LIVIVO - Search results -

Search results

Result 1 - 10 of total 30

Search options

Article ; Online: Functional Regulation of PPARs through Post-Translational Modifications.

Brunmeir, Reinhard / Xu, Feng

International journal of molecular sciences

2018 Volume 19, Issue 6

Abstract: Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily and they are essential regulators of cell differentiation, tissue development, and energy metabolism. Given their central roles in sensing the cellular ... ...

Abstract	Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily and they are essential regulators of cell differentiation, tissue development, and energy metabolism. Given their central roles in sensing the cellular metabolic state and controlling metabolic homeostasis, PPARs became important targets of drug development for the management of metabolic disorders. The function of PPARs is mainly regulated through ligand binding, which induces structural changes, further affecting the interactions with co-activators or co-repressors to stimulate or inhibit their functions. In addition, PPAR functions are also regulated by various Post-translational modifications (PTMs). These PTMs include phosphorylation, SUMOylation, ubiquitination, acetylation, and
MeSH term(s)	Animals ; Humans ; PPAR alpha/genetics ; PPAR alpha/metabolism ; PPAR delta/genetics ; PPAR delta/metabolism ; PPAR gamma/genetics ; PPAR gamma/metabolism ; PPAR-beta/genetics ; PPAR-beta/metabolism ; Peroxisome Proliferator-Activated Receptors/genetics ; Peroxisome Proliferator-Activated Receptors/metabolism ; Protein Processing, Post-Translational/genetics ; Protein Processing, Post-Translational/physiology ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism
Chemical Substances	PPAR alpha ; PPAR delta ; PPAR gamma ; PPAR-beta ; Peroxisome Proliferator-Activated Receptors ; Receptors, Cytoplasmic and Nuclear
Language	English
Publishing date	2018-06-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19061738
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.

Article ; Online: Functional Regulation of PPARs through Post-Translational Modifications

Reinhard Brunmeir / Feng Xu

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

2018 Volume 1738

Abstract	Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily and they are essential regulators of cell differentiation, tissue development, and energy metabolism. Given their central roles in sensing the cellular metabolic state and controlling metabolic homeostasis, PPARs became important targets of drug development for the management of metabolic disorders. The function of PPARs is mainly regulated through ligand binding, which induces structural changes, further affecting the interactions with co-activators or co-repressors to stimulate or inhibit their functions. In addition, PPAR functions are also regulated by various Post-translational modifications (PTMs). These PTMs include phosphorylation, SUMOylation, ubiquitination, acetylation, and O-GlcNAcylation, which are found at numerous modification sites. The addition of these PTMs has a wide spectrum of consequences on protein stability, transactivation function, and co-factor interaction. Moreover, certain PTMs in PPAR proteins have been associated with the status of metabolic diseases. In this review, we summarize the PTMs found on the three PPAR isoforms PPARα, PPARβ/δ, and PPARγ, and their corresponding modifying enzymes. We also discuss the functional roles of these PTMs in regulating metabolic homeostasis and provide a perspective for future research in this intriguing field.
Keywords	nuclear receptors ; PPARα ; PPARγ ; PPARβ/δ ; post-translational modifications ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2018-06-01T00:00:00Z
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: Epigenetic dysregulation of eukaryotic initiation factor 3 subunit E (eIF3E) by lysine methyltransferase REIIBP confers a pro-inflammatory phenotype in t(4;14) myeloma.

Chong, Phyllis S Y / Chooi, Jing Yuan / Lim, Sze Lynn Julia / Chung, Tae-Hoon / Brunmeir, Reinhard / Leow, Aaron Chung Yong / Toh, Sabrina Hui Min / Balan, Kalpnaa / Azaman, Muhamad Irfan Bin / Wu, Zhengwei / Subramaniam, Nagavidya / Vardy, Leah A / Chng, Wee-Joo

Haematologica

2023

Abstract: REIIBP is a lysine methyltransferase aberrantly expressed through alternative promoter usage of NSD2 locus in t(4;14)-translocated multiple myeloma (MM). Clinically, t(4;14) translocation is an adverse prognostic factor found in approximately 15% of MM ... ...

