ATRAID Gene Editing


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ATRAID Gene Editing    

ATRAID (all-trans retinoic acid-induced differentiation factor), also known as apoptosis-related protein 3, APR3, or C2orf28, is a new gene, first cloned to induce cell differentiation and apoptosis from HL60 cells treated with all-trans retinoic acid (ATRA). ATRAID expression is elevated in heart, lung, liver and kidney tissues of aging mice.

AIRAID is a transmembrane protein that is localized on the lysosomal membrane and contains the N-terminal signal sequence, followed by the EGF-like domain, the C-terminus of the transmembrane and intracellular regions.

  • Functions of ATRAID

ATRAID overexpression causes G1/S phase arrest, which may be because overexpression of ATRAID significantly reduces cyclin D1 promoter activity and reduces endogenous cyclin D1 expression at mRNA and protein levels. Studies have confirmed that ATRAID is a direct binding protein of NELL-1. The functional analysis of cell proliferation and osteoblast differentiation showed that ATRAID binding is a potential mechanism for NELL-1 to promote osteoblast differentiation while inhibiting cell proliferation. However, the molecular mechanism by which ATRAID affects the cell cycle remains unknown.

ATRA is a key molecule in retinal pigment epithelium RPE cells, which regulates the development of vision and maintains normal visual function. Song Han et al. demonstrated for the first time that ATRAID levels in RPE and prematurely aging RPE cells induced by oxidative stress were significantly increased. In addition, the overexpression of ATRAID in human RPE cells accelerated cell senescence, which was eliminated by truncated ATRAID.

Therefore, targeting ATRAID may represent a new therapeutic strategy that can delay or inhibit the progressive effects of aging on AMD.

ATRAID Gene Editing Service

CRISPR/Cas9 PlatformCB provides you with comprehensive CRISPR/Cas9 gene editing services and products to a wide range of genomics researchers. As a leading biotechnology company specializing in gene editing, we can help you effectively regulate your target genes editing in vivo and in vitro using the CRISPR/Cas9 system.

  • What we offered?

➢ Gene knockout
➢ Conditional knockout/knock-in
➢ Point mutation
➢ Floxed allele insertion
➢ Fluorescent proteins insertion (e.g. GFP, RFP, mCherry, etc.) or immune-tags insertion (e.g. FLAG, HA, etc.)

  • Models we offered
Blood lineage cellsRAW264.7, HMC1.2, K562, U937 etc.
Cancer cell linesHEK293, HEK293T, Hela, MCF7, Neuro2a, HepG2, U87, etc.
Stem cellsiPSC
Other cell linesNIH3T3, MCF10, HEME, SW10 etc.
AnimalsMouse, rat, rabbit, zebrafish, C. elegans, etc.

Related Products at CRISPR/Cas9 PlatformCB

CLKO-1093ATRAID KO Cell Lysate-HEK293TInquiry
CSC-RT1240Human ATRAID Knockout Cell Line-HEK293TInquiry


  1. Song Han. et al. Apr3 accelerates the senescence of human retinal pigment epithelial cells. Molecular Medicine Reports. 2016; 13(4):3121-3126.
  2. XiaoDong Ding. et al. Apoptosis related protein 3 is a lysosomal membrane protein. Biochemical and Biophysical Research Communications. 2015; 460(4):915-922.
  3. Yuan Li. et al. APR3 modulates oxidative stress and mitochondrial function in ARPE-19 cells. The FASEB Journal Vol. 2018; 32(11):5851-5861.
  4. Yu F. et al. Apoptosis related protein 3, an ATRA-upregulated membrane protein arrests the cell cycle at G1/S phase by decreasing the expression of cyclin D1. Biochemical and Biophysical Research Communications. 2007; 358:1041-1046.
  5. Zhu F. et al. Improved PCR-based subtractive hybridization strategy for cloning differentially expressed genes. Biotechniques. 2000; 29:310-313.
  6. Zou X. et al. NELL-1 binds to APR3 affecting human osteoblast proliferation and differentiation. FEBS Lett. 2011; 585:2410-2418.
For research use only. Not intended for any clinical use.


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