Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival

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Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival. / Alexander, Lou-Ella M M; Watters, January; Reusch, Jessica A; Maurin, Michelle; Nepon-Sixt, Brook S; Vrzalikova, Katerina; Alexandrow, Mark G; Murray, Paul G; Wright, Kenneth L.

In: Molecular immunology, Vol. 91, 01.11.2017, p. 8-16.

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Alexander, Lou-Ella M M ; Watters, January ; Reusch, Jessica A ; Maurin, Michelle ; Nepon-Sixt, Brook S ; Vrzalikova, Katerina ; Alexandrow, Mark G ; Murray, Paul G ; Wright, Kenneth L. / Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival. In: Molecular immunology. 2017 ; Vol. 91. pp. 8-16.

Bibtex

@article{39569729cfbd458195b2d0d2344ea013,
title = "Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival",
abstract = "B cell activation is dependent on a large increase in transcriptional output followed by focused expression on secreted immunoglobulin as the cell transitions to an antibody producing plasma cell. The rapid transcriptional induction is facilitated by the release of poised RNA pol II into productive elongation through assembly of the super elongation complex (SEC). We report that a SEC component, the Eleven -nineteen Lysine-rich leukemia (ELL) family member 3 (ELL3) is dynamically up-regulated in mature and activated human B cells followed by suppression as B cells transition to plasma cells in part mediated by the transcription repressor PRDM1. Burkitt's lymphoma and a sub-set of Diffuse Large B cell lymphoma cell lines abundantly express ELL3. Depletion of ELL3 in the germinal center derived lymphomas results in severe disruption of DNA replication and cell division along with increased DNA damage and cell death. This restricted utilization and survival dependence reveal a key step in B cell activation and indicate a potential therapeutic target against B cell lymphoma's with a germinal center origin.",
keywords = "B-Lymphocytes/immunology, Cell Division/genetics, Cell Survival/genetics, DNA Replication/genetics, Gene Expression Regulation/immunology, Humans, Jurkat Cells, RNA Polymerase II/genetics, Transcriptional Elongation Factors/genetics",
author = "Alexander, {Lou-Ella M M} and January Watters and Reusch, {Jessica A} and Michelle Maurin and Nepon-Sixt, {Brook S} and Katerina Vrzalikova and Alexandrow, {Mark G} and Murray, {Paul G} and Wright, {Kenneth L}",
note = "Copyright {\textcopyright} 2017 Elsevier Ltd. All rights reserved.",
year = "2017",
month = nov,
day = "1",
doi = "10.1016/j.molimm.2017.08.016",
language = "English",
volume = "91",
pages = "8--16",
journal = "Molecular immunology",
issn = "0161-5890",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival

AU - Alexander, Lou-Ella M M

AU - Watters, January

AU - Reusch, Jessica A

AU - Maurin, Michelle

AU - Nepon-Sixt, Brook S

AU - Vrzalikova, Katerina

AU - Alexandrow, Mark G

AU - Murray, Paul G

AU - Wright, Kenneth L

N1 - Copyright © 2017 Elsevier Ltd. All rights reserved.

PY - 2017/11/1

Y1 - 2017/11/1

N2 - B cell activation is dependent on a large increase in transcriptional output followed by focused expression on secreted immunoglobulin as the cell transitions to an antibody producing plasma cell. The rapid transcriptional induction is facilitated by the release of poised RNA pol II into productive elongation through assembly of the super elongation complex (SEC). We report that a SEC component, the Eleven -nineteen Lysine-rich leukemia (ELL) family member 3 (ELL3) is dynamically up-regulated in mature and activated human B cells followed by suppression as B cells transition to plasma cells in part mediated by the transcription repressor PRDM1. Burkitt's lymphoma and a sub-set of Diffuse Large B cell lymphoma cell lines abundantly express ELL3. Depletion of ELL3 in the germinal center derived lymphomas results in severe disruption of DNA replication and cell division along with increased DNA damage and cell death. This restricted utilization and survival dependence reveal a key step in B cell activation and indicate a potential therapeutic target against B cell lymphoma's with a germinal center origin.

AB - B cell activation is dependent on a large increase in transcriptional output followed by focused expression on secreted immunoglobulin as the cell transitions to an antibody producing plasma cell. The rapid transcriptional induction is facilitated by the release of poised RNA pol II into productive elongation through assembly of the super elongation complex (SEC). We report that a SEC component, the Eleven -nineteen Lysine-rich leukemia (ELL) family member 3 (ELL3) is dynamically up-regulated in mature and activated human B cells followed by suppression as B cells transition to plasma cells in part mediated by the transcription repressor PRDM1. Burkitt's lymphoma and a sub-set of Diffuse Large B cell lymphoma cell lines abundantly express ELL3. Depletion of ELL3 in the germinal center derived lymphomas results in severe disruption of DNA replication and cell division along with increased DNA damage and cell death. This restricted utilization and survival dependence reveal a key step in B cell activation and indicate a potential therapeutic target against B cell lymphoma's with a germinal center origin.

KW - B-Lymphocytes/immunology

KW - Cell Division/genetics

KW - Cell Survival/genetics

KW - DNA Replication/genetics

KW - Gene Expression Regulation/immunology

KW - Humans

KW - Jurkat Cells

KW - RNA Polymerase II/genetics

KW - Transcriptional Elongation Factors/genetics

U2 - 10.1016/j.molimm.2017.08.016

DO - 10.1016/j.molimm.2017.08.016

M3 - Article

C2 - 28858629

VL - 91

SP - 8

EP - 16

JO - Molecular immunology

JF - Molecular immunology

SN - 0161-5890

ER -