LIVIVO - Search results -

Search results

Result 1 - 10 of total 18

Search options

Article: A laboratory-based, low-energy, multi-modal x-ray microscope with user-defined resolution.

Esposito, Michela / Massimi, Lorenzo / Buchanan, Ian / Ferrara, Joseph D / Endrizzi, Marco / Olivo, Alessandro

2022 Volume 120, Issue 23, Page(s) 234101

Abstract: We report on the development of a low-energy x-ray phase-based microscope using intensity-modulation masks for single-shot retrieval of three contrast channels: transmission, refraction, and ultra-small-angle scattering or dark field. The retrieval ... ...

Abstract	We report on the development of a low-energy x-ray phase-based microscope using intensity-modulation masks for single-shot retrieval of three contrast channels: transmission, refraction, and ultra-small-angle scattering or dark field. The retrieval method is based on beam tracking, an incoherent and phase-based imaging approach. We demonstrate that the spatial resolution of this imaging system does not depend on focal spot size nor detector pixel pitch, as opposed to conventional and propagation-based x-ray imaging, and it is only dependent on the mask aperture size. This result enables the development of a multi-resolution microscope where multi-scale samples can be explored on different length scales by adjusting only the mask aperture size, without other modifications. Additionally, we show an extended capability of the system to resolve periodic structures below the resolution limit imposed by the mask apertures, which potentially extends dark-field imaging beyond its conventional use.
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1469436-0
ISSN	1077-3118 ; 0003-6951
ISSN (online)	1077-3118
ISSN	0003-6951
DOI	10.1063/5.0082968
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: FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.

Pawlikowska, Patrycja / Delestré, Laure / Gregoricchio, Sebastian / Oppezzo, Alessia / Esposito, Michela / Diop, M' Boyba / Rosselli, Filippo / Guillouf, Christel

Oncogene

2023 Volume 42, Issue 37, Page(s) 2764–2775

Abstract: Leukaemia is caused by the clonal evolution of a cell that accumulates mutations/genomic rearrangements, allowing unrestrained cell growth. However, recent identification of leukaemic mutations in the blood cells of healthy individuals revealed that ... ...

Abstract	Leukaemia is caused by the clonal evolution of a cell that accumulates mutations/genomic rearrangements, allowing unrestrained cell growth. However, recent identification of leukaemic mutations in the blood cells of healthy individuals revealed that additional events are required to expand the mutated clones for overt leukaemia. Here, we assessed the functional consequences of deleting the Fanconi anaemia A (Fanca) gene, which encodes a DNA damage response protein, in Spi1 transgenic mice that develop preleukaemic syndrome. FANCA loss increases SPI1-associated disease penetrance and leukaemic progression without increasing the global mutation load of leukaemic clones. However, a high frequency of leukaemic FANCA-depleted cells display heterozygous activating mutations in known oncogenes, such as Kit or Nras, also identified but at low frequency in FANCA-WT mice with preleukaemic syndrome, indicating that FANCA counteracts the emergence of oncogene mutated leukaemic cells. A unique transcriptional signature is associated with the leukaemic status of FANCA-depleted cells, leading to activation of MDM4, NOTCH and Wnt/β-catenin pathways. We show that NOTCH signalling improves the proliferation capacity of FANCA-deficient leukaemic cells. Collectively, our observations indicate that loss of the FANC pathway, known to control genetic instability, fosters the expansion of leukaemic cells carrying oncogenic mutations rather than mutation formation. FANCA loss may contribute to this leukaemogenic progression by reprogramming transcriptomic landscape of the cells.
MeSH term(s)	Animals ; Mice ; Heterozygote ; Leukemia/genetics ; Mutation ; Oncogenes/genetics ; Fanconi Anemia Complementation Group A Protein/genetics
Chemical Substances	Fanca protein, mouse ; Fanconi Anemia Complementation Group A Protein
Language	English
Publishing date	2023-08-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02800-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2218: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Technical note: Cartilage imaging with sub-cellular resolution using a laboratory-based phase-contrast x-ray microscope.