Abstract	REIIBP is a lysine methyltransferase aberrantly expressed through alternative promoter usage of NSD2 locus in t(4;14)-translocated multiple myeloma (MM). Clinically, t(4;14) translocation is an adverse prognostic factor found in approximately 15% of MM patients. The contribution of REIIBP relative to other NSD2 isoforms as a dependency gene in t(4;14)-translocated MM remains to be evaluated. Here, we demonstrated that despite homology with NSD2, REIIBP displayed distinct substrate specificity by preferentially catalyzing H3K4me3 and H3K27me3, with little activity on H3K36me2. Furthermore, REIIBP was regulated through microRNAs by EZH2 in a Dicer-dependent manner, exemplifying a role of REIIBP in SET-mediated H3K27me3. ChIP-sequencing revealed chromatin remodeling characterized by changes in genome-wide and loci-specific occupancy of these opposing histone marks, allowing a bidirectional regulation of its target genes. Transcriptomics indicated that REIIBP induced a pro-inflammatory gene signature through upregulation of TLR7, which in turn led to B-cell receptor (BCR)-independent activation of BTK and driving NFĸB-mediated production of cytokines such as IL-6. Activation of this pathway is targetable using Ibrutinib and partially mitigated bortezomib resistance in an REIIBP xenograft model. Mechanistically, REIIBP upregulated TLR7 through eIF3E, and this relied on eIF3E RNA-binding function instead of its canonical protein synthesis activity, as demonstrated by direct binding to the 3'UTR of TLR7 mRNA. Altogether, we provided a rationale that coexistence of different NSD2 isoforms induced diversified oncogenic programs that should be considered in the strategies for t(4;14)-targeted therapy.
Language	English
Publishing date	2023-12-21
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.283467
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.76: 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: Regulation of Thermogenic Adipocyte Differentiation and Adaptive Thermogenesis Through Histone Acetylation.

Ong, Belinda X / Brunmeir, Reinhard / Zhang, Qiongyi / Peng, Xu / Idris, Muhammad / Liu, Chungang / Xu, Feng

Frontiers in endocrinology

2020 Volume 11, Page(s) 95

Abstract: Over the past decade, the increasing prevalence of obesity and its associated metabolic disorders constitutes one of the most concerning healthcare issues for countries worldwide. In an effort to curb the increased mortality and morbidity derived from ... ...

Abstract	Over the past decade, the increasing prevalence of obesity and its associated metabolic disorders constitutes one of the most concerning healthcare issues for countries worldwide. In an effort to curb the increased mortality and morbidity derived from the obesity epidemic, various therapeutic strategies have been developed by researchers. In the recent years, advances in the field of adipocyte biology have revealed that the thermogenic adipose tissue holds great potential in ameliorating metabolic disorders. Additionally, epigenetic research has shed light on the effects of histone acetylation on adipogenesis and thermogenesis, thereby establishing the essential roles which histone acetyltransferases (HATs) and histone deacetylases (HDACs) play in metabolism and systemic energy homeostasis. In regard to the therapeutic potential of thermogenic adipocytes for the treatment of metabolic diseases, herein, we describe the current state of knowledge of the regulation of thermogenic adipocyte differentiation and adaptive thermogenesis through histone acetylation. Furthermore, we highlight how different HATs and HDACs maintain the epigenetic transcriptional network to mediate the pathogenesis of various metabolic comorbidities. Finally, we provide insights into recent advances of the potential therapeutic applications and development of HAT and HDAC inhibitors to alleviate these pathological conditions.
MeSH term(s)	Acetylation ; Adaptation, Physiological ; Adipocytes/cytology ; Adipocytes/physiology ; Adipogenesis ; Animals ; Cell Differentiation ; Histones/chemistry ; Humans ; Thermogenesis
Chemical Substances	Histones
Language	English
Publishing date	2020-02-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.00095
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: SIRT1 Interacts with and Deacetylates ATP6V1B2 in Mature Adipocytes.

