repression. Kiss1, a puberty-activating gene, is a key target of this silencing mechanism. Using a gain-of-function approach and a systems biology strategy we now show that EED, an essential PcG component, acts in the arcuate nucleus of the hypothalamus to alter the functional organization of a gene network involved in the stimulatory control of puberty. A central node of this network is Kdm6b, which encodes an enzyme that erases the PcG-dependent histone modification H3K27me3. Kiss1 is a first neighbor in the network; genes encoding glutamatergic receptors and potassium channels are second neighbors. By repressing Kdm6b expression, EED increases H3K27me3 abundance at these gene promoters, reducing gene expression throughout a gene network controlling puberty activation. These results indicate that Kdm6b repression is a basic mechanism used by PcG to modulate the biological output of puberty-activating gene networks.
MeSH term(s)	Animals ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Humans ; Hypothalamus/growth & development ; Hypothalamus/metabolism ; Jumonji Domain-Containing Histone Demethylases/genetics ; Kisspeptins/genetics ; Neurons/metabolism ; Neurosecretory Systems/growth & development ; Neurosecretory Systems/metabolism ; Polycomb Repressive Complex 2/genetics ; Polycomb-Group Proteins/genetics ; Promoter Regions, Genetic/genetics ; Puberty/genetics ; Puberty/physiology ; Rats ; Systems Biology
Chemical Substances	EED protein, human ; Kiss1 protein, rat ; Kisspeptins ; Polycomb-Group Proteins ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Kdm6b protein, rat (EC 1.14.11.-) ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2021-01-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-81689-4
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Article ; Online: Emerging Genetic and Epigenetic Mechanisms Underlying Pubertal Maturation in Adolescence.

Aylwin, Carlos F / Toro, Carlos A / Shirtcliff, Elizabeth / Lomniczi, Alejandro

Journal of research on adolescence : the official journal of the Society for Research on Adolescence

2019 Volume 29, Issue 1, Page(s) 54–79

Abstract: The adolescent transition begins with the onset of puberty which, upstream in the brain, is initiated by the gonadotropin-releasing hormone (GnRH) pulse generator that activates the release of peripheral sex hormones. Substantial research in human and ... ...

Abstract	The adolescent transition begins with the onset of puberty which, upstream in the brain, is initiated by the gonadotropin-releasing hormone (GnRH) pulse generator that activates the release of peripheral sex hormones. Substantial research in human and animal models has revealed a myriad of cellular networks and heritable genes that control the GnRH pulse generator allowing the individual to begin the process of reproductive competence and sexual maturation. Here, we review the latest knowledge in neuroendocrine pubertal research with emphasis on genetic and epigenetic mechanisms underlying the pubertal transition.
MeSH term(s)	Adolescent ; Adolescent Health ; Animals ; Epigenesis, Genetic ; Female ; Gonadal Steroid Hormones/metabolism ; Humans ; Kisspeptins ; Luteinizing Hormone ; Male ; Neurosecretory Systems/physiology ; Promoter Regions, Genetic/physiology ; Puberty/genetics ; Sexual Maturation/genetics
Chemical Substances	Gonadal Steroid Hormones ; Kisspeptins ; Luteinizing Hormone (9002-67-9)
Language	English
Publishing date	2019-03-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2017369-6
ISSN	1532-7795 ; 1050-8392
ISSN (online)	1532-7795
ISSN	1050-8392
DOI	10.1111/jora.12385
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Article: Characterization of

Farkas, Carlos / Quiroz, Aracelly / Alvarez, Claudia / Hermosilla, Viviana / Aylwin, Carlos F / Lomniczi, Alejandro / Castro, Ariel F / Hepp, Matias I / Pincheira, Roxana

Frontiers in genetics

2021 Volume 12, Page(s) 613808

Abstract: The SALL2 transcription factor, an evolutionarily conserved gene through vertebrates, is involved in normal development and neuronal differentiation. In disease, SALL2 is associated with eye, kidney, and brain disorders, but mainly is related to cancer. ... ...

Abstract	The SALL2 transcription factor, an evolutionarily conserved gene through vertebrates, is involved in normal development and neuronal differentiation. In disease, SALL2 is associated with eye, kidney, and brain disorders, but mainly is related to cancer. Some studies support a tumor suppressor role and others an oncogenic role for SALL2, which seems to depend on the cancer type. An additional consideration is tissue-dependent expression of different SALL2 isoforms. Human and mouse
Language	English
Publishing date	2021-02-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2021.613808
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Article ; Online: Neurobeachin, a promising target for use in the treatment of alcohol use disorder.

