IKIP antibody
- Known as:
- IKIP (anti-)
- Catalog number:
- orb100026
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- IKIP antibody
Related genes to: IKIP antibody
- Gene:
- IKBIP NIH gene
- Name:
- IKBKB interacting protein
- Previous symbol:
- -
- Synonyms:
- FLJ31051, IKIP
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2009-10-05
- Date modifiied:
- 2014-11-19
Related products to: IKIP antibody
Related articles to: IKIP antibody
- The response of lung cancer to chemoradiotherapy (CRT) is orchestrated by the dynamic interplay between immune microenvironment remodeling and metabolic reprogramming. However, robust biomarkers for predicting patient prognosis remain elusive. In this study, we performed proteomics profiling of 22 pairs of lung cancer specimens and compared CRT-sensitive versus CRT-resistant subtypes. Functional analysis revealed distinct pathway enrichment between the two groups: the CRT-sensitive subtype was predominantly associated with fatty acid oxidation and energy metabolism, whereas the CRT-resistant subtype exhibited elevated immune activation, inflammatory responses, and stress-related signaling. Based on these findings, we developed a LASSO regression-based predictive model that pinpointed a protein signature encompassing IKBKB interacting protein (IKBIP) and citron rho-interacting serine/threonine kinase (CIT) as optimal predictors of CRT efficacy. Subsequent survival analysis further confirmed the prognostic relevance of these proteins. Collectively, our findings emphasize the critical role of the metabolic-immune axis in modulating CRT sensitivity and provide mechanistic insights into the molecular underpinnings of treatment response, thereby offering a clinically translatable tool for guiding precision therapeutic strategies in lung cancer. - Source: PubMed
Publication date: 2026/06/02
Ouyang WeiweiWang YixuanYang JianghuaCao DongdongWang QianjingLuo YuxiTian ChuanHuang HeWang Xinbo - Glioma is the most aggressive tumor of the central nervous system and is associated with poor prognosis, especially in patients with high-grade gliomas. In this study, we investigated the biological role of inhibitor of kappa B kinase interacting protein (IKBIP) in promoting the progression of glioma. Analysis of the TCGA and GTEx databases revealed that IKBIP is upregulated in both lower-grade gliomas (LGG) and glioblastomas (GBM) compared with normal brain tissues. Kaplan-Meier survival analysis demonstrated that IKBIP upregulation is associated with shorter overall survival (OS) and disease-specific survival (DSS) in patients with LGG. Pan-cancer analysis indicated that IKBIP is aberrantly expressed in various malignant tumors, including gliomas. IKBIP knockdown inhibited the proliferation of glioma cells both and . Additionally, IKBIP knockdown in U251 and U87 glioma cell lines significantly suppressed their invasive capacity. Furthermore, IKBIP knockdown resulted in decreased expression of proteins associated with Wnt/β-catenin/epithelial-mesenchymal transition (EMT) pathway, including β-catenin, ZEB1, ZEB2, N-cadherin, whereas the expression of E-cadherin was increased. Conversely, IKBIP overexpression reduced the level of phosphorylated β-catenin (p-β-catenin) while increasing the expression of total β-catenin in glioma cells. Furthermore, we identified that transcription factor SP1 (Specificity Protein 1), which is also upregulated in glioma tissues and cell lines and is associated with the malignant phenotype of glioma, can bind to the promoter region of IKBIP. Upregulation of SPI in glioma cells significantly increased the expression level of IKBIP, while inhibiting the phosphorylation of β-catenin. These findings collectively suggest that upregulation of IKBIP promotes the proliferation and invasive behaviors of glioma cells by activating the Wnt/β-catenin/EMT pathway. Overall, our findings suggest that SP1-IKBIP axis facilitates the proliferation and invasion of glioma through Wnt/β-catenin-associated EMT, and SP1-IKBIP axis may represent a promising target for the clinical diagnosis and treatment of glioma. - Source: PubMed
Publication date: 2026/03/25
Liu NanZhao MingyueXu LeiCui YetingTian YuLi JuanHu XiaoyuZhang TongcunZhen HainingTu Yanyang - BACKGROUND: Cervical cancer (CC) is a significant global health threat for women worldwide. Although IKBIP has been recognized as an oncogene, little is known about its contribution to CC. Therefore, we aimed to analyze IKBIP expression, its correlation with clinicopathological parameters, and its association with the prognosis in CC. METHODS: IKBIP expression in CC tissues was analyzed using the Gene Expression Profiling Interactive Analysis and Gene Expression Omnibus databases. The transcriptomic data and clinical characteristics of 306 patients with CC were obtained from the Cancer Genome Atlas, and clustering was performed using the X-tile software. Additionally, to validate the prognostic significance of IKBIP, protein levels in normal and cancerous tissues were compared by immunohistochemistry. The Tumor Immune Dysfunction and Exclusion score was used as an indicator of potential response to immunotherapy. Furthermore, we investigated the possible connections between IKBIP and immunological genes and their influence on the development of tumor mutation burden (TMB) and drug sensitivity. The impact of IKBIP on CC cell proliferation, invasion, and migration was investigated using CCK-8, EdU, and transwell assays. To clarify the role of IKBIP in controlling the JAK-STAT signaling cascade and its contribution to the progression of CC, we used the JAK-STAT pathway agonist colivelin in rescue experiments. The effect of IKBIP on CC development was validated using a xenograft tumor model. RESULTS: Our study showed that IKBIP is overexpressed in CC tissues, suggesting that it may be an oncogene associated with CC. Based on nomogram creation, receiver operating characteristic curve analysis, and Kaplan–Meier survival analysis, IKBIP was