NFKBIE

From Wikipedia, the free encyclopedia
Jump to: navigation, search
NFKBIE
Identifiers
Aliases NFKBIE, IKBE, NFKB inhibitor epsilon
External IDs MGI: 1194908 HomoloGene: 36160 GeneCards: NFKBIE
Gene location (Human)
Chromosome 6 (human)
Chr. Chromosome 6 (human)[1]
Chromosome 6 (human)
Genomic location for NFKBIE
Genomic location for NFKBIE
Band 6p21.1 Start 44,258,166 bp[1]
End 44,265,788 bp[1]
RNA expression pattern
PBB GE NFKBIE 203927 at fs.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_004556

NM_008690
NM_001304956

RefSeq (protein)

NP_004547

NP_001291885
NP_032716

Location (UCSC) Chr 6: 44.26 – 44.27 Mb Chr 6: 45.56 – 45.56 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon, also known as NFKBIE, is a protein which in humans is encoded by the NFKBIE gene.[5][6]

Function[edit]

NFKBIE protein expression is up-regulated following NF-κB activation and during myelopoiesis. NFKBIE is able to inhibit NF-κB-directed transactivation via cytoplasmic retention of REL proteins.[6]

NFKB1 or NFKB2 is bound to REL, RELA, or RELB to form the NF-κB transcription factor complex. The NF-κB complex is inhibited by I-kappa-B proteins (NFKBIA or NFKBIB), which inactivate NF-kappa-B by trapping it in the cytoplasm. Phosphorylation of serine residues on the I-kappa-B proteins by kinases (IKBKA, or IKBKB) marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B complex. Activated NF-κB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such as 5-prime GGGRNNYYCC 3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine). For some genes, activation requires NF-κB interaction with other transcription factors, such as STAT (see STAT6), AP-1 (JUN), and NFAT (see NFATC1).[5]

Interactions[edit]

NFKBIE has been shown to interact with NFKB2,[7] RELA,[7] NFKB1[7] and REL.[7][8][9]

References[edit]

Further reading[edit]