ENC1

---

title: "ENC1" type: doc version: 1 created: 2026-02-28 author: "Wikipedia contributors" status: active scope: public tags: ["kelch-proteins"] description: "Protein-coding gene in humans" topic_path: "general/kelch-proteins" source: "https://en.wikipedia.org/wiki/ENC1" license: "CC BY-SA 4.0" wikipedia_page_id: 0 wikipedia_revision_id: 0

::summary Protein-coding gene in humans ::

Ectoderm-neural cortex protein 1 is a protein that in humans is encoded by the ENC1 gene.

Function

DNA damage and/or hyperproliferative signals activate wildtype p53 tumor suppressor protein (TP53; MIM 191170), inducing cell cycle arrest or apoptosis. Mutations that inactivate p53 occur in 50% of all tumors. Polyak et al. (1997) used serial analysis of gene expression (SAGE) to evaluate cellular mRNA levels in a colorectal cancer cell line transfected with p53. Of 7,202 transcripts identified, only 14 were expressed at levels more than 10-fold higher in p53-expressing cells than in control cells. Polyak et al. (1997) termed these genes 'p53-induced genes,' or PIGs, several of which were predicted to encode redox-controlling proteins. They noted that reactive oxygen species (ROS) are potent inducers of apoptosis. Flow cytometric analysis showed that p53 expression induces ROS production, which increases as apoptosis progresses under some conditions. The authors stated that the PIG10 gene, also called ENC1, encodes an actin-binding protein.[supplied by OMIM]

Interactions

ENC1 has been shown to interact with Retinoblastoma protein.

References

References

1. (Sep 1997). "A model for p53-induced apoptosis". Nature.
2. (May 1998). "NRP/B, a novel nuclear matrix protein, associates with p110(RB) and is involved in neuronal differentiation". The Journal of Cell Biology.
3. "Entrez Gene: ENC1 ectodermal-neural cortex (with BTB-like domain)".

::callout[type=info title="Wikipedia Source"] This article was imported from Wikipedia and is available under the Creative Commons Attribution-ShareAlike 4.0 License. Content has been adapted to SurfDoc format. Original contributors can be found on the article history page. ::