Kim, Sun-Yee / Zhang, Qiongyi / Brunmeir, Reinhard / Han, Weiping / Xu, Feng

PloS one

2015 Volume 10, Issue 7, Page(s) e0133448

Abstract: SIRT1 plays a key role in maintaining metabolic homeostasis in mammals by directly modulating the activities of various transcription factors and metabolic enzymes through lysine deacetylation. White adipose tissue plays a key role in lipid storage and ... ...

Abstract	SIRT1 plays a key role in maintaining metabolic homeostasis in mammals by directly modulating the activities of various transcription factors and metabolic enzymes through lysine deacetylation. White adipose tissue plays a key role in lipid storage and metabolism. To identify novel molecular targets of SIRT1 in fat cells, we used a non-biased proteomic approach. We identified a number of proteins whose acetylation status was significantly affected by SIRT1 modulator treatment in 3T3-L1 adipocytes. Among them, ATP6V1B2, a subunit of the vacuolar (H+)-ATPase, was further shown to be associated with SIRT1 by co-immunoprecipitation assay. Moreover, SIRT1 deacetylates ATP6V1B2 in vitro and in vivo. Taken together, our study demonstrates that ATP6V1B2 is a molecular target of SIRT1 in fat cells and the role of SIRT1 and ATP6V1B2 acetylation in the vacuolar (H+)-ATPase function warrants further investigation.
MeSH term(s)	3T3-L1 Cells ; Acetylation ; Adipocytes/cytology ; Adipocytes/metabolism ; Animals ; Cell Differentiation ; HEK293 Cells ; Humans ; Mice ; Protein Binding ; Proteomics ; Sirtuin 1/metabolism ; Vacuolar Proton-Translocating ATPases/metabolism
Chemical Substances	Sirtuin 1 (EC 3.5.1.-) ; ATP6V1B2 protein, mouse (EC 3.6.1.-) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0133448
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

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.

Details ▾
- Full text online
- Order with fees

Article ; Online: Histone deacetylase HDAC1/HDAC2-controlled embryonic development and cell differentiation.

Brunmeir, Reinhard / Lagger, Sabine / Seiser, Christian

The International journal of developmental biology

2009 Volume 53, Issue 2-3, Page(s) 275–289

Abstract: During development from the fertilized egg to a multicellular organism, cell fate decisions have to be taken and cell lineage or tissue-specific gene expression patterns are created and maintained. These alterations in gene expression occur in the ... ...

Abstract	During development from the fertilized egg to a multicellular organism, cell fate decisions have to be taken and cell lineage or tissue-specific gene expression patterns are created and maintained. These alterations in gene expression occur in the context of chromatin structure and are controlled by chromatin modifying enzymes. Gene disruption studies in different genetic systems have shown an essential role of various histone deacetylases (HDACs) during early development and cellular differentiation. In this review, we focus on the functions of the class I enzymes HDAC1 and HDAC2 during development in different organisms and summarise the current knowledge about their involvement in neurogenesis, myogenesis, haematopoiesis and epithelial cell differentiation.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Embryonic Development/genetics ; Embryonic Development/physiology ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Enzymologic ; Histone Deacetylase 1 ; Histone Deacetylase 2 ; Histone Deacetylases/classification ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Mice ; Models, Biological ; Phylogeny ; Repressor Proteins/classification ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
Chemical Substances	Repressor Proteins ; Hdac1 protein, mouse (EC 3.5.1.98) ; Hdac2 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Histone Deacetylase 2 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2009
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036070-0
ISSN	1696-3547 ; 0214-6282
ISSN (online)	1696-3547
ISSN	0214-6282
DOI	10.1387/ijdb.082649rb
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3202: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Comparative Transcriptomic and Epigenomic Analyses Reveal New Regulators of Murine Brown Adipogenesis.

Brunmeir, Reinhard / Wu, Jingyi / Peng, Xu / Kim, Sun-Yee / Julien, Sofi G / Zhang, Qiongyi / Xie, Wei / Xu, Feng

PLoS genetics

2016 Volume 12, Issue 12, Page(s) e1006474

Abstract: Increasing energy expenditure through brown adipocyte recruitment is a promising approach to combat obesity. We report here the comprehensive profiling of the epigenome and transcriptome throughout the lineage commitment and differentiation of C3H10T1/2 ... ...

