# NPAS3

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Protein-coding gene in the species Homo sapiens

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NPAS3 Identifiers Aliases NPAS3, neuronal PAS domain protein 3, MOP6, PASD6, bHLHe12 External IDs OMIM: 609430; MGI: 1351610; HomoloGene: 8461; GeneCards: NPAS3; OMA:NPAS3 - orthologs Gene location (Human) Chr. Chromosome 14 (human)[1] Band 14q13.1 Start 32,934,396 bp[1] End 33,820,863 bp[1] Gene location (Mouse) Chr. Chromosome 12 (mouse)[2] Band 12|12 C1 Start 53,248,677 bp[2] End 54,072,175 bp[2] RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in endothelial cell ventricular zone corpus callosum buccal mucosa cell globus pallidus internal globus pallidus external globus pallidus optic nerve inferior ganglion of vagus nerve entorhinal cortex Top expressed in substantia nigra lumbar subsegment of spinal cord deep cerebellar nuclei dorsal tegmental nucleus fossa globus pallidus dorsomedial hypothalamic nucleus ventral tegmental area condyle lateral hypothalamus More reference expression data BioGPS n/a Gene ontology Molecular function protein dimerization activity DNA binding DNA-binding transcription factor activity, RNA polymerase II-specific protein heterodimerization activity Cellular component nucleoplasm cytosol nucleus Biological process regulation of transcription by RNA polymerase II positive regulation of transcription, DNA-templated transcription, DNA-templated regulation of transcription, DNA-templated developmental process positive regulation of transcription by RNA polymerase II Sources:Amigo / QuickGO Orthologs Species Human Mouse Entrez 64067 27386 Ensembl ENSG00000151322 ENSMUSG00000021010 UniProt Q8IXF0 Q9QZQ0 RefSeq (mRNA) NM_001164749 NM_001165893 NM_022123 NM_173159 NM_001394988 NM_001394989 NM_013780 RefSeq (protein) NP_001158221 NP_001159365 NP_071406 NP_775182 NP_038808 Location (UCSC) Chr 14: 32.93 – 33.82 Mb Chr 12: 53.25 – 54.07 Mb PubMed search [3] [4] Wikidata View/Edit Human View/Edit Mouse

**NPAS3** or **Neuronal PAS domain protein 3** is a brain-enriched [transcription factor](/source/Transcription_factor) belonging to the [bHLH-PAS superfamily of transcription factors](/source/Basic_helix-loop-helix), the members of which carry out diverse functions, including [circadian oscillations](/source/Circadian_oscillations), [neurogenesis](/source/Neurogenesis), [toxin](/source/Toxin) [metabolism](/source/Metabolism), [hypoxia](/source/Hypoxia_(medical)), and [tracheal](/source/Vertebrate_trachea) development. NPAS3 contains a [basic helix-loop-helix](/source/Basic_helix-loop-helix) structural motif and two [PAS domain](/source/PAS_domain), like the other proteins in the superfamily.

It functions as an heterodimer by binding [ARNT2](/source/ARNT2), another member of the bHLH-PAS superfamily.[5]

## Function

*NPAS3* harbors the largest cluster of [human accelerated regions](/source/Human_accelerated_regions), suggesting it may have played a key role in [human evolution](/source/Human_evolution).[6] Among this accelerated elements, HAR202 is particularly fascinating due to its differential activity between modern humans and [archaic species](/source/Homo), even though it has only been reported in animal reporter assays.[7]

From the first set of human accelerated regions described in 2006, *NPAS3* *locus* overlaps one of the most accelerated sequences, HAR21 .[8]

[NPAS1](/source/NPAS1) and NPAS3-deficient mice display behavioral abnormalities typical to the [animal models](/source/Animal_models_of_schizophrenia) of [schizophrenia](/source/Schizophrenia).[9] Targeting the gene in astrocytes leads to autistic-like behaviours such as reduced vocalization and socialization.[10]

According to the same study, *[NPAS1](/source/NPAS1)* and *NPAS3* disruption leads to reduced expression of [reelin](/source/Reelin), which is also consistently found to be reduced in the brains of human patients with [schizophrenia](/source/Schizophrenia) and psychotic [bipolar disorder](/source/Bipolar_disorder).

