IKBKE Antibody
- Known as:
- IKBKE Antibody
- Catalog number:
- 32038
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- IKBKE Antibody
Related genes to: IKBKE Antibody
- Gene:
- IKBKE NIH gene
- Name:
- inhibitor of nuclear factor kappa B kinase subunit epsilon
- Previous symbol:
- -
- Synonyms:
- IKKE, IKK-i, KIAA0151
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-02
- Date modifiied:
- 2017-01-13
Related products to: IKBKE Antibody
Related articles to: IKBKE Antibody
- Inhibitor of nuclear factor kappa-B kinase subunit epsilon (IKBKE), a member of the serine/threonine kinase family, is an important oncogene in glioblastoma. IKBKE is involved in the progression of multiple tumours in glioblastoma (GBM), including tumour invasion, migration, and proliferation. Here, we report an IKBKE-angiomotin-like protein 2 (Amotl2)-yes-associated protein 1 (YAP1) axis in which IKBKE inhibits the protein expression of Amotl2, while Amotl2 regulates the nuclear transport of the YAP1 protein, which has been implicated in brain tumour development and progression. Data analysis of multiple IKBKE mRNA databases of glioma and immunohistochemical analysis of a tissue chip indicated that higher IKBKE expression was associated with higher malignancy and shorter survival in glioma patients. IKBKE downregulation significantly inhibited GBM cell proliferation and restrained tumour growth in a GBM mouse model. Moreover, IKBKE phosphorylates Amotl2, promoting Amotl2 ubiquitination and degradation, leading to YAP1 entry into the nucleus and the activation of downstream genes. In summary, our results are the first to show that IKBKE phosphorylates Amotl2 and that GBM cell proliferation is regulated by the IKBKE↑-Amotl2↓-YAP1↑ axis. - Source: PubMed
Publication date: 2026/07/24
Guo GaochaoSun YanHong RujunLu YalinChen XingjieZhao LimingLi ChaoyueLiu YangHuang Qiang - Macrophages undergo rapid transcriptional reprogramming upon LPS stimulation, but the early regulatory mechanisms (≤6 hours) remain poorly understood. This study investigates the immediate molecular responses in the RAW264.7 murine macrophage cell line, focusing on the interplay between immune activation, cell cycle modulation, and metabolic-epigenetic crosstalk. The metabolic and epigenetic crosstalk mentioned in this study is only inferred from transcriptomic data, and no direct experimental verification was performed. Transcriptomic profiling (RNA-seq) was performed on LPS-stimulated (6-hour) and control macrophages. Differentially expressed genes (DEGs) were analyzed via GO/KEGG enrichment and protein-protein interaction (PPI) networks. Key findings were validated by qPCR and Western blot. Identified 2,715 DEGs (716 upregulated, 1,999 downregulated), with Ikbke identified as a multi-pathway gene (14 pathways). LPS triggered activation of inflammatory pathways (NF-κB, TNF) and downregulation of cell cycle regulators. Ikbke and C5ar1 co-enriched in COVID-19 and viral infection pathways, reflecting their involvement in general innate immune signaling pathways. Transcriptomic findings were validated by qPCR and Western blot, confirming a 6.2-fold induction of Ikbke and significant downregulation of Ezh2. This study identifies Ikbke as a potential correlational candidate of early macrophage responses, linking TLR signaling, metabolic shifts, and viral defense mechanisms. All conclusions in this study are limited to the RAW264.7 immortalized murine macrophage cell line and require further verification in primary cells and in vivo models. These findings in the RAW264.7 cell model provide potential molecular targets for further investigating the modulation of early hyperinflammatory responses. - Source: PubMed
Publication date: 2026/07/15
