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The C-type lectin homologue gene (EP153R) of African swine fever virus inhibits apoptosis both in virus infection and in heterologous expression

Hurtado, Carolina ; Granja, Aitor G ; Bustos, Marı́a J ; [et al.]

Elsevier BV ; 2004

In: Virology Vol. 326, No. 1 ( 2004-08), p. 160-170

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In: Virology, Elsevier BV, Vol. 326, No. 1 ( 2004-08), p. 160-170

Type of Medium: Online Resource

ISSN: 0042-6822

URL: Article

DOI: 10.1016/j.virol.2004.05.019

RVK:

WA 15000

Language: English

Publisher: Elsevier BV

Publication Date: 2004

detail.hit.zdb_id: 1471925-3

SSG: 12

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Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma

Delgado, Pilar ; Álvarez-Prado, Ángel F. ; Marina-Zárate, Ester ; [et al.]

Public Library of Science (PLoS) ; 2020

In: PLOS Genetics Vol. 16, No. 12 ( 2020-12-23), p. e1008960-

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In: PLOS Genetics, Public Library of Science (PLoS), Vol. 16, No. 12 ( 2020-12-23), p. e1008960-

Abstract: Most B cell lymphomas originate from B cells that have germinal center (GC) experience and bear chromosome translocations and numerous point mutations. GC B cells remodel their immunoglobulin (Ig) genes by somatic hypermutation (SHM) and class switch recombination (CSR) in their Ig genes. Activation Induced Deaminase (AID) initiates CSR and SHM by generating U:G mismatches on Ig DNA that can then be processed by Uracyl-N-glycosylase (UNG). AID promotes collateral damage in the form of chromosome translocations and off-target SHM, however, the exact contribution of AID activity to lymphoma generation and progression is not completely understood. Here we show using a conditional knock-in strategy that AID supra-activity alone is not sufficient to generate B cell transformation. In contrast, in the absence of UNG, AID supra-expression increases SHM and promotes lymphoma. Whole exome sequencing revealed that AID heavily contributes to lymphoma SHM, promoting subclonal variability and a wider range of oncogenic variants. Thus, our data provide direct evidence that UNG is a brake to AID-induced intratumoral heterogeneity and evolution of B cell lymphoma.

Type of Medium: Online Resource

ISSN: 1553-7404

URL: Article

DOI: 10.1371/journal.pgen.1008960

DOI: 10.1371/journal.pgen.1008960.g001

DOI: 10.1371/journal.pgen.1008960.g002

DOI: 10.1371/journal.pgen.1008960.g003

DOI: 10.1371/journal.pgen.1008960.g004

DOI: 10.1371/journal.pgen.1008960.g005

DOI: 10.1371/journal.pgen.1008960.g006

DOI: 10.1371/journal.pgen.1008960.s001

DOI: 10.1371/journal.pgen.1008960.s002

DOI: 10.1371/journal.pgen.1008960.s003

DOI: 10.1371/journal.pgen.1008960.s004

DOI: 10.1371/journal.pgen.1008960.s005

DOI: 10.1371/journal.pgen.1008960.s006

DOI: 10.1371/journal.pgen.1008960.s007

DOI: 10.1371/journal.pgen.1008960.s008

DOI: 10.1371/journal.pgen.1008960.s009

DOI: 10.1371/journal.pgen.1008960.s010

DOI: 10.1371/journal.pgen.1008960.s011

DOI: 10.1371/journal.pgen.1008960.s012

DOI: 10.1371/journal.pgen.1008960.s013

DOI: 10.1371/journal.pgen.1008960.r001

DOI: 10.1371/journal.pgen.1008960.r002

DOI: 10.1371/journal.pgen.1008960.r003

DOI: 10.1371/journal.pgen.1008960.r004

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2020

detail.hit.zdb_id: 2186725-2

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miR-181b negatively regulates activation-induced cytidine deaminase in B cells

de Yébenes, Virginia G. ; Belver, Laura ; Pisano, David G. ; [et al.]

Rockefeller University Press ; 2008

In: The Journal of Experimental Medicine Vol. 205, No. 10 ( 2008-09-29), p. 2199-2206

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In: The Journal of Experimental Medicine, Rockefeller University Press, Vol. 205, No. 10 ( 2008-09-29), p. 2199-2206

Abstract: Activated B cells reshape their primary antibody repertoire after antigen encounter by two molecular mechanisms: somatic hypermutation (SHM) and class switch recombination (CSR). SHM and CSR are initiated by activation-induced cytidine deaminase (AID) through the deamination of cytosine residues on the immunoglobulin loci, which leads to the generation of DNA mutations or double-strand break intermediates. As a bystander effect, endogenous AID levels can also promote the generation of chromosome translocations, suggesting that the fine tuning of AID expression may be critical to restrict B cell lymphomagenesis. To determine whether microRNAs (miRNAs) play a role in the regulation of AID expression, we performed a functional screening of an miRNA library and identified miRNAs that regulate CSR. One such miRNA, miR-181b, impairs CSR when expressed in activated B cells, and results in the down-regulation of AID mRNA and protein levels. We found that the AID 3′ untranslated region contains multiple putative binding sequences for miR-181b and that these sequences can be directly targeted by miR-181b. Overall, our results provide evidence for a new regulatory mechanism that restricts AID activity and can therefore be relevant to prevent B cell malignant transformation.

