Early B-cell factor 1 (EBF1) is critical for transcriptional control of SLAMF1 gene in human B cells

Schwartz, Anton M.; Putlyaeva, Lidia V.; Covich, Milica; Klepikova, Anna V.; Akulich, Kseniya A.; Vorontsov, Ilya E.; Korneev, Kirill V.; Dmitriev, Sergey E.; Polanovsky, O. L.; Sidorenko, Svetlana P.; Kulakovskiy, Ivan V.; Kuprash, Dmitry V.

doi:10.1016/j.bbagrm.2016.07.004

Cited by 19 publications

(16 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LMP1-, CD40-, IL-1β-and TLRs-mediated upregulation of CD150 expression is probably effected by regulation of NF-kB or AP1 transcription factors [73]. Despite the absence of classical TATA-box region in SLAMF1 promoter it has several binding sites for transcription factors such as SP1, STAT6, IRF4, EBF1, NF-kB, ELF1, TCF3, and PU.1 [76]. The EBF1 is the key regulator of SLAMF1 promoter activity in mice and human B cells that affect dimethylation of H3K4 leading to the "open" state of chromatin [76,77].…”

Section: Regulation Of Cd150 Expressionmentioning

confidence: 99%

“…Despite the absence of classical TATA-box region in SLAMF1 promoter it has several binding sites for transcription factors such as SP1, STAT6, IRF4, EBF1, NF-kB, ELF1, TCF3, and PU.1 [76]. The EBF1 is the key regulator of SLAMF1 promoter activity in mice and human B cells that affect dimethylation of H3K4 leading to the "open" state of chromatin [76,77]. In distinct cellular types at different stages of differentiation various combinations of transcription factors are involved in CD150 gene regulation.…”

Section: Regulation Of Cd150 Expressionmentioning

confidence: 99%

See 1 more Smart Citation

SLAMF1/CD150 in hematologic malignancies: Silent marker or active player?

Gordiienko

Shlapatska

Kovalevska

et al. 2019

Clinical Immunology

Self Cite

View full text Add to dashboard Cite

SLAMF1/CD150 receptor is a founder of signaling lymphocyte activation molecule (SLAM) family of cell-surface receptors. It is widely expressed on cells within hematopoietic system. In hematologic malignancies CD150 cell surface expression is restricted to cutaneous T-cell lymphomas, few types of B-cell non-Hodgkin's lymphoma, near half of cases of chronic lymphocytic leukemia, Hodgkin's lymphoma, and multiple myeloma. Differential expression among various types of hematological malignancies allows considering CD150 as diagnostical and potential prognostic marker. Moreover, CD150 may be a target for antibody-based or measles virus oncolytic therapy. Due to CD150 signaling properties it is involved in regulation of malignant cell fate decision and tumor microenvironment in Hodgkin's lymphoma and chronic lymphocytic leukemia. This review summarizes evidence for the important role of CD150 in pathogenesis of hematologic malignancies.

show abstract

Section: Regulation Of Cd150 Expressionmentioning

confidence: 99%

Section: Regulation Of Cd150 Expressionmentioning

confidence: 99%

SLAMF1/CD150 in hematologic malignancies: Silent marker or active player?

Gordiienko

Shlapatska

Kovalevska

et al. 2019

Clinical Immunology

Self Cite

View full text Add to dashboard Cite

show abstract

“…These results are consistent with observations of nucleosome structure at active promoters; and, the additional information given by MNase-sensitivity reflects the regulatory potential of loci that contain sensitive nucleosomes, as reported in yeast, plants, and drosophila (Vera et al 2014, Mieczkowski et al, 2016, Pass et al, 2017, Brahma and Henikoff 2019). We demonstrate that immune transcription factors NFkB, Pu1, and Ebf1 are associated with positioned sensitive nucleosomes (Garrett-Sinha et al, 1999, Somasundaram et al, 2015, Schwartz et al, 2016, Willis et al 2017, Zhang et al, 2017). Time course studies have shown early and late gene expression changes during B-cell activation, commensurate with the chromatin structure changes found at promoters following HKST treatment (Fowler et al, 2015, Hawkins et al 2015).…”

Section: Discussionmentioning

confidence: 84%

MNase profiling of promoter chromatin inS. typhimurium-stimulated GM12878 cells reveals dynamic and response-specific nucleosome architecture

