ZNF703

Zinc-finger nucleases (ZFNs) are artificial restriction enzymes generated by fusing a zinc finger DNA-binding domain to a DNA-cleavage domain. Zinc finger domains can be engineered to target specific desired DNA sequences and this enables zinc-finger nucleases to target unique sequences within complex genomes. By taking advantage of endogenous DNA repair machinery, these reagents can be used to precisely alter the genomes of higher organisms. Alongside CRISPR/Cas9 and TALEN, ZFN is a prominent tool in the field of genome editing.

Full Name

zinc finger protein 703

Function

Transcriptional corepressor which does not bind directly to DNA and may regulate transcription through recruitment of histone deacetylases to gene promoters. Regulates cell adhesion, migration and proliferation. May be required for segmental gene expression during hindbrain development.

Biological Process

Biological Process adherens junction assembly Source:UniProtKB
Biological Process cellular response to estradiol stimulus Source:UniProtKB1 Publication
Biological Process mammary gland epithelial cell differentiation Source:UniProtKB1 Publication
Biological Process negative regulation of DNA-templated transcription Source:UniProtKB1 Publication
Biological Process negative regulation of homotypic cell-cell adhesion Source:UniProtKB
Biological Process positive regulation of cell migration Source:UniProtKB
Biological Process positive regulation of cell population proliferation Source:UniProtKB1 Publication
Biological Process positive regulation of epithelial to mesenchymal transition Source:UniProtKB
Biological Process positive regulation of mammary gland epithelial cell proliferation Source:UniProtKB1 Publication
Biological Process regulation of canonical Wnt signaling pathway Source:UniProtKB
Biological Process regulation of cell cycle Source:UniProtKB1 Publication
Biological Process regulation of DNA-templated transcription Source:UniProtKB1 Publication
Biological Process regulation of transforming growth factor beta receptor signaling pathway Source:UniProtKB1 Publication

Cellular Location

Nucleus
Cytoplasm

Involvement in disease

Nucleus 2 Publications
Cytoplasm.