Type of Medium: Online Resource

ISSN: 1540-9538 , 0022-1007

URL: Article

DOI: 10.1084/jem.20080579

RVK:

XA 10000

Language: English

Publisher: Rockefeller University Press

Publication Date: 2008

detail.hit.zdb_id: 1477240-1

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In vivo conditional deletion of HDAC7 reveals its requirement to establish proper B lymphocyte identity and development

Azagra, Alba ; Román-González, Lidia ; Collazo, Olga ; [et al.]

Rockefeller University Press ; 2016

In: Journal of Experimental Medicine Vol. 213, No. 12 ( 2016-11-14), p. 2591-2601

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In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 213, No. 12 ( 2016-11-14), p. 2591-2601

Abstract: Class IIa histone deacetylase (HDAC) subfamily members are tissue-specific gene repressors with crucial roles in development and differentiation processes. A prominent example is HDAC7, a class IIa HDAC that shows a lymphoid-specific expression pattern within the hematopoietic system. In this study, we explored its potential role in B cell development by generating a conditional knockout mouse model. Our study demonstrates for the first time that HDAC7 deletion dramatically blocks early B cell development and gives rise to a severe lymphopenia in peripheral organs, while also leading to pro–B cell lineage promiscuity. We find that HDAC7 represses myeloid and T lymphocyte genes in B cell progenitors through interaction with myocyte enhancer factor 2C (MEFC2). In B cell progenitors, HDAC7 is recruited to promoters and enhancers of target genes, and its absence leads to increased enrichment of histone active marks. Our results prove that HDAC7 is a bona fide transcriptional repressor essential for B cell development.

Type of Medium: Online Resource

ISSN: 0022-1007 , 1540-9538

URL: Article

DOI: 10.1084/jem.20150821

RVK:

XA 10000

Language: English

Publisher: Rockefeller University Press

Publication Date: 2016

detail.hit.zdb_id: 1477240-1

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MYC directly transactivates CR2/CD21, the receptor of the Epstein–Barr virus, enhancing the viral infection of Burkitt lymphoma cells

Molina, Ester ; García-Gutiérrez, Lucía ; Junco, Vanessa ; [et al.]

Springer Science and Business Media LLC ; 2023

In: Oncogene

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In: Oncogene, Springer Science and Business Media LLC

Type of Medium: Online Resource

ISSN: 0950-9232 , 1476-5594

URL: Article

DOI: 10.1038/s41388-023-02846-9

RVK:

XA 10000

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2023

detail.hit.zdb_id: 2008404-3

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UNG shapes the specificity of AID-induced somatic hypermutation

Pérez-Durán, Pablo ; Belver, Laura ; de Yébenes, Virginia G. ; [et al.]

Rockefeller University Press ; 2012

In: Journal of Experimental Medicine Vol. 209, No. 7 ( 2012-07-02), p. 1379-1389

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In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 209, No. 7 ( 2012-07-02), p. 1379-1389

Abstract: Secondary diversification of antibodies through somatic hypermutation (SHM) and class switch recombination (CSR) is a critical component of the immune response. Activation-induced deaminase (AID) initiates both processes by deaminating cytosine residues in immunoglobulin genes. The resulting U:G mismatch can be processed by alternative pathways to give rise to a mutation (SHM) or a DNA double-strand break (CSR). Central to this processing is the activity of uracil-N-glycosylase (UNG), an enzyme normally involved in error-free base excision repair. We used next generation sequencing to analyze the contribution of UNG to the resolution of AID-induced lesions. Loss- and gain-of-function experiments showed that UNG activity can promote both error-prone and high fidelity repair of U:G lesions. Unexpectedly, the balance between these alternative outcomes was influenced by the sequence context of the deaminated cytosine, with individual hotspots exhibiting higher susceptibility to UNG-triggered error-free or error-prone resolution. These results reveal UNG as a new molecular layer that shapes the specificity of AID-induced mutations and may provide new insights into the role of AID in cancer development.

Type of Medium: Online Resource

ISSN: 1540-9538 , 0022-1007

URL: Article

DOI: 10.1084/jem.20112253

RVK:

XA 10000

Language: English

Publisher: Rockefeller University Press

Publication Date: 2012

detail.hit.zdb_id: 1477240-1

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Regulation of B‐cell development and function by micro RNA s

de Yébenes, Virginia G ; Bartolomé‐Izquierdo, Nahikari ; Ramiro, Almudena R.