Esposito, Michela / Astolfo, Alberto / Cipiccia, Silvia / Jones, Charlotte Maughan / Savvidis, Savvas / Ferrara, Joseph D / Endrizzi, Marco / Dudhia, Jayesh / Olivo, Alessandro

Medical physics

2023 Volume 50, Issue 10, Page(s) 6130–6136

Abstract: Background: Microscopic imaging of cartilage is a key tool for the study and development of treatments for osteoarthritis. When cellular and sub-cellular resolution is required, histology remains the gold standard approach, albeit limited by the lack of ...

Abstract	Background: Microscopic imaging of cartilage is a key tool for the study and development of treatments for osteoarthritis. When cellular and sub-cellular resolution is required, histology remains the gold standard approach, albeit limited by the lack of volumetric information as well as by processing artifacts. Cartilage imaging with the sub-cellular resolution has only been demonstrated in the synchrotron environment. Purpose: To provide a proof-of-concept demonstration of the capability of a laboratory-based x-ray phase-contrast microscope to resolve sub-cellular features in a cartilage sample. Methods: This work is based on a laboratory-based x-ray microscope using intensity-modulation masks. The structured nature of the beam, resulting from the mask apertures, allows the retrieval of three contrast channels, namely, transmission, refraction and dark-field, with resolution depending only on the mask aperture width. An ex vivo equine cartilage sample was imaged with the x-ray microscope and results were validated with synchrotron tomography and histology. Results: Individual chondrocytes, that is, cells responsible for cartilage formation, could be detected with the laboratory-based microscope. The complementarity of the three retrieved contrast channels allowed the detection of sub-cellular features in the chondrocytes. Conclusions: We provide the first proof-of-concept of imaging cartilage tissue with sub-cellular resolution using a laboratory-based x-ray microscope.
MeSH term(s)	Animals ; Horses ; X-Rays ; Radiography ; Cartilage/diagnostic imaging ; Microscopy ; Laboratories
Language	English
Publishing date	2023-07-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	188780-4
ISSN	2473-4209 ; 0094-2405
ISSN (online)	2473-4209
ISSN	0094-2405
DOI	10.1002/mp.16599
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1210: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Contribution of ERMES subunits to mature peroxisome abundance.

Esposito, Michela / Hermann-Le Denmat, Sylvie / Delahodde, Agnès

PloS one

2019 Volume 14, Issue 3, Page(s) e0214287

Abstract: Eukaryotic organelles share different components and establish physical contacts to communicate throughout the cell. One of the best-recognized examples of such interplay is the metabolic cooperation and crosstalk between mitochondria and peroxisomes, ... ...

Abstract	Eukaryotic organelles share different components and establish physical contacts to communicate throughout the cell. One of the best-recognized examples of such interplay is the metabolic cooperation and crosstalk between mitochondria and peroxisomes, both organelles being functionally and physically connected and linked to the endoplasmic reticulum (ER). In Saccharomyces cerevisiae, mitochondria are linked to the ER by the ERMES complex that facilitates inter-organelle calcium and phospholipid exchanges. Recently, peroxisome-mitochondria contact sites (PerMit) have been reported and among Permit tethers, one component of the ERMES complex (Mdm34) was shown to interact with the peroxin Pex11, suggesting that the ERMES complex or part of it may be involved in two membrane contact sites (ER-mitochondria and peroxisome- mitochondria). This opens the possibility of exchanges between these three membrane compartments. Here, we investigated in details the role of each ERMES subunit on peroxisome abundance. First, we confirmed previous studies from other groups showing that absence of Mdm10 or Mdm12 leads to an increased number of mature peroxisomes. Secondly, we showed that this is not simply due to respiratory function defect, mitochondrial DNA (mtDNA) loss or mitochondrial network alteration. Finally, we present evidence that the contribution of ERMES subunits Mdm10 and Mdm12 to peroxisome number involves two different mechanisms.
MeSH term(s)	Calcium/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Peroxisomes/metabolism ; Phospholipids/metabolism ; Point Mutation ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	MDM10 protein, S cerevisiae ; MMM1 protein, S cerevisiae ; Mdm12 protein, S cerevisiae ; Membrane Proteins ; Mitochondrial Proteins ; Phospholipids ; Saccharomyces cerevisiae Proteins ; mdm34 protein, S cerevisiae ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-03-25
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.0214287
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: CHIPIN: ChIP-seq inter-sample normalization based on signal invariance across transcriptionally constant genes.