Recent advances in mouse models have further characterized *NPAS3* function and identified key roles in [astrogenesis](/source/Gliogenesis), [adult neurogenesis](/source/Adult_neurogenesis) and in [inhibitory interneurons](/source/Interneuron) [differentiation](/source/Cellular_differentiation).[10][11][12]

## Clinical significance

Disruption of NPAS3 was found in one family affected by schizophrenia[13] and NPAS3 gene is thought to be associated with psychiatric illness and learning disability.[14][15] In a genetic study of several hundred subjects conducted in 2008, interacting [haplotypes](/source/Haplotype) at the NPAS3 locus were found to affect the risk of schizophrenia and [bipolar disorder](/source/Bipolar_disorder).[16]

In a [pharmacogenetical](/source/Pharmacogenetics) study, polymorphisms in NPAS3 gene were highly associated with response to [iloperidone](/source/Iloperidone), a proposed atypical antipsychotic.[17]

## References

1. ^ [***a***](#cite_ref-refGRCh38Ensembl_1-0) [***b***](#cite_ref-refGRCh38Ensembl_1-1) [***c***](#cite_ref-refGRCh38Ensembl_1-2) [GRCh38: Ensembl release 89: ENSG00000151322](http://May2017.archive.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000151322) – [Ensembl](/source/Ensembl_genome_database_project), May 2017

1. ^ [***a***](#cite_ref-refGRCm38Ensembl_2-0) [***b***](#cite_ref-refGRCm38Ensembl_2-1) [***c***](#cite_ref-refGRCm38Ensembl_2-2) [GRCm38: Ensembl release 89: ENSMUSG00000021010](http://May2017.archive.ensembl.org/Mus_musculus/Gene/Summary?db=core;g=ENSMUSG00000021010) – [Ensembl](/source/Ensembl_genome_database_project), May 2017

1. **[^](#cite_ref-3)** ["Human PubMed Reference:"](https://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=Link&LinkName=gene_pubmed&from_uid=64067). *National Center for Biotechnology Information, U.S. National Library of Medicine*.

1. **[^](#cite_ref-4)** ["Mouse PubMed Reference:"](https://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=Link&LinkName=gene_pubmed&from_uid=27386). *National Center for Biotechnology Information, U.S. National Library of Medicine*.

1. **[^](#cite_ref-5)** Rossi JJ, Rosenfeld JA, Chan KM, Streff H, Nankivell V, Peet DJ, et al. (March 2021). ["Molecular characterisation of rare loss-of-function NPAS3 and NPAS4 variants identified in individuals with neurodevelopmental disorders"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987981). *Scientific Reports*. **11** (1) 6602. [Bibcode](/source/Bibcode_(identifier)):[2021NatSR..11.6602R](https://ui.adsabs.harvard.edu/abs/2021NatSR..11.6602R). [doi](/source/Doi_(identifier)):[10.1038/s41598-021-86041-4](https://doi.org/10.1038%2Fs41598-021-86041-4). [PMC](/source/PMC_(identifier)) [7987981](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987981). [PMID](/source/PMID_(identifier)) [33758288](https://pubmed.ncbi.nlm.nih.gov/33758288).

1. **[^](#cite_ref-6)** Kamm GB, Pisciottano F, Kliger R, Franchini LF (May 2013). ["The developmental brain gene NPAS3 contains the largest number of accelerated regulatory sequences in the human genome"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670734). *Molecular Biology and Evolution*. **30** (5): 1088–1102. [doi](/source/Doi_(identifier)):[10.1093/molbev/mst023](https://doi.org/10.1093%2Fmolbev%2Fmst023). [PMC](/source/PMC_(identifier)) [3670734](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670734). [PMID](/source/PMID_(identifier)) [23408798](https://pubmed.ncbi.nlm.nih.gov/23408798).

