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ELL2 Influences Transcription Elongation, Splicing, Ig Secretion and Growth | OMICS International| Abstract

Journal of Mucosal Immunology Research
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  • J Mucosal Immunol Res 2019, Vol 3(1): 112

ELL2 Influences Transcription Elongation, Splicing, Ig Secretion and Growth

Anthony Ghobrial, Nathaniel Flick, Ryan Daly, Malcolm Hoffman and Christine Milcarek*
Department of Immunology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
*Corresponding Author : Dr. Christine Milcarek, Department of Immunology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA, Tel: 02-3937-6828, Email: [email protected]

Received Date: Jun 27, 2019 / Accepted Date: Jul 05, 2019 / Published Date: Jul 12, 2019


ELL2 was previously discovered as a member of the Super Elongation Complex. It is involved in driving the maturation of B cells to plasma cells through shifting patterns of RNA processing, favoring generation of the secretory form of heavy chain immunoglobulin (IgH) associated with plasma cells. ELL2 influences the expression and splicing patterns of more than 4,000 genes in antibody secreting cells. The ELL2 gene has been implicated in cancers such as multiple myeloma and salivary gland carcinoma. A member of the ELL family (ELL1) was recently proven to act as an E3 ubiquitin ligase to known proto-oncogene, c-Myc, through a highly conserved cysteine residue in the C-terminal CEYLH region. Comparison of sequence homology shows this region is conserved between the three members of the ELL family, leading us to hypothesize that the other two ELLs (2 and 3) could serve the same role. In this review, we summarize what is known about ELL2 with respect to its role in driving B cell to plasma cell differentiation as well as its potential role in tumor suppression.

Keywords: Gene expression; Homology; Tumour; Proto-oncogene; Immunology

Citation: Ghobrial A, Flick N, Daly R, Hoffman M, Milcarek C (2019) ELL2 Influences Transcription Elongation, Splicing, Ig Secretion and Growth. J Mucosal Immunol Res 3: 112.

Copyright: © 2019 Ghobrial A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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