Polit, Lélia / Kerdivel, Gwenneg / Gregoricchio, Sebastian / Esposito, Michela / Guillouf, Christel / Boeva, Valentina

BMC bioinformatics

2021 Volume 22, Issue 1, Page(s) 407

Abstract: Background: Multiple studies rely on ChIP-seq experiments to assess the effect of gene modulation and drug treatments on protein binding and chromatin structure. However, most methods commonly used for the normalization of ChIP-seq binding intensity ... ...

Abstract	Background: Multiple studies rely on ChIP-seq experiments to assess the effect of gene modulation and drug treatments on protein binding and chromatin structure. However, most methods commonly used for the normalization of ChIP-seq binding intensity signals across conditions, e.g., the normalization to the same number of reads, either assume a constant signal-to-noise ratio across conditions or base the estimates of correction factors on genomic regions with intrinsically different signals between conditions. Inaccurate normalization of ChIP-seq signal may, in turn, lead to erroneous biological conclusions. Results: We developed a new R package, CHIPIN, that allows normalizing ChIP-seq signals across different conditions/samples when spike-in information is not available, but gene expression data are at hand. Our normalization technique is based on the assumption that, on average, no differences in ChIP-seq signals should be observed in the regulatory regions of genes whose expression levels are constant across samples/conditions. In addition to normalizing ChIP-seq signals, CHIPIN provides as output a number of graphs and calculates statistics allowing the user to assess the efficiency of the normalization and qualify the specificity of the antibody used. In addition to ChIP-seq, CHIPIN can be used without restriction on open chromatin ATAC-seq or DNase hypersensitivity data. We validated the CHIPIN method on several ChIP-seq data sets and documented its superior performance in comparison to several commonly used normalization techniques. Conclusions: The CHIPIN method provides a new way for ChIP-seq signal normalization across conditions when spike-in experiments are not available. The method is implemented in a user-friendly R package available on GitHub: https://github.com/BoevaLab/CHIPIN.
MeSH term(s)	Chromatin ; Chromatin Immunoprecipitation ; Chromatin Immunoprecipitation Sequencing ; Protein Binding ; Sequence Analysis, DNA
Chemical Substances	Chromatin
Language	English
Publishing date	2021-08-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-021-04320-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Freestanding high-aspect-ratio gold masks for low-energy, phase-based x-ray microscopy.

Makarova, Olga V / Divan, Ralu / Moldovan, Nicolaie / Czaplewski, David A / Esposito, Michela / Endrizzi, Marco / Tang, Cha-Mei / Ferrara, Joseph D / Olivo, Alessandro

Nanotechnology

2022 Volume 34, Issue 4

Abstract: High-resolution, x-ray phase contrast microscopy, a key technique with promising potential in biomedical imaging and diagnostics, is based on narrow-slit high-aspect-ratio gold gratings. We present the development, fabrication details, and experimental ... ...

Abstract	High-resolution, x-ray phase contrast microscopy, a key technique with promising potential in biomedical imaging and diagnostics, is based on narrow-slit high-aspect-ratio gold gratings. We present the development, fabrication details, and experimental testing of the freestanding 10
Language	English
Publishing date	2022-11-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1362365-5
ISSN	1361-6528 ; 0957-4484
ISSN (online)	1361-6528
ISSN	0957-4484
DOI	10.1088/1361-6528/ac9b5f
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.

Gregoricchio, Sebastian / Polit, Lélia / Esposito, Michela / Berthelet, Jérémy / Delestré, Laure / Evanno, Emilie / Diop, M'Boyba / Gallais, Isabelle / Aleth, Hanna / Poplineau, Mathilde / Zwart, Wilbert / Rosenbauer, Frank / Rodrigues-Lima, Fernando / Duprez, Estelle / Boeva, Valentina / Guillouf, Christel

Nucleic acids research

2022 Volume 50, Issue 14, Page(s) 7938–7958

Abstract: Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms ... ...

