Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-ε and anti-CD28

Dama Laxminarayana, Islam U. Khan, Kenneth S. O'Rourke, Banabihari Giri

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-ε plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and β-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the -2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions -56, -48, -45, -28, -19, -15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-ε and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation.

Original languageEnglish (US)
Pages (from-to)623-633
Number of pages11
JournalImmunology
Volume122
Issue number4
DOIs
StatePublished - Dec 1 2007

Fingerprint

Adenosine Deaminase
RNA
T-Lymphocytes
Gene Expression
Systemic Lupus Erythematosus
Genes
RNA Editing
Enzymes
Natural Killer Cells
Interleukin-2
Actins
Blood Cells
B-Lymphocytes
Up-Regulation
Research Personnel

Keywords

  • Gene transcripts
  • Mutations
  • RNA editing
  • T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-ε and anti-CD28. / Laxminarayana, Dama; Khan, Islam U.; O'Rourke, Kenneth S.; Giri, Banabihari.

In: Immunology, Vol. 122, No. 4, 01.12.2007, p. 623-633.

Research output: Contribution to journalArticle

Laxminarayana, Dama ; Khan, Islam U. ; O'Rourke, Kenneth S. ; Giri, Banabihari. / Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-ε and anti-CD28. In: Immunology. 2007 ; Vol. 122, No. 4. pp. 623-633.
@article{1910db8406924c4abc2518602b6cf244,
title = "Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-ε and anti-CD28",
abstract = "We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-ε plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and β-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the -2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions -56, -48, -45, -28, -19, -15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-ε and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation.",
keywords = "Gene transcripts, Mutations, RNA editing, T cells",
author = "Dama Laxminarayana and Khan, {Islam U.} and O'Rourke, {Kenneth S.} and Banabihari Giri",
year = "2007",
month = "12",
day = "1",
doi = "10.1111/j.1365-2567.2007.02709.x",
language = "English (US)",
volume = "122",
pages = "623--633",
journal = "Immunology",
issn = "0019-2805",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-ε and anti-CD28

AU - Laxminarayana, Dama

AU - Khan, Islam U.

AU - O'Rourke, Kenneth S.

AU - Giri, Banabihari

PY - 2007/12/1

Y1 - 2007/12/1

N2 - We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-ε plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and β-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the -2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions -56, -48, -45, -28, -19, -15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-ε and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation.

AB - We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-ε plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and β-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the -2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions -56, -48, -45, -28, -19, -15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-ε and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation.

KW - Gene transcripts

KW - Mutations

KW - RNA editing

KW - T cells

UR - http://www.scopus.com/inward/record.url?scp=35948959077&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35948959077&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2567.2007.02709.x

DO - 10.1111/j.1365-2567.2007.02709.x

M3 - Article

C2 - 17897325

AN - SCOPUS:35948959077

VL - 122

SP - 623

EP - 633

JO - Immunology

JF - Immunology

SN - 0019-2805

IS - 4

ER -