Zfp335 (zinc finger protein 335; also known as NRC-interacting factor 1 (Nif1)) is a regulator of vertebrate neurogenesis. As a component of the trithorax H3K4-methylation complex that regulates REST/NRSF, it is essential for neural cell progenitor self-renewal, neurogenesis, and neuronal differentiation. A c.3332g&gt;a mutation in the human gene is associated with severe microcephaly, neuronal degeneration, and neonatal death. 

In this targeted mutation strain, the mouse Zfp335 promoter, exon 1, and exon 2 are flanked by loxP sites. Cre-mediated excision of this floxed region enables the generation of tissue-specific knockouts. Widespread loss of ZNF335 protein in mice leads to embryonic lethality as early as embryonic day 7.5 (E7.5). 

When crossed with Emx1-cre mice (see Stock No. <a href="https://www.jax.org/strain/005628">005628</a>), progeny lack almost all cortical structure and cortical neurons, leading to the formation of a small brain with a thin sheath of tissue and enlarged ventricles.

Zfp335 (zinc finger protein 335; also known as identified as a NRC-interacting factor 1 (Nif1)) is a regulator of vertebrate neurogenesis. A c.3332g&gt;a mutation in the human gene is associated with severe microcephaly, neuronal degeneration, and neonatal death. The mouse Zfp335 promoter, exon 1, and exon 2 are flanked by loxP sites in this conditional targeted mutation strain, enabling tissue-specific knockouts mediated by Cre recombinase.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

<a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> for more information.