Neuronal PAS domain protein 4

Protein-coding gene in the species Homo sapiens

NPAS4
Identifiers
AliasesNPAS4, Le-PAS, NXF, PASD10, bHLHe79, neuronal PAS domain protein 4
External IDsOMIM: 608554; MGI: 2664186; HomoloGene: 15333; GeneCards: NPAS4; OMA:NPAS4 - orthologs
Gene location (Human)
Chromosome 11 (human)
Chr.Chromosome 11 (human)[1]
Chromosome 11 (human)
Genomic location for NPAS4
Genomic location for NPAS4
Band11q13.2Start66,421,004 bp[1]
End66,426,707 bp[1]
Gene location (Mouse)
Chromosome 19 (mouse)
Chr.Chromosome 19 (mouse)[2]
Chromosome 19 (mouse)
Genomic location for NPAS4
Genomic location for NPAS4
Band19|19 AStart5,034,383 bp[2]
End5,040,344 bp[2]
RNA expression pattern
Bgee
HumanMouse (ortholog)
Top expressed in
  • pituitary gland

  • anterior pituitary

  • gonad

  • left uterine tube

  • body of uterus

  • muscle layer of sigmoid colon

  • gastric mucosa

  • smooth muscle tissue

  • popliteal artery

  • tibial arteries
Top expressed in
  • islet of Langerhans

  • female urethra

  • superior frontal gyrus

  • primary visual cortex

  • prefrontal cortex

  • nucleus accumbens

  • olfactory bulb

  • dentate gyrus of hippocampal formation granule cell

  • neural layer of retina

  • cerebellar cortex
More reference expression data
BioGPS
n/a
Gene ontology
Molecular function
  • DNA binding
  • DNA-binding transcription activator activity, RNA polymerase II-specific
  • protein dimerization activity
  • RNA polymerase II cis-regulatory region sequence-specific DNA binding
  • protein binding
  • protein heterodimerization activity
  • DNA-binding transcription factor activity, RNA polymerase II-specific
Cellular component
  • postsynapse
  • transcription regulator complex
  • nucleus
Biological process
  • positive regulation of transcription, DNA-templated
  • regulation of transcription, DNA-templated
  • cellular response to corticosterone stimulus
  • positive regulation of transcription by RNA polymerase II
  • transcription, DNA-templated
  • transcription by RNA polymerase II
  • nervous system development
  • learning
  • short-term memory
  • long-term memory
  • cell differentiation
  • regulation of synaptic transmission, GABAergic
  • social behavior
  • regulation of synaptic plasticity
  • excitatory postsynaptic potential
  • inhibitory postsynaptic potential
  • inhibitory synapse assembly
  • regulation of transcription by RNA polymerase II
Sources:Amigo / QuickGO
Orthologs
SpeciesHumanMouse
Entrez

266743

225872

Ensembl

ENSG00000174576

ENSMUSG00000045903

UniProt

Q8IUM7

Q8BGD7

RefSeq (mRNA)

NM_178864
NM_001318804

NM_153553

RefSeq (protein)

NP_001305733
NP_849195

NP_705781

Location (UCSC)Chr 11: 66.42 – 66.43 MbChr 19: 5.03 – 5.04 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Neuronal PAS domain protein 4 is a protein that in humans is encoded by the NPAS4 gene.[5] The NPAS4 gene is a neuronal activity-dependent immediate early gene that has been identified as a transcription factor. The protein regulates the transcription of genes that control inhibitory synapse development, synaptic plasticity and most recently reported also behavior.[6]


Function

NPAS4 is a member of the basic helix-loop-helix-PER-ARNT-SIM (bHLH-PAS) class of transcriptional regulators, which are involved in a wide range of physiologic and developmental events (Ooe et al., 2004 [PubMed 14701734]).[supplied by OMIM, Mar 2008].

NPAS4 has been shown by Dr. Brenda Bloodgood to play critical roles in regulating the plasticity of inhibitory neurons. She found that NPAS4 helps to regulate plasticity by orchestrating a redistribution of inhibitory synapses, wherein they are lost from proximal apical dendrites of CA1 pyramidal neurons and increased on the somata.[7]

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000174576 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000045903 – Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ "Entrez Gene: Neuronal PAS domain protein 4". Retrieved 2017-10-15.
  6. ^ Funahashi Y, Ariza A, Emi R, Xu Y, Shan W, Suzuki K, Kozawa K, Ahammad RU, Wu M, Takano T, Yura Y, Kuroda K, Nagai T, Amano M, Yamada K, Kaibuchi K (2019). "Phosphorylation of Npas4 by MAPK Regulates Reward-Related Gene Expression and Behaviors". Cell Reports. 29 (10): 3235–3252.e9. doi:10.1016/j.celrep.2019.10.116. PMID 31801086.
  7. ^ Bloodgood BL, Sharma N, Browne HA, Trepman AZ, Greenberg ME (2013-11-07). "The activity-dependent transcription factor NPAS4 regulates domain-specific inhibition". Nature. 503 (7474): 121–125. Bibcode:2013Natur.503..121B. doi:10.1038/nature12743. ISSN 1476-4687. PMC 4169177. PMID 24201284.

Further reading

  • Ooe N, Saito K, Mikami N, Nakatuka I, Kaneko H (2004). "Identification of a novel basic helix-loop-helix-PAS factor, NXF, reveals a Sim2 competitive, positive regulatory role in dendritic-cytoskeleton modulator drebrin gene expression". Mol. Cell. Biol. 24 (2): 608–16. doi:10.1128/mcb.24.2.608-616.2004. PMC 343817. PMID 14701734.
  • Bersten DC, Bruning JB, Peet DJ, Whitelaw ML (2014). "Human variants in the neuronal basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) transcription factor complex NPAS4/ARNT2 disrupt function". PLOS ONE. 9 (1): e85768. Bibcode:2014PLoSO...985768B. doi:10.1371/journal.pone.0085768. PMC 3894988. PMID 24465693.
  • Klaric TS, Thomas PQ, Dottori M, Leong WK, Koblar SA, Lewis MD (2014). "A reduction in Npas4 expression results in delayed neural differentiation of mouse embryonic stem cells". Stem Cell Res Ther. 5 (3): 64. doi:10.1186/scrt453. PMC 4076635. PMID 24887558.
  • Funahashi Y, Ariza A, Emi R, Xu Y, Shan W, Suzuki K, Kozawa K, Ahammad RU, Wu M, Takano T, Yura Y, Kuroda K, Nagai T, Amano M, Yamada K, Kaibuchi K (2019). "Phosphorylation of Npas4 by MAPK Regulates Reward-Related Gene Expression and Behaviors". Cell Reports. 29 (10): 3235–3252.e9. doi:10.1016/j.celrep.2019.10.116. PMID 31801086.


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This article incorporates text from the United States National Library of Medicine, which is in the public domain.