Abstract	Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.
MeSH term(s)	Acetylation ; Animals ; Chromatin/genetics ; Histone Deacetylase 1/genetics ; Leukemia, Erythroblastic, Acute/genetics ; Mice ; Polycomb Repressive Complex 2/genetics ; Polycomb Repressive Complex 2/metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics ; Trans-Activators/genetics
Chemical Substances	Chromatin ; Proto-Oncogene Proteins ; Trans-Activators ; proto-oncogene protein Spi-1 ; Polycomb Repressive Complex 2 (EC 2.1.1.43) ; Hdac1 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98)
Language	English
Publishing date	2022-07-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac613
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1067: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Integrity of the Saccharomyces cerevisiae Rpn11 protein is critical for formation of proteasome storage granules (PSG) and survival in stationary phase.

Saunier, Rémy / Esposito, Michela / Dassa, Emmanuel P / Delahodde, Agnès

PloS one

2013 Volume 8, Issue 8, Page(s) e70357

Abstract: Decline of proteasome activity has been reported in mammals, flies and yeasts during aging. In the yeast Saccharomyces cerevisiae, the reduction of proteolysis in stationary phase is correlated with disassembly of the 26S proteasomes into their 20S and ... ...

Abstract	Decline of proteasome activity has been reported in mammals, flies and yeasts during aging. In the yeast Saccharomyces cerevisiae, the reduction of proteolysis in stationary phase is correlated with disassembly of the 26S proteasomes into their 20S and 19S subcomplexes. However a recent report showed that upon entry into the stationary phase, proteasome subunits massively re-localize from the nucleus into mobile cytoplasmic structures called proteasome storage granules (PSGs). Whether proteasome subunits in PSG are assembled into active complexes remains an open question that we addressed in the present study. We showed that a particular mutant of the RPN11 gene (rpn11-m1), encoding a proteasome lid subunit already known to exhibit proteasome assembly/stability defect in vitro, is unable to form PSGs and displays a reduced viability in stationary phase. Full restoration of long-term survival and PSG formation in rpn11-m1 cells can be achieved by the expression in trans of the last 45 amino acids of the C-terminal domain of Rpn11, which was moreover found to co-localize with PSGs. In addition, another rpn11 mutant leading to seven amino acids change in the Rpn11 C-terminal domain, which exhibits assembled-26S proteasomes, is able to form PSGs but with a delay compared to the wild type situation. Altogether, our findings indicate that PSGs are formed of fully assembled 26S proteasomes and suggest a critical role for the Rpn11 protein in this process.
MeSH term(s)	Amino Acid Sequence ; Cytosol/metabolism ; Endopeptidases/chemistry ; Endopeptidases/genetics ; Endopeptidases/metabolism ; Enzyme Stability ; Molecular Sequence Data ; Mutation ; Proteasome Endopeptidase Complex/metabolism ; Protein Structure, Tertiary ; Protein Subunits/metabolism ; Protein Transport ; Saccharomyces cerevisiae/cytology ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/chemistry ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Survival Analysis
Chemical Substances	Protein Subunits ; RPN11 protein, S cerevisiae ; Saccharomyces cerevisiae Proteins ; Endopeptidases (EC 3.4.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; ATP dependent 26S protease (EC 3.4.99.-)
Language	English
Publishing date	2013-08-06
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.0070357
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.

Delestré, Laure / Cui, Hengxiang / Esposito, Michela / Quiveron, Cyril / Mylonas, Elena / Penard-Lacronique, Virginie / Bischof, Oliver / Guillouf, Christel

Haematologica

2017 Volume 102, Issue 11, Page(s) 1850–1860

Abstract: Transcriptional deregulation caused by epigenetic or genetic alterations is a major cause of leukemic transformation. The Spi1/PU.1 transcription factor is a key regulator of many steps of hematopoiesis, and limits self-renewal of hematopoietic stem ... ...

