# ID3

Source: https://onco.cc/targets/id3/  
OnCo record `id3` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

ID3 (DNA-binding protein inhibitor ID-3) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Burkitt lymphoma and Diffuse large B-cell lymphoma.

## Summary

Transcriptional regulator (lacking a basic DNA binding domain) which negatively regulates the basic helix-loop-helix (bHLH) transcription factors by forming heterodimers and inhibiting their DNA binding and transcriptional activity. Implicated in regulating a variety of cellular processes, including cellular growth, senescence, differentiation, apoptosis, angiogenesis, and neoplastic transformation. Involved in myogenesis by inhibiting skeletal muscle and cardiac myocyte differentiation and promoting muscle precursor cells proliferation.

CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. IntOGen calls it a driver in 5 cohorts (0 activating, 5 loss-of-function), covering Burkitt Lymphoma, Diffuse Large B-Cell Lymphoma, NOS, Malignant Lymphoma, Non-Hodgkin Lymphoma.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: inhibitor of DNA binding 3; DNA-binding protein inhibitor ID-3; HEIR-1; bHLHb25
- Tags: cancer-genes-wave
- Symbol: ID3
- Class: tumor-suppressor
- Biology: Transcriptional regulator (lacking a basic DNA binding domain) which negatively regulates the basic helix-loop-helix (bHLH) transcription factors by forming heterodimers and inhibiting their DNA binding and transcriptional activity. Implicated in regulating a variety of cellular processes, including cellular growth, senescence, differentiation, apoptosis, angiogenesis, and neoplastic transformation. Involved in myogenesis by inhibiting skeletal muscle and cardiac myocyte differentiation and promoting muscle precursor cells proliferation. Inhibits the binding of E2A-containing protein complexes to muscle creatine kinase E-box enhancer. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-BMAL1 heterodimer. Location: Nucleus (UniProt). Locus 1p36.12 (HGNC).
- Where found: Non-Hodgkin lymphoma: Open Targets association 0.61 with non-Hodgkin lymphoma (MONDO_0018908); IntOGen driver in 2 cohorts (MLYM, NHL); Burkitt lymphoma: Open Targets association 0.51 with Burkitt lymphoma (MONDO_0007243); CIViC evidence names this disease; Diffuse large B-cell lymphoma: IntOGen driver in 1 cohort (DLBCLNOS)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 5 cohorts; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:5362: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:5362
- UniProt Q02535: https://www.uniprot.org/uniprotkb/Q02535/entry
- NCBI Gene 3399: https://www.ncbi.nlm.nih.gov/gene/3399
- Ensembl ENSG00000117318: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000117318

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Burkitt lymphoma](https://onco.cc/cancers/burkitt-lymphoma/), [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/)

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JSON: https://onco.cc/api/v1/entities/id3.json