Abstract	Increasing energy expenditure through brown adipocyte recruitment is a promising approach to combat obesity. We report here the comprehensive profiling of the epigenome and transcriptome throughout the lineage commitment and differentiation of C3H10T1/2 mesenchymal stem cell line into brown adipocytes. Through direct comparison to datasets from differentiating white adipocytes, we systematically identify stage- and lineage-specific coding genes, lncRNAs and microRNAs. Utilizing chromatin state maps, we also define stage- and lineage-specific enhancers, including super-enhancers, and their associated transcription factor binding motifs and genes. Through these analyses, we found that in brown adipocytes, brown lineage-specific genes are pre-marked by both H3K4me1 and H3K27me3, and the removal of H3K27me3 at the late stage is necessary but not sufficient to promote brown gene expression, while the pre-deposition of H3K4me1 plays an essential role in poising the brown genes for expression in mature brown cells. Moreover, we identify SOX13 as part of a p38 MAPK dependent transcriptional response mediating early brown cell lineage commitment. We also identify and subsequently validate PIM1, SIX1 and RREB1 as novel regulators promoting brown adipogenesis. Finally, we show that SIX1 binds to adipogenic and brown marker genes and interacts with C/EBPα, C/EBPβ and EBF2, suggesting their functional cooperation during adipogenesis.
MeSH term(s)	Adipogenesis/genetics ; Adipose Tissue, Brown/growth & development ; Adipose Tissue, Brown/metabolism ; Animals ; Autoantigens/genetics ; Basic Helix-Loop-Helix Transcription Factors/biosynthesis ; Basic Helix-Loop-Helix Transcription Factors/genetics ; CCAAT-Enhancer-Binding Protein-beta/biosynthesis ; CCAAT-Enhancer-Binding Protein-beta/genetics ; CCAAT-Enhancer-Binding Protein-beta/metabolism ; CCAAT-Enhancer-Binding Proteins/biosynthesis ; CCAAT-Enhancer-Binding Proteins/genetics ; CCAAT-Enhancer-Binding Proteins/metabolism ; Cell Differentiation/genetics ; Cell Lineage/genetics ; DNA-Binding Proteins/biosynthesis ; DNA-Binding Proteins/genetics ; Energy Metabolism/genetics ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Mesenchymal Stromal Cells ; Mice ; Obesity/genetics ; Obesity/metabolism ; Obesity/pathology ; RNA, Long Noncoding/biosynthesis ; Transcription Factors/biosynthesis ; Transcription Factors/genetics ; Transcriptome/genetics
Chemical Substances	Autoantigens ; Basic Helix-Loop-Helix Transcription Factors ; CCAAT-Enhancer-Binding Protein-beta ; CCAAT-Enhancer-Binding Proteins ; CEBPA protein, mouse ; Cebpb protein, mouse ; DNA-Binding Proteins ; Ebf2 protein, mouse ; Homeodomain Proteins ; RNA, Long Noncoding ; Rreb1 protein, mouse ; Six1 protein, mouse ; Sox13 protein, mouse ; Transcription Factors
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1006474
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: SIRT1 Interacts with and Deacetylates ATP6V1B2 in Mature Adipocytes.

