Preferential binding of HIF-1 to transcriptionally active loci determines cell-type specific response to hypoxia
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1474-760X
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
Preferential binding of HIF-1 to transcriptionally active loci determines cell-type specific response to hypoxia ; volume:10 ; number:10 ; day:14 ; month:10 ; year:2009 ; pages:1-12 ; date:10.2009
Genome biology ; 10, Heft 10 (14.10.2009), 1-12, 10.2009
- Urheber
-
Xia, Xiaobo
- Beteiligte Personen und Organisationen
-
Kung, Andrew L.
SpringerLink (Online service)
- DOI
-
10.1186/gb-2009-10-10-r113
- URN
-
urn:nbn:de:1111-2016050147442
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
14.08.2025, 10:46 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Xia, Xiaobo
- Kung, Andrew L.
- SpringerLink (Online service)
Ähnliche Objekte (12)
NREP, transcriptionally upregulated by HIF-1α, aggravates breast cancer cell growth and metastasis by promoting glycolysis
KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development
ΔNp63 transcriptionally regulates ATM to control p53 Serine-15 phosphorylation
SP1 transcriptionally regulates UBE2N expression to promote lung adenocarcinoma progression
Are preferential agreements stepping stones to other markets?
O-GlcNAc transferase couples MRE11 to transcriptionally active chromatin to suppress DNA damage
Preferential trade and investment agreements : from recalibration to reintegration
Morphology of transcriptionally active chromatin
TAp73 transcriptionally represses BNIP3 expression
Jagged1 intracellular domain/SMAD3 complex transcriptionally regulates TWIST1 to drive glioma invasion
Transcriptionally induced enhancers in the macrophage immune response to Mycobacterium tuberculosis infection
LINC01106 post-transcriptionally regulates ELK3 and HOXD8 to promote bladder cancer progression
NREP, transcriptionally upregulated by HIF-1α, aggravates breast cancer cell growth and metastasis by promoting glycolysis
KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development
ΔNp63 transcriptionally regulates ATM to control p53 Serine-15 phosphorylation
SP1 transcriptionally regulates UBE2N expression to promote lung adenocarcinoma progression
Are preferential agreements stepping stones to other markets?
O-GlcNAc transferase couples MRE11 to transcriptionally active chromatin to suppress DNA damage
Preferential trade and investment agreements : from recalibration to reintegration
Morphology of transcriptionally active chromatin
TAp73 transcriptionally represses BNIP3 expression
Jagged1 intracellular domain/SMAD3 complex transcriptionally regulates TWIST1 to drive glioma invasion
Transcriptionally induced enhancers in the macrophage immune response to Mycobacterium tuberculosis infection
LINC01106 post-transcriptionally regulates ELK3 and HOXD8 to promote bladder cancer progression
NREP, transcriptionally upregulated by HIF-1α, aggravates breast cancer cell growth and metastasis by promoting glycolysis
KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development
ΔNp63 transcriptionally regulates ATM to control p53 Serine-15 phosphorylation
SP1 transcriptionally regulates UBE2N expression to promote lung adenocarcinoma progression
Are preferential agreements stepping stones to other markets?
O-GlcNAc transferase couples MRE11 to transcriptionally active chromatin to suppress DNA damage
Preferential trade and investment agreements : from recalibration to reintegration
Morphology of transcriptionally active chromatin
TAp73 transcriptionally represses BNIP3 expression
Jagged1 intracellular domain/SMAD3 complex transcriptionally regulates TWIST1 to drive glioma invasion
Transcriptionally induced enhancers in the macrophage immune response to Mycobacterium tuberculosis infection