Cuzon Carlson, Verginia C / Aylwin, Carlos F / Carlson, Timothy L / Ford, Matthew / Mesnaoui, Houda / Lomniczi, Alejandro / Ferguson, Betsy / Cervera-Juanes, Rita P

Addiction biology

2021 Volume 27, Issue 1, Page(s) e13107

Abstract: Hazardous, heavy drinking increases risk for developing alcohol use disorder (AUD), which affects ~7% of adult Americans. Thus, understanding the molecular mechanisms promoting risk for heavy drinking is essential to developing more effective AUD ... ...

Abstract	Hazardous, heavy drinking increases risk for developing alcohol use disorder (AUD), which affects ~7% of adult Americans. Thus, understanding the molecular mechanisms promoting risk for heavy drinking is essential to developing more effective AUD pharmacotherapies than those currently approved by the FDA. Using genome-wide bisulfate sequencing, we identified DNA methylation (DNAm) signals within the nucleus accumbens core (NAcC) that differentiate nonheavy and heavy ethanol-drinking rhesus macaques. One differentially DNAm region (D-DMR) located within the gene neurobeachin (NBEA), which promotes synaptic membrane protein trafficking, was hypermethylated in heavy drinking macaques. A parallel study identified a similar NBEA D-DMR in human NAcC that distinguished alcoholic and nonalcoholic individuals. To investigate the role of NBEA in heavy ethanol drinking, we engineered a viral vector carrying a short hairpin RNA (shRNA) to reduce the expression of NBEA. Using two murine models of ethanol consumption: 4 days of drinking-in-the-dark and 4 weeks of chronic intermittent access, the knockdown of NBEA expression did not alter average ethanol consumption in either model. However, it did lead to a significant increase in the ethanol preference ratio. Following withdrawal, whole-cell patch clamp electrophysiological experiments revealed that Nbea knockdown led to an increase in spontaneous excitatory postsynaptic current amplitude with no alteration in spontaneous inhibitory postsynaptic currents, suggesting a specific role of NBEA in trafficking of glutamatergic receptors. Together, our findings suggest that NBEA could be targeted to modulate the preference for alcohol use.
MeSH term(s)	Adult ; Aged ; Alcohol Drinking/genetics ; Alcoholism/genetics ; Animals ; Carrier Proteins/genetics ; DNA Methylation/drug effects ; Humans ; Macaca mulatta ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Nerve Tissue Proteins/genetics ; Nucleus Accumbens/drug effects
Chemical Substances	Carrier Proteins ; NBEA protein, human ; Nerve Tissue Proteins
Language	English
Publishing date	2021-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1324314-7
ISSN	1369-1600 ; 1355-6215
ISSN (online)	1369-1600
ISSN	1355-6215
DOI	10.1111/adb.13107
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Article ; Online: Trithorax dependent changes in chromatin landscape at enhancer and promoter regions drive female puberty.

Toro, Carlos A / Wright, Hollis / Aylwin, Carlos F / Ojeda, Sergio R / Lomniczi, Alejandro

Nature communications

2018 Volume 9, Issue 1, Page(s) 57

Abstract: Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons. Here we identify two members of the Trithorax group (TrxG) of modifiers, mixed-lineage leukemia 1 (MLL1), and 3 (MLL3), ...

Abstract	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons. Here we identify two members of the Trithorax group (TrxG) of modifiers, mixed-lineage leukemia 1 (MLL1), and 3 (MLL3), as central components of an activating epigenetic machinery that dynamically counteracts PcG repression. Preceding puberty, MLL1 changes the chromatin configuration at the promoters of Kiss1 and Tac3, two genes required for puberty to occur, from repressive to permissive. Concomitantly, MLL3 institutes a chromatin structure that changes the functional status of a Kiss1 enhancer from poised to active. RNAi-mediated, ARC-specific Mll1 knockdown reduced Kiss1 and Tac3 expression, whereas CRISPR-Cas9-directed epigenome silencing of the Kiss1 enhancer selectively reduced Kiss1 activity. Both interventions delay puberty and disrupt reproductive cyclicity. Our results demonstrate that an epigenetic switch from transcriptional repression to activation is crucial to the regulatory mechanism controlling the timing of mammalian puberty.
MeSH term(s)	Animals ; CRISPR-Cas Systems ; Chromatin ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental/genetics ; Gene Knockdown Techniques ; Gene Silencing ; Hypothalamus/metabolism ; Kisspeptins/genetics ; Macaca mulatta ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Polycomb-Group Proteins/metabolism ; Promoter Regions, Genetic ; Puberty/genetics ; Rats ; Rats, Sprague-Dawley ; Tachykinins/genetics
Chemical Substances	Chromatin ; Kisspeptins ; Mllt1 protein, rat ; Polycomb-Group Proteins ; Tachykinins ; Myeloid-Lymphoid Leukemia Protein (149025-06-9)
Language	English
Publishing date	2018-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-017-02512-1
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Article ; Online: Sex-specific pubertal and metabolic regulation of Kiss1 neurons via Nhlh2.