Wiley ; 2013

In: Immunological Reviews Vol. 253, No. 1 ( 2013-05), p. 25-39

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In: Immunological Reviews, Wiley, Vol. 253, No. 1 ( 2013-05), p. 25-39

Abstract: Micro RNA s (mi RNA s) have emerged as a new class of gene expression regulators whose functions influence a myriad of biological processes, from developmental decisions through immune responses and numerous pathologies, including cancer and autoimmunity. mi RNA s are small RNA molecules that drive post‐transcriptional negative regulation of gene expression by promoting the degradation or translational block of their target m RNA s. Here, we review some of the data relating to the role of mi RNA s in the regulation of the B‐cell lineage, with a special focus on results obtained in vivo . We start by giving a general overview of mi RNA activity, including the issue of target specificity and the experimental approaches more widely used to analyze the function of these molecules. We then go on to discuss the function of mi RNA s during B‐cell differentiation in the bone marrow and in the periphery as well as during the humoral immune response. Finally, we describe a few examples of the contribution of mi RNA s, both as oncogenes and tumor suppressors, to the development of B‐cell neoplasias.

Type of Medium: Online Resource

ISSN: 0105-2896 , 1600-065X

URL: Issue

URL: Article

DOI: 10.1111/imr.2013.253.issue-1

DOI: 10.1111/imr.12046

Language: English

Publisher: Wiley

Publication Date: 2013

detail.hit.zdb_id: 2038276-5

SSG: 12

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Activation-induced deaminase: light and dark sides

de Yébenes, Virginia G. ; Ramiro, Almudena R.

Elsevier BV ; 2006

In: Trends in Molecular Medicine Vol. 12, No. 9 ( 2006-9), p. 432-439

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In: Trends in Molecular Medicine, Elsevier BV, Vol. 12, No. 9 ( 2006-9), p. 432-439

Type of Medium: Online Resource

ISSN: 1471-4914

URL: Article

DOI: 10.1016/j.molmed.2006.07.001

Language: English

Publisher: Elsevier BV

Publication Date: 2006

detail.hit.zdb_id: 2155736-6

SSG: 12

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MicroRNAs Prevent the Generation of Autoreactive Antibodies

Belver, Laura ; de Yébenes, Virginia G. ; Ramiro, Almudena R.

Elsevier BV ; 2010

In: Immunity Vol. 33, No. 5 ( 2010-11), p. 713-722

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In: Immunity, Elsevier BV, Vol. 33, No. 5 ( 2010-11), p. 713-722

Type of Medium: Online Resource

ISSN: 1074-7613

URL: Article

DOI: 10.1016/j.immuni.2010.11.010

RVK:

XA 48754.8

Language: English

Publisher: Elsevier BV

Publication Date: 2010

detail.hit.zdb_id: 2001966-X

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Aging-Associated miR-217 Aggravates Atherosclerosis and Promotes Cardiovascular Dysfunction

de Yébenes, Virginia G. ; Briones, Ana M. ; Martos-Folgado, Inmaculada ; [et al.]

Ovid Technologies (Wolters Kluwer Health) ; 2020

In: Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 40, No. 10 ( 2020-10), p. 2408-2424

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In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 40, No. 10 ( 2020-10), p. 2408-2424

Abstract: microRNAs are master regulators of gene expression with essential roles in virtually all biological processes. miR-217 has been associated with aging and cellular senescence, but its role in vascular disease is not understood. Approach and Results: We have used an inducible endothelium-specific knock-in mouse model to address the role of miR-217 in vascular function and atherosclerosis. miR-217 reduced NO production and promoted endothelial dysfunction, increased blood pressure, and exacerbated atherosclerosis in proatherogenic apoE −/ − mice. Moreover, increased endothelial miR-217 expression led to the development of coronary artery disease and altered left ventricular heart function, inducing diastolic and systolic dysfunction. Conversely, inhibition of endogenous vascular miR-217 in apoE −/− mice improved vascular contractility and diminished atherosclerosis. Transcriptome analysis revealed that miR-217 regulates an endothelial signaling hub and downregulates a network of eNOS (endothelial NO synthase) activators, including VEGF (vascular endothelial growth factor) and apelin receptor pathways, resulting in diminished eNOS expression. Further analysis revealed that human plasma miR-217 is a biomarker of vascular aging and cardiovascular risk. Conclusions: Our results highlight the therapeutic potential of miR-217 inhibitors in aging-related cardiovascular disease.

Type of Medium: Online Resource

ISSN: 1079-5642 , 1524-4636

URL: Article

DOI: 10.1161/ATVBAHA.120.314333

Language: English

Publisher: Ovid Technologies (Wolters Kluwer Health)

Publication Date: 2020

detail.hit.zdb_id: 1494427-3

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