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 NFKBIEgene.[5][6]
Function
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]
Emmerich F, Theurich S, Hummel M, et al. (2004). "Inactivating I kappa B epsilon mutations in Hodgkin/Reed-Sternberg cells". J. Pathol. 201 (3): 413–20.
doi:
10.1002/path.1454.
PMID14595753.
S2CID33577004.
Bouwmeester T, Bauch A, Ruffner H, et al. (2004). "A physical and functional map of the human TNF-alpha/NF-kappa B signal transduction pathway". Nat. Cell Biol. 6 (2): 97–105.
doi:
10.1038/ncb1086.
PMID14743216.
S2CID11683986.
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 NFKBIEgene.[5][6]
Function
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]
Emmerich F, Theurich S, Hummel M, et al. (2004). "Inactivating I kappa B epsilon mutations in Hodgkin/Reed-Sternberg cells". J. Pathol. 201 (3): 413–20.
doi:
10.1002/path.1454.
PMID14595753.
S2CID33577004.
Bouwmeester T, Bauch A, Ruffner H, et al. (2004). "A physical and functional map of the human TNF-alpha/NF-kappa B signal transduction pathway". Nat. Cell Biol. 6 (2): 97–105.
doi:
10.1038/ncb1086.
PMID14743216.
S2CID11683986.