Leon, Silvia / Talbi, Rajae / McCarthy, Elizabeth A / Ferrari, Kaitlin / Fergani, Chrysanthi / Naule, Lydie / Choi, Ji Hae / Carroll, Rona S / Kaiser, Ursula B / Aylwin, Carlos F / Lomniczi, Alejandro / Navarro, Víctor M

eLife

2021 Volume 10

Abstract: Hypothalamic Kiss1 neurons control gonadotropin-releasing hormone release through the secretion of kisspeptin. Kiss1 neurons serve as a nodal center that conveys essential regulatory cues for the attainment and maintenance of reproductive function. ... ...

Abstract	Hypothalamic Kiss1 neurons control gonadotropin-releasing hormone release through the secretion of kisspeptin. Kiss1 neurons serve as a nodal center that conveys essential regulatory cues for the attainment and maintenance of reproductive function. Despite this critical role, the mechanisms that control kisspeptin synthesis and release remain largely unknown. Using Drop-Seq data from the arcuate nucleus of adult mice and in situ hybridization, we identified Nescient Helix-Loop-Helix 2 (
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/physiology ; Cell Line ; Chromatin ; DNA/genetics ; Estradiol/pharmacology ; Female ; Fertility ; Gene Expression Regulation/drug effects ; Immunoprecipitation ; Kisspeptins/genetics ; Kisspeptins/metabolism ; Kisspeptins/pharmacology ; Leptin/pharmacology ; Luteinizing Hormone/metabolism ; Male ; Mice ; Mice, Knockout ; Neurons/physiology ; Peptide Fragments/pharmacology ; Polymerase Chain Reaction/methods ; Sex Factors ; Sexual Maturation/physiology ; Substance P/analogs & derivatives ; Substance P/pharmacology
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Chromatin ; KISS1 protein, human ; Kiss1 protein, mouse ; Kisspeptins ; Leptin ; Nhlh2 protein, mouse ; Peptide Fragments ; senktide (106128-89-6) ; Substance P (33507-63-0) ; Estradiol (4TI98Z838E) ; Luteinizing Hormone (9002-67-9) ; DNA (9007-49-2)
Language	English
Publishing date	2021-09-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.69765
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Article ; Online: MKRN3 inhibits the reproductive axis through actions in kisspeptin-expressing neurons.

Abreu, Ana Paula / Toro, Carlos A / Song, Yong Bhum / Navarro, Victor M / Bosch, Martha A / Eren, Aysegul / Liang, Joy N / Carroll, Rona S / Latronico, Ana Claudia / Rønnekleiv, Oline K / Aylwin, Carlos F / Lomniczi, Alejandro / Ojeda, Sergio / Kaiser, Ursula B

The Journal of clinical investigation

2020 Volume 130, Issue 8, Page(s) 4486–4500

Abstract: The identification of loss-of-function mutations in MKRN3 in patients with central precocious puberty in association with the decrease in MKRN3 expression in the medial basal hypothalamus of mice before the initiation of reproductive maturation suggests ... ...

Abstract	The identification of loss-of-function mutations in MKRN3 in patients with central precocious puberty in association with the decrease in MKRN3 expression in the medial basal hypothalamus of mice before the initiation of reproductive maturation suggests that MKRN3 is acting as a brake on gonadotropin-releasing hormone (GnRH) secretion during childhood. In the current study, we investigated the mechanism by which MKRN3 prevents premature manifestation of the pubertal process. We showed that, as in mice, MKRN3 expression is high in the hypothalamus of rats and nonhuman primates early in life, decreases as puberty approaches, and is independent of sex steroid hormones. We demonstrated that Mkrn3 is expressed in Kiss1 neurons of the mouse hypothalamic arcuate nucleus and that MKRN3 repressed promoter activity of human KISS1 and TAC3, 2 key stimulators of GnRH secretion. We further showed that MKRN3 has ubiquitinase activity, that this activity is reduced by MKRN3 mutations affecting the RING finger domain, and that these mutations compromised the ability of MKRN3 to repress KISS1 and TAC3 promoter activity. These results indicate that MKRN3 acts to prevent puberty initiation, at least in part, by repressing KISS1 and TAC3 transcription and that this action may involve an MKRN3-directed ubiquitination-mediated mechanism.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Arcuate Nucleus of Hypothalamus/pathology ; Female ; Gene Expression Regulation ; Gonadotropin-Releasing Hormone/genetics ; Gonadotropin-Releasing Hormone/metabolism ; HEK293 Cells ; Humans ; Kisspeptins/biosynthesis ; Kisspeptins/genetics ; Male ; Mice ; Neurokinin B/genetics ; Neurokinin B/metabolism ; Neurons/metabolism ; Neurons/pathology ; Promoter Regions, Genetic ; Puberty, Precocious/genetics ; Puberty, Precocious/metabolism ; Puberty, Precocious/pathology ; Rats, Sprague-Dawley ; Transcription, Genetic ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	KISS1 protein, human ; Kiss1 protein, mouse ; Kiss1 protein, rat ; Kisspeptins ; TAC3 protein, human ; Gonadotropin-Releasing Hormone (33515-09-2) ; Neurokinin B (86933-75-7) ; MKRN3 protein, human (EC 2.3.2.27) ; Mkrn3 protein, mouse (EC 2.3.2.27) ; Mkrn3 protein, rat (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2020-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI136564
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Article: Data on SVCT2 transporter expression and localization in cancer cell lines and tissues

