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Mouse Anti-IKBKB Recombinant Antibody (10A2) (CBMAB-I0334-YY)

This product is Mouse antibody that recognizes IKBKB. The antibody 10A2 can be used for immunoassay techniques such as: ELISA, WB, IHC-P, IF, FC
See all IKBKB antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
10A2
Antibody Isotype
IgG1
Application
ELISA, WB, IHC-P, IF, FC

Basic Information

Specificity
Human
Antibody Isotype
IgG1
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Preservative
.03% sodium azide
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Beta
Introduction
The protein encoded by this gene phosphorylates the inhibitor in the inhibitor/NF-kappa-B complex, causing dissociation of the inhibitor and activation of NF-kappa-B. The encoded protein itself is found in a complex of proteins. Several transcript variants, some protein-coding and some not, have been found for this gene.
Entrez Gene ID
3551
UniProt ID
O14920
Alternative Names
Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Beta
Function
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses (PubMed:30337470).

Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation. Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE (PubMed:11297557, PubMed:20410276).

IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs. Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor (PubMed:15084260).

Also phosphorylates other substrates including NCOA3, BCL10 and IRS1 (PubMed:17213322).

Within the nucleus, acts as an adapter protein for NFKBIA degradation in UV-induced NF-kappa-B activation (PubMed:11297557).

Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity).

Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus (PubMed:25326418).
Biological Process
Antigen processing and presentation of exogenous peptide antigen via MHC class I, TAP-dependent Source: Reactome
Cellular response to tumor necrosis factor Source: UniProtKB
Cortical actin cytoskeleton organization Source: UniProtKB
Fc-epsilon receptor signaling pathway Source: Reactome
I-kappaB kinase/NF-kappaB signaling Source: UniProtKB
Inflammatory response Source: UniProtKB
Innate immune response Source: UniProtKB
Interleukin-1-mediated signaling pathway Source: UniProtKB
Negative regulation of bicellular tight junction assembly Source: UniProtKB
Negative regulation of myosin-light-chain-phosphatase activity Source: UniProtKB
Peptidyl-serine phosphorylation Source: UniProtKB
Positive regulation of I-kappaB kinase/NF-kappaB signaling Source: UniProtKB
Positive regulation of NF-kappaB transcription factor activity Source: MGI
Positive regulation of transcription, DNA-templated Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Protein localization to plasma membrane Source: UniProtKB
Protein phosphorylation Source: UniProtKB
Regulation of establishment of endothelial barrier Source: UniProtKB
Regulation of phosphorylation Source: ParkinsonsUK-UCL
Regulation of tumor necrosis factor-mediated signaling pathway Source: Reactome
Response to virus Source: UniProtKB
Stimulatory C-type lectin receptor signaling pathway Source: Reactome
Stress-activated MAPK cascade Source: Reactome
T cell receptor signaling pathway Source: Reactome
Tumor necrosis factor-mediated signaling pathway Source: UniProtKB
Cellular Location
Nucleus; Cytoplasm; Membrane raft. Colocalized with DPP4 in membrane rafts.
Involvement in disease
Immunodeficiency 15B (IMD15B):
An autosomal recessive primary immunodeficiency disorder characterized by onset in infancy of life-threatening bacterial, fungal, and viral infections and failure to thrive. Laboratory studies show hypo- or agammaglobulinemia with relatively normal numbers of B and T-cells, and impaired differentiation and activation of immune cells.
Immunodeficiency 15A (IMD15A):
An autosomal dominant primary immunodeficiency disorder characterized by lymphopenia, inflammation and immune activation of both CD4+ and CD8+ T cells. Patients suffer from recurrent respiratory tract infections, oral candidiasis, and otitis media.
PTM
Upon cytokine stimulation, phosphorylated on Ser-177 and Ser-181 by MEKK1 and/or MAP3K14/NIK as well as TBK1 and PRKCZ; which enhances activity. Once activated, autophosphorylates on the C-terminal serine cluster; which decreases activity and prevents prolonged activation of the inflammatory response. Phosphorylated by the IKK-related kinases TBK1 and IKBKE, which is associated with reduced CHUK/IKKA and IKBKB activity and NF-kappa-B-dependent gene transcription. Dephosphorylated at Ser-177 and Ser-181 by PPM1A and PPM1B.
(Microbial infection) Acetylation of Thr-180 by Yersinia YopJ prevents phosphorylation and activation, thus blocking the I-kappa-B pathway.
Ubiquitinated. Monoubiquitination involves TRIM21 that leads to inhibition of Tax-induced NF-kappa-B signaling. According to PubMed:19675099, 'Ser-163' does not serve as a monoubiquitination site. According to PubMed:16267042, ubiquitination on 'Ser-163' modulates phosphorylation on C-terminal serine residues.
(Microbial infection) Monoubiquitination by TRIM21 is disrupted by Yersinia YopJ.
Hydroxylated by PHD1/EGLN2, loss of hydroxylation under hypoxic conditions results in activation of NF-kappa-B.