1. **[^](#cite_ref-7)** Caporale AL, Cinalli AR, Rubinstein M, Franchini LF (October 2024). Wittkopp P (ed.). ["The Human Accelerated Region HAR202 Controls NPAS3 Expression in the Developing Forebrain Displaying Differential Enhancer Activity Between Modern and Archaic Human Sequences"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11461159). *Molecular Biology and Evolution*. **41** (10) msae186. [doi](/source/Doi_(identifier)):[10.1093/molbev/msae186](https://doi.org/10.1093%2Fmolbev%2Fmsae186). [PMC](/source/PMC_(identifier)) [11461159](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11461159). [PMID](/source/PMID_(identifier)) [39241178](https://pubmed.ncbi.nlm.nih.gov/39241178).

1. **[^](#cite_ref-Pollard_2006_8-0)** Pollard KS, Salama SR, Lambert N, Lambot MA, Coppens S, Pedersen JS, et al. (September 2006). "An RNA gene expressed during cortical development evolved rapidly in humans". *Nature*. **443** (7108): 167–172. [Bibcode](/source/Bibcode_(identifier)):[2006Natur.443..167P](https://ui.adsabs.harvard.edu/abs/2006Natur.443..167P). [doi](/source/Doi_(identifier)):[10.1038/nature05113](https://doi.org/10.1038%2Fnature05113). [hdl](/source/Hdl_(identifier)):[2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/51805](https://hdl.handle.net/2013%2FULB-DIPOT%3Aoai%3Adipot.ulb.ac.be%3A2013%2F51805). [PMID](/source/PMID_(identifier)) [16915236](https://pubmed.ncbi.nlm.nih.gov/16915236). [S2CID](/source/S2CID_(identifier)) [18107797](https://api.semanticscholar.org/CorpusID:18107797).

1. **[^](#cite_ref-ErbelSieler_2004_9-0)** Erbel-Sieler C, Dudley C, Zhou Y, Wu X, Estill SJ, Han T, et al. (September 2004). ["Behavioral and regulatory abnormalities in mice deficient in the NPAS1 and NPAS3 transcription factors"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC518807). *Proceedings of the National Academy of Sciences of the United States of America*. **101** (37): 13648–13653. [Bibcode](/source/Bibcode_(identifier)):[2004PNAS..10113648E](https://ui.adsabs.harvard.edu/abs/2004PNAS..10113648E). [doi](/source/Doi_(identifier)):[10.1073/pnas.0405310101](https://doi.org/10.1073%2Fpnas.0405310101). [PMC](/source/PMC_(identifier)) [518807](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC518807). [PMID](/source/PMID_(identifier)) [15347806](https://pubmed.ncbi.nlm.nih.gov/15347806).

1. ^ [***a***](#cite_ref-Li_2022_10-0) [***b***](#cite_ref-Li_2022_10-1) Li Y, Fan T, Li X, Liu L, Mao F, Li Y, et al. (August 2022). ["Npas3 deficiency impairs cortical astrogenesis and induces autistic-like behaviors"](https://doi.org/10.1016%2Fj.celrep.2022.111289). *Cell Reports*. **40** (9) 111289. [doi](/source/Doi_(identifier)):[10.1016/j.celrep.2022.111289](https://doi.org/10.1016%2Fj.celrep.2022.111289). [PMID](/source/PMID_(identifier)) [36044858](https://pubmed.ncbi.nlm.nih.gov/36044858).

1. **[^](#cite_ref-11)** Pieper AA, Wu X, Han TW, Estill SJ, Dang Q, Wu LC, et al. (September 2005). ["The neuronal PAS domain protein 3 transcription factor controls FGF-mediated adult hippocampal neurogenesis in mice"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1216832). *Proceedings of the National Academy of Sciences of the United States of America*. **102** (39): 14052–14057. [Bibcode](/source/Bibcode_(identifier)):[2005PNAS..10214052P](https://ui.adsabs.harvard.edu/abs/2005PNAS..10214052P). [doi](/source/Doi_(identifier)):[10.1073/pnas.0506713102](https://doi.org/10.1073%2Fpnas.0506713102). [PMC](/source/PMC_(identifier)) [1216832](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1216832). [PMID](/source/PMID_(identifier)) [16172381](https://pubmed.ncbi.nlm.nih.gov/16172381).

