IKBKB & CHUK Protein Protein Interaction Antibody Pair
- Known as:
- IKBKB & CHUK Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0096
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IKBKB & CHUK Protein Interaction Antibody Pair
Related genes to: IKBKB & CHUK Protein Protein Interaction Antibody Pair
- Gene:
- CHUK NIH gene
- Name:
- component of inhibitor of nuclear factor kappa B kinase complex
- Previous symbol:
- TCF16
- Synonyms:
- IKK1, IKK-alpha, IkBKA, NFKBIKA, IKKA
- Chromosome:
- 10q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-15
- Date modifiied:
- 2019-02-21
- Gene:
- IKBKB NIH gene
- Name:
- inhibitor of nuclear factor kappa B kinase subunit beta
- Previous symbol:
- -
- Synonyms:
- IKK2, NFKBIKB, IKK-beta, IKKB
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2019-04-23
- Gene:
- TRAPPC9 NIH gene
- Name:
- trafficking protein particle complex 9
- Previous symbol:
- -
- Synonyms:
- IKBKBBP, NIBP, KIAA1882, T1, TRS120, MRT13
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-05-07
- Date modifiied:
- 2019-04-23
Related products to: IKBKB & CHUK Protein Protein Interaction Antibody Pair
Related articles to: IKBKB & CHUK Protein Protein Interaction Antibody Pair
- The transcription factor NF-kappaB plays an important role in both physiological and pathological events in the central nervous system. Nevertheless, the mechanisms of NF-kappaB-mediated regulation of gene expression, and the signaling molecules participating in the NF-kappaB pathway in the central nervous system are, to date, poorly understood. To identify such molecules, we conducted a yeast two-hybrid screen of a human brain cDNA library using NIK as bait. As a result, we identified a novel NIK and IKK(beta) binding protein designated NIBP that is mainly expressed in brain, muscle, heart, and kidney. Interestingly, low levels of expression were detected in immune tissues such as spleen, thymus, and peripheral blood leukocytes, where NF-kappaB is known to modulate immune function. We demonstrated by immunohistochemistry that NIBP expression in the brain is localized to neurons. NIBP physically interacts with NIK, IKK(beta), but not IKK(alpha) or IKK(gamma). NIBP overexpression potentiates tumor necrosis factor-alpha-induced NF-kappaB activation through increased phosphorylation of the IKK complex and its downstream I(kappa)B(alpha) and p65 substrates. Finally, knockdown of NIBP expression by small interfering RNA reduces tumor necrosis factor-alpha-induced NF-kappaB activation, prevents nerve growth factor-induced neuronal differentiation, and decreases Bcl-xL gene expression in PC12 cells. Our data demonstrate that NIBP, by interacting with NIK and IKK(beta), is a new enhancer of the cytokine-induced NF-(kappa)B signaling pathway. Because of its neuronal expression, we propose that NIBP may be a potential target for modulating the NF-(kappa)B signaling cascade in neuronal pathologies dependent upon abnormal activation of this pathway. - Source: PubMed
Publication date: 2005/06/10
Hu Wen-HuiPendergast Julie SMo Xian-MingBrambilla RobertaBracchi-Ricard ValerieLi FangWalters Winston MBlits BasHe LiSchaal Sandra MBethea John R