Li DingYe QinsongLiu TiantianYing DiqiYe SongZheng JishanSun Zhiqiang - Rebuilding human naïve pluripotency from primed stem cells is essential for generating pre-implantation epiblast-like cells, a key source for regenerative medicine. Here we present a defined, feeder-free protocol that efficiently converts primed human pluripotent stem cells (hPSCs) to a naïve-like state within 12 days. Integrated ATAC-seq, RNA-seq and miRNA-seq analyses reveal a rapid chromatin rewiring marked by increased accessibility at OCT/KLF motifs, closure at ZIC/RFX/NFκB sites, upregulation of miR-372/373 and miR-182/183, and downregulation of miR-302 and miR-363/106 clusters. Functional assays demonstrate that the inflammatory transcription factor NFκB/RELA blocks naïve induction by activating peri-implantation barrier genes, including IKBKE and VEGFR1. Conversely, enforced miR-372/373 expression accelerates conversion by directly targeting RELA. These data delineate an NFκB/RELA axis that orchestrates the epigenetic switch to human naïve pluripotency, offering a tractable framework for studying early human development and advancing cell-based therapies. - Source: PubMed
Publication date: 2026/07/07
Wang LuqinXiao LizhanZou GaoyangMao HuipingZhang ShihaoYang QiushengYin ChunkouWan JianiKumar ManishWu HaokaifengWang HaoxianZhang XiaoliZeng LihuaZhou ChunhuaYu ShengyongLi YiZheng LinglingLiu YuliangLiao BaojianZhang ZhenLiu Jing - Cytotoxic T cells produce the cytokine interferon-γ (IFN-γ). We sought to determine whether IFN-γ directly kills target cells and found that T cells used IFN-γ to kill murine melanoma cells lacking the kinases TBK1 and IKKε. In the absence of both kinases, IFN-γ induced the production of TNF receptor 1 (TNFR1) and the sensor Z-DNA binding protein 1 (ZBP1) in the tumor cells to stimulate receptor-interacting protein kinase 1 (RIPK1)-dependent apoptosis in a cell-autonomous manner. IFN-γ also enhanced the activation of nuclear factor κB (NF-κB) signaling in a TNFR1-dependent manner in cells deficient in both TBK1 and IKKε. Because IFN-γ-induced apoptosis occurred in a transcription-dependent manner with slow kinetics, STAT1 and NF-κB cooperated to activate the expression of inflammatory genes in the dying cells. Thus, IFN-γ-induced cell death was accompanied by an inflammatory signature in the absence of TBK1 and IKKε. TBK1 and IKKε not only mediated the induction of type I IFN but also inhibited RIPK1-dependent death and NF-κB-dependent inflammation. Therefore, we propose that these kinases may have gained these intertwined functions so that cells infected by pathogens that produce antagonists of TBK1 and IKKε are eliminated by IFN-γ-secreting T cells in an inflammatory manner to compensate for the inhibition of type I IFN production. - Source: PubMed
Publication date: 2026/07/07
Sun Nicholas DCarr Allison RKrogman Erica NChawla YogeshZhong JunGuttormson Matthew CChan MarkHsu Michelle ADong HaidongBogunovic DusanPandey AkhileshRogers Laura MTing Adrian T - Premature ovarian insufficiency (POI) impairs fertility and health in reproductive-age women, with autoimmune factors contributing to 4-30% of cases. To investigate immune dysregulation in POI, we developed two mouse models using pZP3 induction: regular immune (RE-POI) and enhanced immune (EN-POI) cycles. The EN-POI model exhibited stable, irreversible ovarian dysfunction, including disrupted estrous cycles, hormonal changes (elevated FSH, decreased AMH, and estradiol), follicular depletion, and infertility. Immune profiling demonstrated consistent T-lymphocyte imbalance across both RE-POI and EN-POI model groups, characterized by expanded splenic CD4 T cells, diminished regulatory T cells, elevated systemic inflammatory cytokines, and ovarian fibrosis. Proteomic comparison between the control and EN-POI groups identified 198 differentially expressed proteins, mainly enriched in immune and inflammatory pathways. Based on these differential proteins, subsequent network analysis further identified six key hub proteins, namely Mmp9, Isg15, Ikbke, Siglec1, Pf4, and Cdkn1b. This study establishes a stable autoimmune POI model, elucidates T-cell imbalance with cytokine storm and fibrosis, and identifies key molecules linking immune abnormalities to ovarian failure, offering new insights into POI research. - Source: PubMed
Publication date: 2026/05/11
Tian YingZhou JiaqiPei XinyiLiu FeiranDiao Feiyang