1. **[^](#cite_ref-12)** Stanco A, Pla R, Vogt D, Chen Y, Mandal S, Walker J, et al. (December 2014). ["NPAS1 represses the generation of specific subtypes of cortical interneurons"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258152). *Neuron*. **84** (5): 940–953. [doi](/source/Doi_(identifier)):[10.1016/j.neuron.2014.10.040](https://doi.org/10.1016%2Fj.neuron.2014.10.040). [PMC](/source/PMC_(identifier)) [4258152](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258152). [PMID](/source/PMID_(identifier)) [25467980](https://pubmed.ncbi.nlm.nih.gov/25467980).

1. **[^](#cite_ref-Kamnasaran_2003_13-0)** Kamnasaran D, Muir WJ, Ferguson-Smith MA, Cox DW (May 2003). ["Disruption of the neuronal PAS3 gene in a family affected with schizophrenia"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1735455). *Journal of Medical Genetics*. **40** (5): 325–332. [doi](/source/Doi_(identifier)):[10.1136/jmg.40.5.325](https://doi.org/10.1136%2Fjmg.40.5.325). [PMC](/source/PMC_(identifier)) [1735455](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1735455). [PMID](/source/PMID_(identifier)) [12746393](https://pubmed.ncbi.nlm.nih.gov/12746393).

1. **[^](#cite_ref-Pickard_2005_14-0)** Pickard BS, Malloy MP, Porteous DJ, Blackwood DH, Muir WJ (July 2005). "Disruption of a brain transcription factor, NPAS3, is associated with schizophrenia and learning disability". *American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics*. **136B** (1): 26–32. [doi](/source/Doi_(identifier)):[10.1002/ajmg.b.30204](https://doi.org/10.1002%2Fajmg.b.30204). [PMID](/source/PMID_(identifier)) [15924306](https://pubmed.ncbi.nlm.nih.gov/15924306). [S2CID](/source/S2CID_(identifier)) [33879828](https://api.semanticscholar.org/CorpusID:33879828).

1. **[^](#cite_ref-Pickard_2006_15-0)** Pickard BS, Pieper AA, Porteous DJ, Blackwood DH, Muir WJ (2006). ["The NPAS3 gene--emerging evidence for a role in psychiatric illness"](https://doi.org/10.1080%2F07853890600946500). *Annals of Medicine*. **38** (6): 439–448. [doi](/source/Doi_(identifier)):[10.1080/07853890600946500](https://doi.org/10.1080%2F07853890600946500). [PMID](/source/PMID_(identifier)) [17008307](https://pubmed.ncbi.nlm.nih.gov/17008307).

1. **[^](#cite_ref-Pickard_2009_16-0)** Pickard BS, Christoforou A, Thomson PA, Fawkes A, Evans KL, Morris SW, et al. (September 2009). ["Interacting haplotypes at the NPAS3 locus alter risk of schizophrenia and bipolar disorder"](https://doi.org/10.1038%2Fmp.2008.24). *Molecular Psychiatry*. **14** (9): 874–884. [doi](/source/Doi_(identifier)):[10.1038/mp.2008.24](https://doi.org/10.1038%2Fmp.2008.24). [PMID](/source/PMID_(identifier)) [18317462](https://pubmed.ncbi.nlm.nih.gov/18317462).

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## Further reading

- Kamnasaran D, Muir WJ, Ferguson-Smith MA, Cox DW (May 2003). ["Disruption of the neuronal PAS3 gene in a family affected with schizophrenia"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1735455). *Journal of Medical Genetics*. **40** (5): 325–332. [doi](/source/Doi_(identifier)):[10.1136/jmg.40.5.325](https://doi.org/10.1136%2Fjmg.40.5.325). [PMC](/source/PMC_(identifier)) [1735455](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1735455). [PMID](/source/PMID_(identifier)) [12746393](https://pubmed.ncbi.nlm.nih.gov/12746393).