Roa, Francisco J. / Peña, Eduardo / Inostroza, Eveling / Sotomayor, Kirsty / González, Mauricio / Gutierrez-Castro, Francisco A. / Maurin, Michelle / Sweet, Karen / Labrousse, Claire / Gatica, Marcell / Aylwin, Carlos F. / Mendoza, Pamela / Maldonado, Mafalda / Delgado, Carolina / Madariaga, Jaime / Panes, Jessica / Silva-Grecchi, Tiare / Concha, Ilona I. / Moraga-Cid, Gustavo /

Reyes, Alejandro M. / Muñoz-Montesino, Carola / Vera, Juan Carlos / Rivas, Coralia I.

Data in Brief. 2019 Aug., v. 25

2019

Abstract: The data presented in this article are related to the research paper entitled “Increased expression of mitochondrial sodium-coupled ascorbic acid transporter-2 (mitSVCT2) as a central feature in breast cancer”, available in Free Radical Biology and ... ...

Abstract	The data presented in this article are related to the research paper entitled “Increased expression of mitochondrial sodium-coupled ascorbic acid transporter-2 (mitSVCT2) as a central feature in breast cancer”, available in Free Radical Biology and Medicine Journal [1]. In this article, we examined the SVCT2 transporter expression in various breast cancer cell lines using RT-PCR and Western blot assays. In addition, we analyzed the subcellular localization of SVCT2 by immunofluorescence colocalization assays and cellular fractionation experiments. Finally, an analysis of different cancer tissue microarrays immunostained for SVCT2 and imaged by The Human Protein Atlas (https://www.proteinatlas.org) is presented.
Keywords	Western blotting ; ascorbic acid ; breast neoplasms ; fluorescent antibody technique ; fractionation ; mitochondria ; neoplasm cells
Language	English
Dates of publication	2019-08
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2019.103972
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Article ; Online: Data on SVCT2 transporter expression and localization in cancer cell lines and tissues.

Roa, Francisco J / Peña, Eduardo / Inostroza, Eveling / Sotomayor, Kirsty / González, Mauricio / Gutierrez-Castro, Francisco A / Maurin, Michelle / Sweet, Karen / Labrousse, Claire / Gatica, Marcell / Aylwin, Carlos F / Mendoza, Pamela / Maldonado, Mafalda / Delgado, Carolina / Madariaga, Jaime / Panes, Jessica / Silva-Grecchi, Tiare / Concha, Ilona I / Moraga-Cid, Gustavo /

Reyes, Alejandro M / Muñoz-Montesino, Carola / Vera, Juan Carlos / Rivas, Coralia I

Data in brief

2019 Volume 25, Page(s) 103972

Abstract: The data presented in this article are related to the research paper entitled "Increased expression of mitochondrial sodium-coupled ascorbic acid transporter-2 (mitSVCT2) as a central feature in breast cancer", available in Free Radical Biology and ... ...

Abstract	The data presented in this article are related to the research paper entitled "Increased expression of mitochondrial sodium-coupled ascorbic acid transporter-2 (mitSVCT2) as a central feature in breast cancer", available in Free Radical Biology and Medicine Journal [1]. In this article, we examined the SVCT2 transporter expression in various breast cancer cell lines using RT-PCR and Western blot assays. In addition, we analyzed the subcellular localization of SVCT2 by immunofluorescence colocalization assays and cellular fractionation experiments. Finally, an analysis of different cancer tissue microarrays immunostained for SVCT2 and imaged by The Human Protein Atlas (https://www.proteinatlas.org) is presented.
Language	English
Publishing date	2019-05-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409 ; 2352-3409
ISSN (online)	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2019.103972
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