Sun-Yee Kim / Qiongyi Zhang / Reinhard Brunmeir / Weiping Han / Feng Xu

PLoS ONE, Vol 10, Iss 7, p e

2015 Volume 0133448

Abstract	SIRT1 plays a key role in maintaining metabolic homeostasis in mammals by directly modulating the activities of various transcription factors and metabolic enzymes through lysine deacetylation. White adipose tissue plays a key role in lipid storage and metabolism. To identify novel molecular targets of SIRT1 in fat cells, we used a non-biased proteomic approach. We identified a number of proteins whose acetylation status was significantly affected by SIRT1 modulator treatment in 3T3-L1 adipocytes. Among them, ATP6V1B2, a subunit of the vacuolar (H+)-ATPase, was further shown to be associated with SIRT1 by co-immunoprecipitation assay. Moreover, SIRT1 deacetylates ATP6V1B2 in vitro and in vivo. Taken together, our study demonstrates that ATP6V1B2 is a molecular target of SIRT1 in fat cells and the role of SIRT1 and ATP6V1B2 acetylation in the vacuolar (H+)-ATPase function warrants further investigation.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
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: Dose imbalance of DYRK1A kinase causes systemic progeroid status in Down syndrome by increasing the un-repaired DNA damage and reducing LaminB1 levels.

Murray, Aoife / Gough, Gillian / Cindrić, Ana / Vučković, Frano / Koschut, David / Borelli, Vincenzo / Petrović, Dražen J / Bekavac, Ana / Plećaš, Ante / Hribljan, Valentina / Brunmeir, Reinhard / Jurić, Julija / Pučić-Baković, Maja / Slana, Anita / Deriš, Helena / Frkatović, Azra / Groet, Jűrgen / O'Brien, Niamh L / Chen, Hong Yu /

Yeap, Yee Jie / Delom, Frederic / Havlicek, Steven / Gammon, Luke / Hamburg, Sarah / Startin, Carla / D'Souza, Hana / Mitrečić, Dinko / Kero, Mijana / Odak, Ljubica / Krušlin, Božo / Krsnik, Željka / Kostović, Ivica / Foo, Jia Nee / Loh, Yuin-Han / Dunn, Norris Ray / de la Luna, Susana / Spector, Tim / Barišić, Ingeborg / Thomas, Michael S C / Strydom, Andre / Franceschi, Claudio / Lauc, Gordan / Krištić, Jasminka / Alić, Ivan / Nižetić, Dean

EBioMedicine

2023 Volume 94, Page(s) 104692

Abstract: Background: People with Down syndrome (DS) show clinical signs of accelerated ageing. Causative mechanisms remain unknown and hypotheses range from the (essentially untreatable) amplified-chromosomal-instability explanation, to potential actions of ... ...

Abstract	Background: People with Down syndrome (DS) show clinical signs of accelerated ageing. Causative mechanisms remain unknown and hypotheses range from the (essentially untreatable) amplified-chromosomal-instability explanation, to potential actions of individual supernumerary chromosome-21 genes. The latter explanation could open a route to therapeutic amelioration if the specific over-acting genes could be identified and their action toned-down. Methods: Biological age was estimated through patterns of sugar molecules attached to plasma immunoglobulin-G (IgG-glycans, an established "biological-ageing-clock") in n = 246 individuals with DS from three European populations, clinically characterised for the presence of co-morbidities, and compared to n = 256 age-, sex- and demography-matched healthy controls. Isogenic human induced pluripotent stem cell (hiPSCs) models of full and partial trisomy-21 with CRISPR-Cas9 gene editing and two kinase inhibitors were studied prior and after differentiation to cerebral organoids. Findings: Biological age in adults with DS is (on average) 18.4-19.1 years older than in chronological-age-matched controls independent of co-morbidities, and this shift remains constant throughout lifespan. Changes are detectable from early childhood, and do not require a supernumerary chromosome, but are seen in segmental duplication of only 31 genes, along with increased DNA damage and decreased levels of LaminB1 in nucleated blood cells. We demonstrate that these cell-autonomous phenotypes can be gene-dose-modelled and pharmacologically corrected in hiPSCs and derived cerebral organoids. Using isogenic hiPSC models we show that chromosome-21 gene DYRK1A overdose is sufficient and necessary to cause excess unrepaired DNA damage. Interpretation: Explanation of hitherto observed accelerated ageing in DS as a developmental progeroid syndrome driven by DYRK1A overdose provides a target for early pharmacological preventative intervention strategies. Funding: Main funding came from the "Research Cooperability" Program of the Croatian Science Foundation funded by the European Union from the European Social Fund under the Operational Programme Efficient Human Resources 2014-2020, Project PZS-2019-02-4277, and the Wellcome Trust Grants 098330/Z/12/Z and 217199/Z/19/Z (UK). All other funding is described in details in the "Acknowledgements".
MeSH term(s)	Adult ; Humans ; Aging ; Cell Differentiation ; Down Syndrome/genetics ; Induced Pluripotent Stem Cells ; Dyrk Kinases
Language	English
Publishing date	2023-07-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2023.104692
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 7090: 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: Dynamic and distinct histone modifications modulate the expression of key adipogenesis regulatory genes.