- Moreira F, Kiehl TR, So K, Ajeawung NF, Honculada C, Gould P, et al. (July 2011). ["NPAS3 demonstrates features of a tumor suppressive role in driving the progression of Astrocytomas"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123785). *The American Journal of Pathology*. **179** (1): 462–476. [doi](/source/Doi_(identifier)):[10.1016/j.ajpath.2011.03.044](https://doi.org/10.1016%2Fj.ajpath.2011.03.044). [PMC](/source/PMC_(identifier)) [3123785](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123785). [PMID](/source/PMID_(identifier)) [21703424](https://pubmed.ncbi.nlm.nih.gov/21703424).

- Kamnasaran D, Ajewung N, Rana M, Gould P (2010). "393 NPAS3 is a novel late-stage acting progression factor in gliomas with tumour suppressive functions". *European Journal of Cancer Supplements*. **8** (5): 100. [doi](/source/Doi_(identifier)):[10.1016/S1359-6349(10)71194-0](https://doi.org/10.1016%2FS1359-6349%2810%2971194-0).

- Long PM, Wesley UV, Jaworski DM (2010). ["CB-01. Regulation of aminoacylase expression in neuroblastoma"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199169). *Neuro-Oncology*. **12** (Supplement 4): iv7–iv25. [doi](/source/Doi_(identifier)):[10.1093/neuonc/noq116.s2](https://doi.org/10.1093%2Fneuonc%2Fnoq116.s2). [PMC](/source/PMC_(identifier)) [3199169](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199169).

- Wong J, Duncan CE, Beveridge NJ, Webster MJ, Cairns MJ, Weickert CS (March 2013). ["Expression of NPAS3 in the human cortex and evidence of its posttranscriptional regulation by miR-17 during development, with implications for schizophrenia"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576160). *Schizophrenia Bulletin*. **39** (2): 396–406. [doi](/source/Doi_(identifier)):[10.1093/schbul/sbr177](https://doi.org/10.1093%2Fschbul%2Fsbr177). [PMC](/source/PMC_(identifier)) [3576160](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576160). [PMID](/source/PMID_(identifier)) [22228753](https://pubmed.ncbi.nlm.nih.gov/22228753).

- Shin J, Jeong HY, Lee KE, Kim J (September 2010). ["Isolation and Characterization of Chicken NPAS3"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214776). *Experimental Neurobiology*. **19** (2): 71–74. [doi](/source/Doi_(identifier)):[10.5607/en.2010.19.2.71](https://doi.org/10.5607%2Fen.2010.19.2.71). [PMC](/source/PMC_(identifier)) [3214776](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214776). [PMID](/source/PMID_(identifier)) [22110344](https://pubmed.ncbi.nlm.nih.gov/22110344).

- Fonseca DJ, Prada CF, Siza LM, Angel D, Gomez YM, Restrepo CM, et al. (March 2012). "A de novo 14q12q13.3 interstitial deletion in a patient affected by a severe neurodevelopmental disorder of unknown origin". *American Journal of Medical Genetics. Part A*. **158A** (3): 689–693. [doi](/source/Doi_(identifier)):[10.1002/ajmg.a.35215](https://doi.org/10.1002%2Fajmg.a.35215). [PMID](/source/PMID_(identifier)) [22315208](https://pubmed.ncbi.nlm.nih.gov/22315208). [S2CID](/source/S2CID_(identifier)) [9506804](https://api.semanticscholar.org/CorpusID:9506804).

