- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1742-4690
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Suppression of HTLV-1 transcription by SIRT1 deacetylase ; volume:12 ; number:1 ; day:28 ; month:8 ; year:2015 ; pages:1 ; date:12.2015
Retrovirology ; 12, Heft 1 (28.8.2015), 1, 12.2015
- Creator
-
Jin, Dong-Yan
Tang, Hei-Man Vincent
Gao, Wei-Wei
Chan, Chi-Ping
Iha, Hidekatsu
Yuen, Kit-San
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1186/1742-4690-12-S1-P53
- URN
-
urn:nbn:de:101:1-2020100521015722339027
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:48 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Jin, Dong-Yan
- Tang, Hei-Man Vincent
- Gao, Wei-Wei
- Chan, Chi-Ping
- Iha, Hidekatsu
- Yuen, Kit-San
- SpringerLink (Online service)
Other Objects (12)
Transcription factor NFκB regulates the expression of the histone deacetylase SIRT1
SIRT1 ISGylation accelerates tumor progression by unleashing SIRT1 from the inactive state to promote its deacetylase activity
Regulation of pituitary growth hormone synthesis by NAD + dependent deacetylase Sirt1
Regulation of pituitary growth hormone synthesis by NAD+ dependent deacetylase Sirt1
O-GlcNAcylation of SIRT1 enhances its deacetylase activity and promotes cytoprotection under stress
Molecular mechanisms of apoptosis suppression by HTLV-1 bZIP factor in HTLV-1 infected cells
HTLV-1 inhibits stress granules formation by interacting with the histone deacetylase 6 (HDAC6)
The Hda1 histone deacetylase limits divergent non‐coding transcription and restricts transcription initiation frequency
HTLV-3 and HTLV-4 antisense proteins activate JunB-, c-Jun- and JunD-dependent transcription
Checkpoint suppressor 1 suppresses transcriptional activity of ERα and breast cancer cell proliferation via deacetylase SIRT1
Integration of the deacetylase SIRT1 in the response to nucleolar stress:metabolic implications for neurodegenerative diseases
JunD/HBZ enhances HBZ enhances HTLV-1 antisense transcription
Transcription factor NFκB regulates the expression of the histone deacetylase SIRT1
SIRT1 ISGylation accelerates tumor progression by unleashing SIRT1 from the inactive state to promote its deacetylase activity
Regulation of pituitary growth hormone synthesis by NAD + dependent deacetylase Sirt1
Regulation of pituitary growth hormone synthesis by NAD+ dependent deacetylase Sirt1
O-GlcNAcylation of SIRT1 enhances its deacetylase activity and promotes cytoprotection under stress
Molecular mechanisms of apoptosis suppression by HTLV-1 bZIP factor in HTLV-1 infected cells
HTLV-1 inhibits stress granules formation by interacting with the histone deacetylase 6 (HDAC6)
The Hda1 histone deacetylase limits divergent non‐coding transcription and restricts transcription initiation frequency
HTLV-3 and HTLV-4 antisense proteins activate JunB-, c-Jun- and JunD-dependent transcription
Checkpoint suppressor 1 suppresses transcriptional activity of ERα and breast cancer cell proliferation via deacetylase SIRT1
Integration of the deacetylase SIRT1 in the response to nucleolar stress:metabolic implications for neurodegenerative diseases
JunD/HBZ enhances HBZ enhances HTLV-1 antisense transcription
Transcription factor NFκB regulates the expression of the histone deacetylase SIRT1
SIRT1 ISGylation accelerates tumor progression by unleashing SIRT1 from the inactive state to promote its deacetylase activity
Regulation of pituitary growth hormone synthesis by NAD + dependent deacetylase Sirt1
Regulation of pituitary growth hormone synthesis by NAD+ dependent deacetylase Sirt1
O-GlcNAcylation of SIRT1 enhances its deacetylase activity and promotes cytoprotection under stress
Molecular mechanisms of apoptosis suppression by HTLV-1 bZIP factor in HTLV-1 infected cells
HTLV-1 inhibits stress granules formation by interacting with the histone deacetylase 6 (HDAC6)
The Hda1 histone deacetylase limits divergent non‐coding transcription and restricts transcription initiation frequency
HTLV-3 and HTLV-4 antisense proteins activate JunB-, c-Jun- and JunD-dependent transcription
Checkpoint suppressor 1 suppresses transcriptional activity of ERα and breast cancer cell proliferation via deacetylase SIRT1
Integration of the deacetylase SIRT1 in the response to nucleolar stress:metabolic implications for neurodegenerative diseases