found to be a biomarker for poor prognosis in CC. Furthermore, IKBIP expression was strongly correlated with immune infiltration, TMB, and drug sensitivity in CC. In vitro experiments indicated that IKBIP functions as an oncogene because inhibiting its expression dramatically reduced the capacity of CC cells to proliferate, migrate, and invade, as indicated using the CCK8, EdU, and transwell assays. Additionally, our findings suggested that IKBIP promotes CC progression by regulating the JAK-STAT signaling pathway. Rescue experiments demonstrated that the JAK-STAT pathway activator colivelin mitigated the inhibitory effects of IKBIP knockdown on CC cell behavior. We successfully constructed a CC xenograft mouse model, and in vivo experiments demonstrated that the expression of IKBIP is closely correlated with the malignancy of CC, providing further evidence that IKBIP contributes to the advancement of CC. CONCLUSION: This study offers novel insights into CC by establishing IKBIP as a robust prognostic marker. Our findings suggest that IKBIP not only correlates with adverse clinical outcomes but also influences tumor immunogenicity and treatment response. Furthermore, IKBIP was significantly correlated with CC progression mediated by the JAK/STAT3 signaling pathway and may be an effective therapeutic target. - Source: PubMed
Publication date: 2026/03/20
Wang YanQiao HuiYu PanpanGao WeiRuiZhao ZouyuYang Ping - BACKGROUND: I Kappa B Kinase Interacting Protein (IKBIP) has been reported to promote tumor progression in diverse cancers. however, the role of IKBIP in hepatocellular carcinoma (HCC) has remained unclear. METHODS: Multi-omics analysis was performed using data from publicly databases, to systematically assess the expression patterns, prognostic value and immune landscape of IKBIP in HCC. The prognostic value of IKBIP was further verified using immunohistochemical (IHC) examination in two independent clinical cohorts. Furthermore, human HCC cell lines (Huh7, MHCC-97 H and HepG2) were knocked down for IKBIP using small-interfering RNA (siRNA), and cell proliferation, and migration ability were assessed. RNA-sequencing was performed on Huh7 cells with IKBIP knockdown to explore the effect of IKBIP in HCC cells. A nomogram was constructed by combining IKBIP expression and clinicopathological parameters to predict prognosis for individual patient. Functional enrichment analysis was performed to identify key pathways associated with IKBIP. Immune infiltration analyses were conducted to explore the relationship between IKBIP expression and immune microenvironment. RESULTS: The bioinformatics analyses indicated that IKBIP expression was significantly upregulated in tumor tissue and correlated with unfavorable prognosis. IHC experimental in both the Peking University Shenzhen Hospital (PKUSZ) and Shanghai Outdo cohorts demonstrated that IKBIP overexpression was associated with poorer survival. We found that IKBIP knockdown significantly inhibits HCC cell proliferation, colony formation, and migration in vitro. RNA-sequencing on IKBIP-knockdown Huh7 cells suggested that IKBIP played a role in promoting cell proliferation. The univariable and multivariable Cox analysis revealed that IKBIP expression was an independent factor for overall survival and diseases free survival. The nomogram by incorporating the IKBIP and clinicopathological features showed good performance in predicting prognosis. GSEA analysis revealed that IKBIP was associated with the cell cycle-related, epithelial-to-mesenchymal transition and angiogenesis pathways. We also found that IKBIP expression holds potential for predicting immunotherapeutic benefits. CONCLUSIONS: The comprehensive multi-omics analysis and experimental findings demonstrate that IKBIP may be a biomarker with prognostic and functional significance in HCC. - Source: PubMed
Publication date: 2026/03/19
Jiao YuanjunGuo LinglingLu YubinLi MengqingZhong YanfengWu BoDong HanxingWang TingChen Erbao - Early diagnosis and biomarker discovery to bolster the therapeutic pipeline for Parkinson's disease (PD) are urgently needed. In this study, we leverage the large-scale, whole-blood total RNA and DNA sequencing data from the Accelerating Medicines Partnership in Parkinson's Disease (AMP PD) program to identify PD-associated RNAs, including both known genes and novel circular RNAs (circRNA) and enhancer RNAs (eRNAs). Initially, 874 known genes, 783 eRNAs, and 35 circRNAs were found differentially expressed in PD blood in the PPMI cohort (FDR < 0.05). Based on these findings, a novel multi-omics machine learning model was built to predict PD diagnosis with high performance (AUC = 0.89), which was superior to previous models. We further replicated this discovery in an independent PDBP/BioFIND cohort and confirmed 1,111 significant marker genes, including 491 known genes, 599 eRNAs, and 21 circRNAs. Functional enrichment analysis showed that the PD-associated genes are involved in neutrophil activation and degranulation, as well as the TNF-α signaling pathway. By comparing the PD-associated genes in blood with those in human brain dopamine neurons in our BRAINcode cohort, we found only 44 genes (9% of the known genes) showing significant changes with the same direction in both PD brain neurons and PD blood, among which are neuroinflammation-associated genes IKBIP, CXCR2, and NFKBIB. Our findings demonstrated consistently lower SNCA mRNA levels and the increased expression levels of VDR gene in the blood of early-stage PD patients. In summary, this study provides a generally useful computational framework for further biomarker development and early disease prediction. We also delineate a wide spectrum of the known and novel RNAs linked to PD that are detectable in circulating blood cells in a harmonized, large-scale dataset. - Source: PubMed
Publication date: 2025/06/20
Dong XianjunHu RuifengWang RuoxuanYuan JieLin ZechuanHutchins ElizabethLandin BarryLiao ZhixiangLiu GanqiangScherzer Clemens