v t e Transcription factors and intracellular receptors (1) Basic domains (1.1) Basic leucine zipper (bZIP) Activating transcription factor AATF 1 2 3 4 5 6 7 AP-1 c-Fos FOSB FOSL1 FOSL2 JDP2 c-Jun JUNB JunD BACH 1 2 BATF BLZF1 C/EBP α β γ δ ε ζ CREB 1 3 L1 CREM DBP DDIT3 GABPA GCN4 HLF MAF B sMaf F G K NFE 2 L1 L2 L3 NFIL3 NRL NRF 1 2 3 XBP1 (1.2) Basic helix–loop–helix (bHLH) Group A AS-C ASCL1 ASCL2 ATOH1 HAND 1 2 MESP2 Myogenic regulatory factors MyoD Myogenin MYF5 MYF6 NeuroD 1 2 Neurogenins 1 2 3 OLIG 1 2 Paraxis TCF15 Scleraxis SLC LYL1 TAL 1 2 Twist Group B FIGLA Myc c-Myc l-Myc n-Myc MXD4 TCF4 Group C bHLH-PAS AhR AHRR ARNT ARNTL ARNTL2 CLOCK HIF 1A EPAS1 3A NPAS 1 2 3 PER 1 2 3 Period SIM 1 2 Group D DEC 1 2 BHLHA9 Pho4 ID 1 2 3 4 Group E HES 1 2 3 4 5 6 7 HEY 1 2 L Group F bHLH-COE EBF1 (1.3) bHLH-ZIP AP-4 MAX MXD1 MXD3 MITF MNT MLX MLXIPL MXI1 Myc SREBP 1 2 USF1 (1.4) NF-1 NFI A B C X SMAD R-SMAD 1 2 3 5 9 I-SMAD 6 7 4) (1.5) RF-X RFX 1 2 3 4 5 6 ANK (1.6) Basic helix-span-helix (bHSH) AP-2 α β γ δ ε (2) Zinc finger DNA-binding domains (2.1) Nuclear receptor (Cys4) subfamily 1 Thyroid hormone α β CAR FXR LXR α β PPAR α β/δ γ PXR RAR α β γ ROR α β γ Rev-ErbA α β VDR subfamily 2 COUP-TF (I II Ear-2 HNF4 α γ PNR RXR α β γ Testicular receptor 2 4 TLX subfamily 3 Steroid hormone Androgen Estrogen α β Glucocorticoid Mineralocorticoid Progesterone Estrogen related α β γ subfamily 4 NUR NGFIB NOR1 NURR1 subfamily 5 LRH-1 SF1 subfamily 6 GCNF subfamily 0 DAX1 SHP (2.2) Other Cys4 GATA 1 2 3 4 5 6 MTA 1 2 3 TRPS1 (2.3) Cys2His2 General transcription factors TFIIA TFIIB TFIID TFIIE 1 2 TFIIF 1 2 TFIIH 1 2 4 2I 3A 3C1 3C2 ATBF1 BCL 6 11A 11B CTCF E4F1 EGR 1 2 3 4 ERV3 GFI1 GLI family 1 2 3 REST S1 S2 YY1 HIC 1 2 HIVEP 1 2 3 IKZF 1 2 3 ILF 2 3 Sp/KLF family KLF 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 17 SP 1 2 4 7 8 MTF1 MYT1 OSR1 PRDM9 SALL 1 2 3 4 TSHZ3 WT1 Zbtb7 7A 7B ZBTB 11 16 17 20 21 32 33 40 zinc finger 3 7 9 10 19 22 24 33B 34 35 41 43 44 51 74 143 146 148 165 202 217 219 238 239 259 267 268 281 300 318 330 346 350 365 366 384 423 451 452 471 593 638 644 649 655 804A (2.4) Cys6 HIVEP1 (2.5) Alternating composition AIRE DIDO1 GRLF1 ING 1 2 4 JARID 1A 1B 1C 1D 2 JMJD1B (2.6) WRKY WRKY (3) Helix-turn-helix domains (3.1) Homeodomain Antennapedia ANTP class protoHOX Hox-like ParaHox Gsx 1 2 