|Positive WB detected in||L02 cells, HeLa cells, HepG2 cells|
|Positive IP detected in||HepG2 cells|
|Positive IF detected in||L02 cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:200-1:1000 for WB|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
14662-1-AP targets AFF4 in WB, IP, IF, ELISA applications and shows reactivity with human samples.
|Host / Isotype||Rabbit / IgG|
|Immunogen||AFF4 fusion protein Ag6336|
|Full Name||AF4/FMR2 family, member 4|
|Calculated molecular weight||127 kDa|
|Observed molecular weight||140 kDa|
|GenBank accession number||BC063007|
|Gene ID (NCBI)||27125|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Transcriptional controled by RNA polymerase II (Pol II) is a multi-step process requiring the concerted action of multiple factors and contacts with the DNA template for the proper synthesis of nascent RNA [PMID:12676794]. ELL1 was demonstrated to be a Pol II elongation factor capable of enhancing the catalytic rate of transcription elongation by reducing transient pausing by the enzyme [PMID:8596958]. AFF4 was initially identified as a fusion partner of the MLL (mixed-lineage leukemia) gene participated in infant acute lymphoblastic leukemia, and a component of the ELL/p-TEFb elongation complex. AFF4 interacts with positive transcription elongation factor-b while also repressing Tat transactivation of HIV-1 [PMID:17389929].
Structural and functional insight into the effect of AFF4 dimerization on activation of HIV-1 proviral transcription.
A chalcone derivative reactivates latent HIV-1 transcription through activating P-TEFb and promoting Tat-SEC interaction on viral promoter.
Nucleic Acids Res
Multiple P-TEFbs cooperatively regulate the release of promoter-proximally paused RNA polymerase II.
Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy.