The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines: Role of specific PKC isoforms

Rachel Chamias; Mahmoud Huleihel; Mordechai Aboud

doi:10.1016/j.leukres.2009.03.032

The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines: Role of specific PKC isoforms

Rachel Chamias, Mahmoud Huleihel, Mordechai Aboud

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

We demonstrate here that TPA activates HTLV-1 LTR expression in Jurkat and H9 T-cell lines, by strictly different mechanisms. In Jurkat cells this activation is exerted by a PKCα- and PKCε-antagonized mechanism which operates through an Sp1 binding site residing within the Est responsive region 1 of the LTR. On the other hand, in H9 cells TPA activates the LTR by two consecutive mechanisms; the first depends on PKCη activity and is exerted through the 21 bp repeats of the LTR, whereas the second is analogous to that observed in Jurkat cells, except that it is antagonized by PKCδ.

Original language	English
Pages (from-to)	93-99
Number of pages	7
Journal	Leukemia Research
Volume	34
Issue number	1
DOIs	https://doi.org/10.1016/j.leukres.2009.03.032
State	Published - 1 Jan 2010

Keywords

21 bp TRE
ERR-1
HTLV-1 LTR
Jurkat and H9 T-cell lines
PKC isoforms
Sp1 site
TPA

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.leukres.2009.03.032

Cite this

@article{bc37ea8126ca418ba1dd895d4e214be9,

title = "The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines: Role of specific PKC isoforms",

abstract = "We demonstrate here that TPA activates HTLV-1 LTR expression in Jurkat and H9 T-cell lines, by strictly different mechanisms. In Jurkat cells this activation is exerted by a PKCα- and PKCε-antagonized mechanism which operates through an Sp1 binding site residing within the Est responsive region 1 of the LTR. On the other hand, in H9 cells TPA activates the LTR by two consecutive mechanisms; the first depends on PKCη activity and is exerted through the 21 bp repeats of the LTR, whereas the second is analogous to that observed in Jurkat cells, except that it is antagonized by PKCδ.",

keywords = "21 bp TRE, ERR-1, HTLV-1 LTR, Jurkat and H9 T-cell lines, PKC isoforms, Sp1 site, TPA",

author = "Rachel Chamias and Mahmoud Huleihel and Mordechai Aboud",

note = "Funding Information: Financial support: This study was supported by a grant from the Israel Science Foundation (ISF), Israel Cancer Research Fund (ICRF) and the Chief Scientist Office of the Israeli Health Ministry. ",

year = "2010",

month = jan,

day = "1",

doi = "10.1016/j.leukres.2009.03.032",

language = "English",

volume = "34",

pages = "93--99",

journal = "Leukemia Research",

issn = "0145-2126",

publisher = "Elsevier Ltd.",

number = "1",

}

TY - JOUR

T1 - The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines

T2 - Role of specific PKC isoforms

AU - Chamias, Rachel

AU - Huleihel, Mahmoud

AU - Aboud, Mordechai

N1 - Funding Information: Financial support: This study was supported by a grant from the Israel Science Foundation (ISF), Israel Cancer Research Fund (ICRF) and the Chief Scientist Office of the Israeli Health Ministry.

PY - 2010/1/1

Y1 - 2010/1/1

N2 - We demonstrate here that TPA activates HTLV-1 LTR expression in Jurkat and H9 T-cell lines, by strictly different mechanisms. In Jurkat cells this activation is exerted by a PKCα- and PKCε-antagonized mechanism which operates through an Sp1 binding site residing within the Est responsive region 1 of the LTR. On the other hand, in H9 cells TPA activates the LTR by two consecutive mechanisms; the first depends on PKCη activity and is exerted through the 21 bp repeats of the LTR, whereas the second is analogous to that observed in Jurkat cells, except that it is antagonized by PKCδ.

AB - We demonstrate here that TPA activates HTLV-1 LTR expression in Jurkat and H9 T-cell lines, by strictly different mechanisms. In Jurkat cells this activation is exerted by a PKCα- and PKCε-antagonized mechanism which operates through an Sp1 binding site residing within the Est responsive region 1 of the LTR. On the other hand, in H9 cells TPA activates the LTR by two consecutive mechanisms; the first depends on PKCη activity and is exerted through the 21 bp repeats of the LTR, whereas the second is analogous to that observed in Jurkat cells, except that it is antagonized by PKCδ.

KW - 21 bp TRE

KW - ERR-1

KW - HTLV-1 LTR

KW - Jurkat and H9 T-cell lines

KW - PKC isoforms

KW - Sp1 site

KW - TPA

UR - http://www.scopus.com/inward/record.url?scp=73249143109&partnerID=8YFLogxK

U2 - 10.1016/j.leukres.2009.03.032

DO - 10.1016/j.leukres.2009.03.032

M3 - Article

AN - SCOPUS:73249143109

SN - 0145-2126

VL - 34

SP - 93

EP - 99

JO - Leukemia Research

JF - Leukemia Research

IS - 1

ER -

The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines: Role of specific PKC isoforms

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this