Abstract	Transcriptional deregulation caused by epigenetic or genetic alterations is a major cause of leukemic transformation. The Spi1/PU.1 transcription factor is a key regulator of many steps of hematopoiesis, and limits self-renewal of hematopoietic stem cells. The deregulation of its expression or activity contributes to leukemia, in which Spi1 can be either an oncogene or a tumor suppressor. Herein we explored whether cellular senescence, an anti-tumoral pathway that restrains cell proliferation, is a mechanism by which Spi1 limits hematopoietic cell expansion, and thus prevents the development of leukemia. We show that Spi1 overexpression triggers cellular senescence both in primary fibroblasts and hematopoietic cells. Erythroid and myeloid lineages are both prone to Spi1-induced senescence. In hematopoietic cells, Spi1-induced senescence requires its DNA-binding activity and a functional p38MAPK14 pathway but is independent of a DNA-damage response. In contrast, in fibroblasts, Spi1-induced senescence is triggered by a DNA-damage response. Importantly, using our well-established Spi1 transgenic leukemia mouse model, we demonstrate that Spi1 overexpression also induces senescence in erythroid progenitors of the bone marrow
MeSH term(s)	Animals ; Biomarkers ; Bone Marrow/metabolism ; Bone Marrow/pathology ; Cell Line ; Cell Proliferation ; Cellular Senescence/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Ectopic Gene Expression ; Fibroblasts/metabolism ; Hematopoietic Stem Cells/metabolism ; Humans ; Immunohistochemistry ; Leukemia/genetics ; Leukemia/metabolism ; Leukemia/pathology ; Mice ; Mice, Transgenic ; Mutation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism
Chemical Substances	Biomarkers ; DNA-Binding Proteins ; Proto-Oncogene Proteins ; Trans-Activators ; proto-oncogene protein Spi-1
Language	English
Publishing date	2017-09-14
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2016.157636
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 ; Online: PLZF limits enhancer activity during hematopoietic progenitor aging.

Poplineau, Mathilde / Vernerey, Julien / Platet, Nadine / N'guyen, Lia / Hérault, Léonard / Esposito, Michela / Saurin, Andrew J / Guilouf, Christel / Iwama, Atsushi / Duprez, Estelle

Nucleic acids research

2019 Volume 47, Issue 9, Page(s) 4509–4520

Abstract: PLZF (promyelocytic leukemia zinc finger) is a transcription factor acting as a global regulator of hematopoietic commitment. PLZF displays an epigenetic specificity by recruiting chromatin-modifying factors but little is known about its role in ... ...

Abstract	PLZF (promyelocytic leukemia zinc finger) is a transcription factor acting as a global regulator of hematopoietic commitment. PLZF displays an epigenetic specificity by recruiting chromatin-modifying factors but little is known about its role in remodeling chromatin of cells committed toward a given specific hematopoietic lineage. In murine myeloid progenitors, we decipher a new role for PLZF in restraining active genes and enhancers by targeting acetylated lysine 27 of Histone H3 (H3K27ac). Functional analyses reveal that active enhancers bound by PLZF are involved in biological processes related to metabolism and associated with hematopoietic aging. Comparing the epigenome of young and old myeloid progenitors, we reveal that H3K27ac variation at active enhancers is a hallmark of hematopoietic aging. Taken together, these data suggest that PLZF, associated with active enhancers, appears to restrain their activity as an epigenetic gatekeeper of hematopoietic aging.
MeSH term(s)	Aging/genetics ; Animals ; Cell Differentiation/genetics ; Enhancer Elements, Genetic ; Epigenesis, Genetic/genetics ; Gene Expression Regulation, Developmental/genetics ; Hematopoietic Stem Cells/metabolism ; Histones/genetics ; Humans ; Jumonji Domain-Containing Histone Demethylases/genetics ; Mice ; Myeloid Progenitor Cells/metabolism ; Promyelocytic Leukemia Zinc Finger Protein/genetics ; Protein Binding ; Regulatory Sequences, Nucleic Acid/genetics ; Transcription, Genetic
Chemical Substances	Histones ; Promyelocytic Leukemia Zinc Finger Protein ; Zbtb16 protein, mouse ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Kdm6b protein, mouse (EC 1.5.-)
Language	English
Publishing date	2019-05-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkz174
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1067: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.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

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

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

In stock of ZB MED Cologne/Königswinter

Order via subito