Salama, A. A., Elgohary, R., & Fahmy, M. I. (2023). Protocatechuic acid ameliorates lipopolysaccharide‐induced kidney damage in mice via downregulation of TLR‐4‐mediated IKBKB/NF‐κB and MAPK/Erk signaling pathways. Journal of Applied Toxicology.

Sacco, K., Kuehn, H. S., Kawai, T., Alsaati, N., Smith, L., Davila, B., ... & Keller, M. D. (2023). A Heterozygous Gain-of-Function Variant in IKBKB Associated with Autoimmunity and Autoinflammation. Journal of Clinical Immunology, 43(2), 512-520.

Long, D., Xu, Y., Mao, G., Xin, R., Deng, Z., Liao, H., ... & Kang, Y. (2022). tRNA-derived fragment TRF365 regulates the metabolism of anterior cruciate ligament cells by targeting IKBKB. Cell Death Discovery, 8(1), 19.

Lee, S., Shin, H. J., Noh, C., Kim, S. I., Ko, Y. K., Lee, S. Y., ... & Kim, Y. H. (2021). Ikbkb sirna-encapsulated poly (Lactic-co-glycolic acid) nanoparticles diminish neuropathic pain by inhibiting microglial activation. International journal of molecular sciences, 22(11), 5657.

Pan, F., Zhang, J., Tang, B., Jing, L., Qiu, B., & Zha, Z. (2020). The novel circ_0028171/miR-218-5p/IKBKB axis promotes osteosarcoma cancer progression. Cancer Cell International, 20(1), 1-14.

Bialek, K., Czarny, P., Watala, C., Wigner, P., Talarowska, M., Galecki, P., ... & Sliwinski, T. (2020). Novel association between TGFA, TGFB1, IRF1, PTGS2 and IKBKB single-nucleotide polymorphisms and occurrence, severity and treatment response of major depressive disorder. PeerJ, 8, e8676.

Cuvelier, G. D., Rubin, T. S., Junker, A., Sinha, R., Rosenberg, A. M., Wall, D. A., & Schroeder, M. L. (2019). Clinical presentation, immunologic features, and hematopoietic stem cell transplant outcomes for IKBKB immune deficiency. Clinical Immunology, 205, 138-147.

Krazinski, B. E., Kowalczyk, A. E., Sliwinska‑Jewsiewicka, A., Grzegrzolka, J., Godlewski, J., Kwiatkowski, P., ... & Kiewisz, J. (2019). IKBKB expression in clear cell renal cell carcinoma is associated with tumor grade and patient outcomes. Oncology Reports, 41(2), 1189-1197.

Huang, Y., Chen, G., Wang, Y., He, R., Du, J., Jiao, X., & Tai, Q. (2018). Inhibition of microRNA-16 facilitates the paclitaxel resistance by targeting IKBKB via NF-κB signaling pathway in hepatocellular carcinoma. Biochemical and biophysical research communications, 503(2), 1035-1041.

Cardinez, C., Miraghazadeh, B., Tanita, K., Da Silva, E., Hoshino, A., Okada, S., ... & Cook, M. C. (2018). Gain-of-function IKBKB mutation causes human combined immune deficiency. Journal of Experimental Medicine, 215(11), 2715-2724.

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For research use only. Not intended for any clinical use.

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