The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer

Ran Tur-Kaspa; Yosef Shaul; David D. Moore; Robert D. Burk; Sam Okret; Lorenz Poellinger; David A. Shafritz

doi:10.1016/0042-6822(88)90127-4

The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer

Ran Tur-Kaspa
, Yosef Shaul
, David D. Moore
, Robert D. Burk
, Sam Okret
, Lorenz Poellinger
, David A. Shafritz

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

164 Scopus citations

Abstract

The hepatitis B virus (HBV) genome contains a specific DNA binding site for the glucocorticoid receptor. Using DNase I footprinting, this binding site was localized at HBV map positions 341–370 clockwise from theEcoRI site. The DNA sequence protected in the footprint contains two tandem copies of the GRE core hexanucleotide 5′-TGT_c^TCT-3′. Deletion analysis and reconstruction experiments in plasmid expression vectors demonstrated that this glucocorticoid receptor binding sequence serves as a signal for augmenting glucocorticoid-dependent activity of the HBV enhancer, which is located ∼ 730 nucleotides downstream in the HBV genome. Even though it does not serve as an independent enhancer element, the HBV glucocorticoid receptor domain can therefore be categorized as a functional GRE.

Original language	English
Pages (from-to)	630-633
Number of pages	4
Journal	Virology
Volume	167
Issue number	2
DOIs	https://doi.org/10.1016/0042-6822(88)90127-4
State	Published - Dec 1988
Externally published	Yes

Bibliographical note

Funding Information:
Research supported in part by NIH Grant CA-32605 (to D.A.S.) and CA-45476 (to R.D.B.), by a grant from Hoechst AG (to D.D.M.), and by grants from the Israeli Ministry of Health and the IsraeliA ssocia-tion for the Fight against Cancer (to R.T-K.). Duringp art of these studies, Ran Tur-Kaspaw as an NIH John E. Fogarty internationalF ellow on leavef rom Hadassah Medical School, Jerusalem, Israel.

Funding

Research supported in part by NIH Grant CA-32605 (to D.A.S.) and CA-45476 (to R.D.B.), by a grant from Hoechst AG (to D.D.M.), and by grants from the Israeli Ministry of Health and the IsraeliA ssocia-tion for the Fight against Cancer (to R.T-K.). Duringp art of these studies, Ran Tur-Kaspaw as an NIH John E. Fogarty internationalF ellow on leavef rom Hadassah Medical School, Jerusalem, Israel.

Funders	Funder number
National Cancer Institute	R01CA032605

UN SDGs

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

SDG 3 Good Health and Well-being

Access to Document

10.1016/0042-6822(88)90127-4

Cite this

@article{11f6c5559b0a47038446ab1fb04b1e5c,

title = "The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer",

abstract = "The hepatitis B virus (HBV) genome contains a specific DNA binding site for the glucocorticoid receptor. Using DNase I footprinting, this binding site was localized at HBV map positions 341–370 clockwise from theEcoRI site. The DNA sequence protected in the footprint contains two tandem copies of the GRE core hexanucleotide 5′-TGTcTCT-3′. Deletion analysis and reconstruction experiments in plasmid expression vectors demonstrated that this glucocorticoid receptor binding sequence serves as a signal for augmenting glucocorticoid-dependent activity of the HBV enhancer, which is located ∼ 730 nucleotides downstream in the HBV genome. Even though it does not serve as an independent enhancer element, the HBV glucocorticoid receptor domain can therefore be categorized as a functional GRE.",

author = "Ran Tur-Kaspa and Yosef Shaul and Moore, \{David D.\} and Burk, \{Robert D.\} and Sam Okret and Lorenz Poellinger and Shafritz, \{David A.\}",

note = "Funding Information: Research supported in part by NIH Grant CA-32605 (to D.A.S.) and CA-45476 (to R.D.B.), by a grant from Hoechst AG (to D.D.M.), and by grants from the Israeli Ministry of Health and the IsraeliA ssocia-tion for the Fight against Cancer (to R.T-K.). Duringp art of these studies, Ran Tur-Kaspaw as an NIH John E. Fogarty internationalF ellow on leavef rom Hadassah Medical School, Jerusalem, Israel.",

year = "1988",

month = dec,

doi = "10.1016/0042-6822(88)90127-4",

language = "אנגלית",

volume = "167",

pages = "630--633",

journal = "Virology",

issn = "0042-6822",

publisher = "Academic Press Inc.",

number = "2",

}

TY - JOUR

T1 - The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer

AU - Tur-Kaspa, Ran

AU - Shaul, Yosef

AU - Moore, David D.

AU - Burk, Robert D.

AU - Okret, Sam

AU - Poellinger, Lorenz

AU - Shafritz, David A.

N1 - Funding Information: Research supported in part by NIH Grant CA-32605 (to D.A.S.) and CA-45476 (to R.D.B.), by a grant from Hoechst AG (to D.D.M.), and by grants from the Israeli Ministry of Health and the IsraeliA ssocia-tion for the Fight against Cancer (to R.T-K.). Duringp art of these studies, Ran Tur-Kaspaw as an NIH John E. Fogarty internationalF ellow on leavef rom Hadassah Medical School, Jerusalem, Israel.

PY - 1988/12

Y1 - 1988/12

N2 - The hepatitis B virus (HBV) genome contains a specific DNA binding site for the glucocorticoid receptor. Using DNase I footprinting, this binding site was localized at HBV map positions 341–370 clockwise from theEcoRI site. The DNA sequence protected in the footprint contains two tandem copies of the GRE core hexanucleotide 5′-TGTcTCT-3′. Deletion analysis and reconstruction experiments in plasmid expression vectors demonstrated that this glucocorticoid receptor binding sequence serves as a signal for augmenting glucocorticoid-dependent activity of the HBV enhancer, which is located ∼ 730 nucleotides downstream in the HBV genome. Even though it does not serve as an independent enhancer element, the HBV glucocorticoid receptor domain can therefore be categorized as a functional GRE.

AB - The hepatitis B virus (HBV) genome contains a specific DNA binding site for the glucocorticoid receptor. Using DNase I footprinting, this binding site was localized at HBV map positions 341–370 clockwise from theEcoRI site. The DNA sequence protected in the footprint contains two tandem copies of the GRE core hexanucleotide 5′-TGTcTCT-3′. Deletion analysis and reconstruction experiments in plasmid expression vectors demonstrated that this glucocorticoid receptor binding sequence serves as a signal for augmenting glucocorticoid-dependent activity of the HBV enhancer, which is located ∼ 730 nucleotides downstream in the HBV genome. Even though it does not serve as an independent enhancer element, the HBV glucocorticoid receptor domain can therefore be categorized as a functional GRE.

UR - https://www.scopus.com/pages/publications/0024266511

U2 - 10.1016/0042-6822(88)90127-4

DO - 10.1016/0042-6822(88)90127-4

M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???

C2 - 3201757

AN - SCOPUS:0024266511

SN - 0042-6822

VL - 167

SP - 630

EP - 633

JO - Virology

JF - Virology

IS - 2

ER -

The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer

Abstract

Bibliographical note

Funding

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this