IRF2 Recombinant Rabbit mAb (一抗) - WB,IHC-P,IHC-F,IF | Bioss

bsm-52115R

重组兔单抗

IRF2 Recombinant Rabbit mAb

干扰素调节因子2重组兔单抗

IRF-2; 9830146E22Rik; IRF2_HUMAN; IRF2; IRF2_MOUSE; interferon regulatory factor 2

Rabbit

A synthesized peptide derived from human IRF2: 300-349

IgG

Liquid

affinity purified by Protein A

Recombinant

5F2

39 kDa

45 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

IRF2 encodes interferon regulatory factor 2, a member of the interferon regulatory transcription factor (IRF) family. IRF2 competitively inhibits the IRF1-mediated transcriptional activation of interferons alpha and beta, and presumably other genes that employ IRF1 for transcription activation. However, IRF2 also functions as a transcriptional activator of histone H4. [provided by RefSeq, Jul 2008]

IRF2

Interferon regulatory factor 2

Nucleus.

Expressed throughout the epithelium of the colon. Also expressed in lamina propria.

Acetylated by CBP/ p300 during cell-growth. Acetylation on Lys-75 is required for stimulation of H4 promoter activity.
The major sites of sumoylation are Lys-137 and Lys-293. Sumoylation by SUMO1 increases its transcriptional repressor activity on IRF1 and diminishes its ability to activate ISRE and H4 promoter.

Belongs to the IRF family.
Contains 1 IRF tryptophan pentad repeat DNA-binding domain.

Specifically binds to the upstream regulatory region of type I IFN and IFN-inducible MHC class I genes (the interferon consensus sequence (ICS)) and represses those genes. Also acts as an activator for several genes including H4 and IL7. Constitutively binds to the ISRE promoter to activate IL7. Involved in cell cycle regulation through binding the site II (HiNF-M) promoter region of H4 and activating transcription during cell growth. Antagonizes IRF1 transcriptional activation.