Cole

Dennis

2019

Preprint

View full text Add to dashboard Cite

The nucleosome is the primary unit of chromatin structure and commonly imputed as a regulator of nuclear events, although the exact mechanisms remain unclear. Recent studies have shown that certain nucleosomes can have different sensitivities to micrococcal nuclease (MNase) digestion, resulting in the release of populations of nucleosomes dependent on the concentration of MNase. Mapping MNase sensitivity of nucleosomes at transcription start sites genome-wide reveals an important functional nucleosome organization that correlates with gene expression levels and transcription factor binding. In order to understand nucleosome distribution and sensitivity dynamics during a robust genome response, we mapped nucleosome position and sensitivity using multiple concentrations of MNase. We use the innate immune response as a model system to understand chromatin-mediated regulation. Herein we demonstrate that stimulation of a human lymphoblastoid cell line (GM12878) with heat-killed Salmonella typhimurium (HKST) results in widespread nucleosome remodeling of response-specific loci. We further show that the response alters the sensitivity of promoter nucleosomes. Finally, we correlate the increased sensitivity with response-specific transcription factor binding. These results indicate that nucleosome distribution and sensitivity dynamics are integral to appropriate cellular response and pave the way for further studies that will deepen our understanding of the specificity of genome response.

show abstract

“…Genetic engineering manipulations were carried out using standard techniques; enzymes produced by Fermentas/ThermoScientific (Lithuania) were used. In order to produce the constructs pGL3-rs3753381 (G) and pGL3-rs11265455 (A), sequences of the enhancers E and D, respectively, were amplified with primers containing the restriction sites SalI and BglII (only SalI in the case of enhancer D) and then cloned into a WT SLAMF1 vector [ 35 ] cleaved at the BamHI-NcoI sites, together with a fragment of the pGL3-basic vector cleaved at the SalI-NcoI sites. Constructs with alternative variants of the respective polymorphisms, rs3753381 (A) and rs11265455 (G), were produced on the basis of the pGL3-rs3753381 (G) and pGL3- rs11265455 (A) constructs.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, we described several regulatory regions that control the expression of the SLAMF1 gene, including the promoter (297-0 with respect to the translation start site) and three enhancer elements of approximately 2.5 kb, two of them located in the third intron and one at a distance of 3 kbp after the coding sequence [ 35 ]. The activity of these regulatory elements was studied in Raji and MP-1 cell lines (Burkitt lymphoma and acute lymphoblastic leukemia models, respectively).…”

Section: Introductionmentioning

confidence: 99%

The Minor Variant of the SingleNucleotide Polymorphism rs3753381 Affects the Activity of a SLAMF1 Enhancer

et al. 2017

View full text Add to dashboard Cite

The SLAMF1 gene encodes CD150, a transmembrane glycoprotein expressed on the surface of T and B-lymphocytes, NK-cells, dendritic cells, and subpopulations of macrophages and basophils. We investigated the functional regulatory polymorphisms of the SLAMF1 locus associated with autoimmune processes, using bioinformatics and a mutational analysis of the regulatory elements overlapping with polymorphic positions. In the reporter gene assay in MP-1 and Raji B-cell lines, the enhancer activity of the regulatory region of the locus containing the rs3753381 polymorphism demonstrated a twofold increase upon the introduction of the rs3753381 minor variant (G → A) associated with myasthenia gravis. An analysis of the nucleotide context in the vicinity of rs3753381 revealed that the minor version of this polymorphism improves several binding sites for the transcription factors of FOX and NFAT, and RXR nuclear receptors. All mutations that disrupt any of these sites lead to a decrease in the enhancer activity both in MP1 and in Raji cells, and each of the two B-cell lines expresses a specific set of these factors. Thus, the minor variant of the rs3753381 polymorphism may contribute to the development of myasthenia gravis by modulating SLAMF1 expression, presumably in pathogenic B-lymphocytes.

show abstract

Early B-cell factor 1 (EBF1) is critical for transcriptional control of SLAMF1 gene in human B cells

Cited by 19 publications

References 80 publications

SLAMF1/CD150 in hematologic malignancies: Silent marker or active player?

SLAMF1/CD150 in hematologic malignancies: Silent marker or active player?

MNase profiling of promoter chromatin inS. typhimurium-stimulated GM12878 cells reveals dynamic and response-specific nucleosome architecture

The Minor Variant of the SingleNucleotide Polymorphism rs3753381 Affects the Activity of a SLAMF1 Enhancer

Contact Info

Product

Resources

About