BRD3 Gene Editing


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BRD3 Gene Editing    

BRD3, also known as RING3 protein-like protein (RING3L), is a member of the the Bromodomain and Extra Terminal (BET) families of Bromodomain proteins (BRD). This gene is located at 9q34, which contains several major histocompatibility complex (MHC) genes.

The structure of BRD3 Figure1: The structure of BRD3 (Lei-lei Fu. 2015)

Structurally similar to other BET family members, it contains two tandem homologous BRDs and a "terminal" motif. Functionally, BRD3 is associated with acetylated lysine residues on histones and transcription factors, and BRD3 is also involved in nuclear small-weight plastics in the transcriptional environment.

The BET families of BRD consisting of four human members (BRD2, BRD3, BRD4, and BRDT) have become promising new cancer target categories for small molecule drug discovery.

BRD3 Gene Editing Service

CRISPR/Cas9 PlatformCB, a global leading biotechnological company specializing in gene editing, is dedicated to offering comprehensive CRISPR/Cas9 gene editing services and products to a wide range of genomics researchers. With deep gene editing knowledge and extensive experience in experimental operation and data processing, we can help you effectively control target genes deleted, inserted or point mutated in cells or animals via CRISPR/Cas9 technology.

  • BRD3 Gene Editing Cell Line Generation

We have successfully implemented BRD3 CRISPR/Cas9 gene edited in both easy-to-transfect cell lines and hard-to-transfect cells. To support your projects, we will offer you full-length custom BRD3 gene editing service from strategy design to final stable cells. Our BRD3 gene editing cell line generation services include:

➢ gRNA design and synthesis
➢ Transfect the cell lines you're interested
➢ Select the high expression cells and sort monoclonal cell
➢ Validate the knockout/knockin/point mutation of BRD3 by PCR and sequencing
➢ Produce cryogenic preserved vials of stable cells and a final report

Typically, we develop CRISPR-mediated gene editing cell lines including HEK239T, Hela, HepG2, U87, but we can use other cell lines according to your requirements.

  • Alternative cell lines

➢ Blood Lineage Cells (RAW264.7, HMC1.2, K562, U937 etc.)
➢ Cancer Cell Lines (HEK293, HEK293T, Hela, MCF7, Neuro2a, HepG2, U87 etc.)
➢ Stem Cells (iPSC)
➢ Other Cell Lines (NIH3T3, MCF10, HEME, SW10 etc.)

  • BRD3 Gene Editing Animal Model Generation

CRISPR/Cas9 PlatformCB also has extensive experience in incorporating CRISPR/Cas9 technology into animal models, which have been fully recognized by our clients. Tell us your needs, we provide a one-stop-shop BRD3 CRISPR/Cas9 gene editing animal service and guarantee at least 2 founders or 3 F1 animals with shorter turnaround time and lower price. Our BRD3 gene editing animal model generation services include:

➢ BRD3 gene conventional knockout animals
➢ BRD3 gene conditional knockout animals
➢ BRD3 point mutation animals
➢ BRD3 knockin animals

Alternative species: mouse, rat, rabbit, zebrafish, C. elegans, etc.

CRISPR/Cas9 PlatformCB is devoted to providing the best gene editing services and products for academic research, biotech research and pharmaceutical drug discovery with excellent quality management and quality assurance capacity. To accelerate the achievement of your research goals, our gene editing expert team provides you with custom CRISPR/Cas9 services for any specific gene to help you solve problems encountered during your research. There is no doubt that CRISPR/Cas9 PlatformCB will be your best partner to support your research.

Related Products at CRISPR/Cas9 PlatformCB

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  1. Isaia Barbieri. et al. Bromodomains as therapeutic targets in cancer. Briefings in Functional Genomics. 2013; 12(3):219-230.
  2. Imran Ali. et al. BET Inhibitors as Anticancer Agents: A Patent Review. Recent Patents on Anti-Cancer Drug Discovery. 2017; 12(4).
  3. LeRoy G. et al. The double bromodomain proteins Brd2 and Brd3 couple histone acetylation to transcription. Molecular Cell. 2008; 30 (1): 51–60.
  4. Stonestrom AJ. et al. Functions of BET proteins in erythroid gene expression. Blood. 2015; 125: 2825–34.
  5. Lei-lei Fu. et al. Inhibition of BET bromodomains as a therapeutic strategy for cancer drug discovery. Oncotarget. 2015; 6(8):5501–5516.
For research use only. Not intended for any clinical use.


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