Zhang, Qiongyi / Ramlee, Muhammad Khairul / Brunmeir, Reinhard / Villanueva, Claudio J / Halperin, Daniel / Xu, Feng

Cell cycle (Georgetown, Tex.)

2012 Volume 11, Issue 23, Page(s) 4310–4322

Abstract: Histone modifications and their modifying enzymes are fundamentally involved in the epigenetic regulation of adipogenesis. This study aimed to define the roles of various histone modifications and their "division of labor" in fat cell differentiation. To ...

Abstract	Histone modifications and their modifying enzymes are fundamentally involved in the epigenetic regulation of adipogenesis. This study aimed to define the roles of various histone modifications and their "division of labor" in fat cell differentiation. To achieve these goals, we examined the distribution patterns of eight core histone modifications at five key adipogenic regulatory genes, Pref-1, C/EBPβ, C/EBPα, PPARγ2 and aP2, during the adipogenesis of C3H 10T1/2 mouse mesenchymal stem cells (MSCs) and 3T3-L1 preadipocytes. We found that the examined histone modifications are globally stable throughout adipogenesis but show distinct and highly dynamic distribution patterns at specific genes. For example, the Pref-1 gene has lower levels of active chromatin markers and significantly higher H3 K27 tri-methylation in MSCs compared with committed preadipocytes; the C/EBPβ gene is enriched in active chromatin markers at its 3'-UTR; the C/EBPα gene is predominantly marked by H3 K27 tri-methylation in adipogenic precursor cells, and this repressive marker decreases dramatically upon induction; the PPARγ2 and aP2 genes show increased histone acetylation on both H3 and H4 tails during adipogenesis. Further functional studies revealed that the decreased level of H3 K27 tri-methylation leads to de-repression of Pref-1 gene, while the increased level of histone acetylation activates the transcription of PPARγ2 and aP2 genes. Moreover, the active histone modification-marked 3'-UTR of C/EBPβ gene was demonstrated as a strong enhancer element by luciferase assay. Our results indicate that histone modifications are gene-specific at adipogenic regulator genes, and they play distinct roles in regulating the transcriptional network during adipogenesis.
MeSH term(s)	3' Untranslated Regions ; 3T3-L1 Cells ; Acetylation ; Adipocytes/cytology ; Adipocytes/metabolism ; Adipogenesis/genetics ; Animals ; CCAAT-Enhancer-Binding Protein-alpha/genetics ; CCAAT-Enhancer-Binding Protein-alpha/metabolism ; CCAAT-Enhancer-Binding Protein-beta/genetics ; CCAAT-Enhancer-Binding Protein-beta/metabolism ; Calcium-Binding Proteins ; Cell Line ; Epigenesis, Genetic ; Fatty Acid-Binding Proteins/genetics ; Fatty Acid-Binding Proteins/metabolism ; Histones/metabolism ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Methylation ; Mice ; PPAR gamma/genetics ; PPAR gamma/metabolism
Chemical Substances	3' Untranslated Regions ; CCAAT-Enhancer-Binding Protein-alpha ; CCAAT-Enhancer-Binding Protein-beta ; Calcium-Binding Proteins ; Dlk1 protein, mouse ; Fabp4 protein, mouse ; Fatty Acid-Binding Proteins ; Histones ; Intercellular Signaling Peptides and Proteins ; PPAR gamma
Language	English
Publishing date	2012-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.22224
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5881: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

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

Full text online

More links

Kategorien

Order via subito

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

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

In stock of ZB MED Cologne/Königswinter

Order via subito