Entity Details

Primary name NFIB
Entity type gene
Source Source Link

Details

PrimaryID4781
RefseqGene
SymbolNFIB
Namenuclear factor I B
Chromosome9
Location9p23-p22.3
TaxID9606
Statuslive
SourceGenomegenomic
SourceOriginnatural
CreationDate1998-08-21
ModificationDate2021-06-11

Ontological Relatives

UniProt IDsNFIB_HUMAN

GO terms

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GOName
GO:0000122 negative regulation of transcription by RNA polymerase II
GO:0000785 chromatin
GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding
GO:0000981 DNA-binding transcription factor activity, RNA polymerase II-specific
GO:0001228 DNA-binding transcription activator activity, RNA polymerase II-specific
GO:0001650 fibrillar center
GO:0002062 chondrocyte differentiation
GO:0003677 DNA binding
GO:0005634 nucleus
GO:0005654 nucleoplasm
GO:0006260 DNA replication
GO:0006357 regulation of transcription by RNA polymerase II
GO:0007420 brain development
GO:0010001 glial cell differentiation
GO:0021740 principal sensory nucleus of trigeminal nerve development
GO:0021960 anterior commissure morphogenesis
GO:0043392 negative regulation of DNA binding
GO:0044300 cerebellar mossy fiber
GO:0045893 positive regulation of transcription, DNA-templated
GO:0045944 positive regulation of transcription by RNA polymerase II
GO:0060486 club cell differentiation
GO:0060509 type I pneumocyte differentiation
GO:0060510 type II pneumocyte differentiation
GO:0061141 lung ciliated cell differentiation
GO:0071679 commissural neuron axon guidance
GO:0140416 transcription regulator inhibitor activity
GO:1902894 negative regulation of pri-miRNA transcription by RNA polymerase II
GO:1990837 sequence-specific double-stranded DNA binding
GO:2000791 negative regulation of mesenchymal cell proliferation involved in lung development
GO:2000795 negative regulation of epithelial cell proliferation involved in lung morphogenesis

Diseases

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Disease IDSourceNameDescription
618286 OMIMMacrocephaly, acquired, with impaired intellectual development (MACID)An autosomal dominant disorder characterized by postnatal macrocephaly and borderline to mild mental retardation. Additional variable neurodevelopmental features include muscular hypotonia, motor and speech delay, attention deficit disorder, autism spectrum disorder, and behavioral abnormalities. Some patients present corpus callosum dysgenesis. The disease is caused by variants affecting the gene represented in this entry.