EAF1
Reaktivität: Human
WB, ELISA
Wirt: Kaninchen
Polyclonal
FITC
Applikationshinweise
WB,1:500 - 1:2000
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Buffer
PBS with 0.02 % sodium azide,50 % glycerol, pH 7.3.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C
Informationen zur Lagerung
Store at -20°C. Avoid freeze / thaw cycles.
Target
EAF1
(ELL Associated Factor 1 (EAF1))
Andere Bezeichnung
EAF1
Hintergrund
Actin is a key regulator of RNA polymerase (Pol) II-dependent transcription. Positive transcription elongation factor b (P-TEFb), a Cdk9/cyclin T1 heterodimer, has been reported to play a critical role in transcription elongation. However, the relationship between actin and P-TEFb is still not clear. In this study, actin was found to interact with Cdk9, a catalytic subunit of P-TEFb, in elongation complexes. Using immunofluorescence and immunoprecipitation assays, Cdk9 was found to bind to G-actin through the conserved Thr-186 in the T-loop. Overexpression and in vitro kinase assays showed that G-actin promotes P-TEFb-dependent phosphorylation of the Pol II C-terminal domain. An in vitro transcription experiment revealed that the interaction between G-actin and Cdk9 stimulated Pol II transcription elongation. ChIP and immobilized template assays indicated that actin recruited Cdk9 to a transcriptional template in vivo and in vitro. Using cytokine IL-6-inducible p21 gene expression system, we revealed that actin recruited Cdk9 to endogenous gene. Moreover, overexpression of actin and Cdk9 increased histone H3 acetylation and acetylized histone H3 binding to a transcriptional template through the interaction with histone acetyltransferase, p300. Taken together, our results suggested that actin participates in transcription elongation by recruiting Cdk9 for phosphorylation of the Pol II C-terminal domain, and the actin-Cdk9 interaction promotes chromatin remodeling.,EAF1,Epigenetics & Nuclear Signaling,EAF1