Xlox PDX1 Cdx 1 2 4 extended Hox: Evx1 Evx2 MEOX1 MEOX2 Homeobox A1 A2 A3 A4 A5 A7 A9 A10 A11 A13 B1 B2 B3 B4 B5 B6 B7 B8 B9 B13 C4 C5 C6 C8 C9 C10 C11 C12 C13 D1 D3 D4 D8 D9 D10 D11 D12 D13 GBX1 GBX2 MNX1 metaHOX NK-like BARHL1 BARHL2 BARX1 BARX2 BSX DBX 1 2 DLX 1 2 3 4 5 6 EMX 1 2 EN 1 2 HHEX HLX LBX1 LBX2 MSX 1 2 NANOG NKX 2-1 2-2 2-3 2-5 3-1 3-2 HMX1 HMX2 HMX3 6-1 6-2 NOTO TLX1 TLX2 TLX3 VAX1 VAX2 other ARX CRX CUTL1 FHL 1 2 3 HESX1 HOPX LMX 1A 1B NOBOX TALE IRX 1 2 3 4 5 6 MKX MEIS 1 2 PBX 1 2 3 PKNOX 1 2 SIX 1 2 3 4 5 PHF 1 3 6 8 10 16 17 20 21A POU domain PIT-1 BRN-3: A B C Octamer transcription factor: 1 2 3/4 6 7 11 SATB2 ZEB 1 2 (3.2) Paired box PAX 1 2 3 4 5 6 7 8 9 PRRX 1 2 PROP1 PHOX 2A 2B RAX SHOX SHOX2 VSX1 VSX2 Bicoid GSC BICD2 OTX 1 2 PITX 1 2 3 (3.3) Fork head / winged helix E2F 1 2 3 4 5 FOX proteins A1 A2 A3 B1 B2 C1 C2 D1 D2 D3 D4 D4L1 D4L3 D4L4 D4L5 D4L6 E1 E3 F1 F2 G1 H1 I1 I2 I3 J1 J2 J3 K1 K2 L1 L2 M1 N1 N2 N3 N4 O1 O3 O4 O6 P1 P2 P3 P4 Q1 R1 R2 S1 (3.4) Heat shock factors HSF 1 2 4 (3.5) Tryptophan clusters ELF 2 4 5 EHF ELK 1 3 4 ERF ETS 1 2 ERG SPIB ETV 1 4 5 6 FLI1 Interferon regulatory factors 1 2 3 4 5 6 7 8 MYB MYBL2 (3.6) TEA domain transcriptional enhancer factor 1 2 3 4 (4) β-Scaffold factors with minor groove contacts (4.1) Rel homology region NF-κB NFKB1 NFKB2 REL RELA RELB NFAT C1 C2 C3 C4 5 (4.2) STAT STAT 1 2 3 4 5 6 (4.3) p53-like p53 p63 p73 family p53 TP63 p73 TBX 1 2 3 5 19 21 22 TBR1 TBR2 TFT MYRF (4.4) MADS box Mef2 A B C D SRF (4.6) TATA-binding proteins TBP TBPL1 (4.7) High-mobility group BBX HMGB 1 2 3 4 HMGN 1 2 3 4 HNF 1A 1B SOX 1 2 3 4 5 6 8 9 10 11 12 13 14 15 17 18 21 SRY SSRP1 TCF/LEF TCF 1 3 4 LEF1 TOX 1 2 3 4 (4.9) Grainyhead TFCP2 (4.10) Cold-shock domain CSDA YBX1 (4.11) Runt CBF CBFA2T2 CBFA2T3 RUNX1 RUNX2 RUNX3 RUNX1T1 (0) Other transcription factors (0.2) HMGI(Y) HMGA 1 2 HBP1 (0.3) Pocket domain Rb RBL1 RBL2 (0.5) AP-2/EREBP-related factors Apetala 2 EREBP B3 (0.6) Miscellaneous ARID 1A 1B 2 3A 3B 4A CAP IFI 16 35 MLL 2 3 T1 MNDA NFY A B C Rho/Sigma see also transcription factor/coregulator deficiencies

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Adapted from the Wikipedia article [NPAS3](https://en.wikipedia.org/wiki/NPAS3) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/NPAS3?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.