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Mouse Anti-IKBKE Recombinant Antibody (6B4B5) (CBMAB-I1548-YY)

This product is Mouse antibody that recognizes IKBKE . The antibody 6B4B5 can be used for immunoassay techniques such as: ELISA, WB, IHC-P, IF, FC
See all IKBKE antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
6B4B5
Antibody Isotype
IgG1
Application
ELISA, WB, IHC-P, IF, FC

Basic Information

Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
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 Epsilon
Introduction
IKBKE is a noncanonical I-kappa-B (see MIM 164008) kinase (IKK) that is essential for regulating antiviral signaling pathways. IKBKE has also been identified as a breast cancer (MIM 114480) oncogene and is amplified and overexpressed in over 30% of breast carcinomas and breast cancer cell lines (Hutti et al., 2009
Entrez Gene ID
9641
UniProt ID
Q14164
Alternative Names
Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Epsilon
Function
Serine/threonine kinase that plays an essential role in regulating inflammatory responses to viral infection, through the activation of the type I IFN, NF-kappa-B and STAT signaling. Also involved in TNFA and inflammatory cytokines, like Interleukin-1, signaling. Following activation of viral RNA sensors, such as RIG-I-like receptors, associates with DDX3X and phosphorylates interferon regulatory factors (IRFs), IRF3 and IRF7, as well as DDX3X. This activity allows subsequent homodimerization and nuclear translocation of the IRF3 leading to transcriptional activation of pro-inflammatory and antiviral genes including IFNB. In order to establish such an antiviral state, IKBKE forms several different complexes whose composition depends on the type of cell and cellular stimuli. Thus, several scaffolding molecules including IPS1/MAVS, TANK, AZI2/NAP1 or TBKBP1/SINTBAD can be recruited to the IKBKE-containing-complexes. Activated by polyubiquitination in response to TNFA and interleukin-1, regulates the NF-kappa-B signaling pathway through, at least, the phosphorylation of CYLD. Phosphorylates inhibitors of NF-kappa-B thus leading to the dissociation of the inhibitor/NF-kappa-B complex and ultimately the degradation of the inhibitor. In addition, is also required for the induction of a subset of ISGs which displays antiviral activity, may be through the phosphorylation of STAT1 at 'Ser-708'. Phosphorylation of STAT1 at 'Ser-708' seems also to promote the assembly and DNA binding of ISGF3 (STAT1:STAT2:IRF9) complexes compared to GAF (STAT1:STAT1) complexes, in this way regulating the balance between type I and type II IFN responses. Protects cells against DNA damage-induced cell death. Also plays an important role in energy balance regulation by sustaining a state of chronic, low-grade inflammation in obesity, wich leads to a negative impact on insulin sensitivity. Phosphorylates AKT1.
Biological Process
Cellular response to virus Source: Ensembl
Gene expression Source: Ensembl
Immune response Source: UniProtKB
Interleukin-17-mediated signaling pathway Source: Ensembl
Intrinsic apoptotic signaling pathway in response to DNA damage Source: UniProtKB
mRNA stabilization Source: Ensembl
Peptidyl-serine phosphorylation Source: GO_Central
Positive regulation of DNA-binding transcription factor activity Source: BHF-UCL
Positive regulation of I-kappaB kinase/NF-kappaB signaling Source: UniProtKB
Positive regulation of lipid storage Source: BHF-UCL
Positive regulation of type I interferon-mediated signaling pathway Source: Ensembl
Protein phosphorylation Source: UniProtKB
Regulation of protein-containing complex assembly Source: Ensembl
Response to interferon-beta Source: UniProtKB
Response to type I interferon Source: Ensembl
Cellular Location
Nucleus; PML body; Cytoplasm. Targeting to PML nuclear bodies upon DNA damage is TOPORS-dependent (PubMed:20188669). Located diffusely throughout the cytoplasm but locates to punctate cytoplasmic bodies when coexpressed with TRIM6 (PubMed:24882218).
PTM
Autophosphorylated and phosphorylated by IKBKB/IKKB. Phosphorylation at Ser-172 is enhanced by the interaction with DDX3X. Phosphorylated at Thr-501 upon IFN activation.
Sumoylation by TOPORS upon DNA damage is required for protection of cells against DNA damage-induced cell death. Desumoylated by SENP1.
'Lys-63'-linked polyubiquitinated at Lys-30 and Lys-401 by TRAF2:BIRC2 and TRAF2:BIRC3 complexes. Ubiquitination is induced by LPS, TNFA and interleukin-1 and required for full kinase activity and KF-kappa-B pathway activation.

Xie, W., Jiang, Q., Wu, X., Wang, L., Gao, B., Sun, Z., ... & Guo, J. (2022). IKBKE phosphorylates and stabilizes Snail to promote breast cancer invasion and metastasis. Cell Death & Differentiation, 29(8), 1528-1540.

Zhu, T., Hong, J., Shuai, Z., Xu, S., Qian, D., Hong, X., ... & Liu, L. (2020). The decreased expression of IKBKE in systemic lupus erythematosus. Clinical Rheumatology, 39, 2611-2617.

Qiao, J., Chen, Y., Mi, Y., Jin, H., Wang, L., Huang, T., ... & Zou, Z. (2020). Macrophages confer resistance to BET inhibition in triple-negative breast cancer by upregulating IKBKE. Biochemical Pharmacology, 180, 114126.

Bainbridge, A., Walker, S., Smith, J., Patterson, K., Dutt, A., Ng, Y. M., ... & Coffey, K. (2020). IKBKE activity enhances AR levels in advanced prostate cancer via modulation of the Hippo pathway. Nucleic Acids Research, 48(10), 5366-5382.

Yin, M., Wang, X., & Lu, J. (2020). Advances in IKBKE as a potential target for cancer therapy. Cancer medicine, 9(1), 247-258.

Zhao, Z., Li, Y., Liu, H., Jain, A., Patel, P. V., & Cheng, K. (2020). Co-delivery of IKBKE siRNA and cabazitaxel by hybrid nanocomplex inhibits invasiveness and growth of triple-negative breast cancer. Science advances, 6(29), eabb0616.

Guo, G., Sun, Y., Hong, R., Xiong, J., Lu, Y., Liu, Y., ... & Huang, Q. (2020). IKBKE enhances TMZ-chemoresistance through upregulation of MGMT expression in glioblastoma. Clinical and Translational Oncology, 22, 1252-1262.

Zhang, Z., Wang, Z., Huang, K., Liu, Y., Wei, C., Zhou, J., ... & Han, L. (2019). PLK4 is a determinant of temozolomide sensitivity through phosphorylation of IKBKE in glioblastoma. Cancer Letters, 443, 91-107.

Leonardi, M., Perna, E., Tronnolone, S., Colecchia, D., & Chiariello, M. (2019). Activated kinase screening identifies the IKBKE oncogene as a positive regulator of autophagy. Autophagy, 15(2), 312-326.

Liu, S., Marneth, A. E., Alexe, G., Walker, S. R., Gandler, H. I., Ye, D. Q., ... & Frank, D. A. (2018). The kinases IKBKE and TBK1 regulate MYC-dependent survival pathways through YB-1 in AML and are targets for therapy. Blood advances, 2(23), 3428-3442.

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

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