Ask about this productRelated genes to: RELB Blocking Peptide
- Gene:
- RELB NIH gene
- Name:
- RELB proto-oncogene, NF-kB subunit
- Previous symbol:
- -
- Synonyms:
- REL-B
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2016-04-29
Related products to: RELB Blocking Peptide
Related articles to: RELB Blocking Peptide
- Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus are gammaherpesviruses associated with multiple human cancers. Kaposi's sarcoma (KS) is a human malignancy associated with KSHV infection. KS lesions are characterized by proliferating endothelial-derived spindle cells, leaky blood vessels, and inflammatory infiltrating leukocytes. The inflammatory leukocytes secrete cytokines and growth factors that may contribute to the survival and proliferation of tumor cells. Unless exposed to inflammatory cytokines, resting endothelial cells usually do not express adhesion molecules. Here, we identify a novel mechanistic link demonstrating that KSHV-infected latent endothelial cells express vascular cell adhesion molecule (VCAM1) and induce leukocyte adhesion and transendothelial migration (TEM) in a VCAM1-dependent manner. Inhibition of VCAM1 function using siRNA knockdown or antibody blockade impairs leukocyte adhesion and TEM, suggesting that cell adhesion and TEM are mediated by VCAM1. VCAM1 expression in KSHV-infected endothelial cells involves the non-canonical NF-кB (NF-κB2) pathway because depletion of NIK, IKKα, RelB, or NF-κB p52 via siRNA results in a decrease of VCAM1 levels, as well as a corresponding impairment of cell adhesion and TEM. Thus, KSHV-infected endothelial cells likely promote the infiltration of immune cells by modulating the expression of adhesion factors like VCAM1 on their surface. Moreover, we report that KSHV vFLIP, a latency protein encoded by the virus, directly induces VCAM1 expression and promotes leukocyte adhesion and transendothelial migration. We further demonstrate that endothelial cells infected with a vFLIP-deleted virus had reduced VCAM1 expression and reduced leukocyte adhesion and transendothelial migration.IMPORTANCEKaposi's sarcoma-associated herpesvirus (KSHV) is associated with the development of Kaposi's sarcoma (KS). KS tumors are characterized by proliferating endothelial-derived spindle cells and infiltrating leukocytes, which secrete cytokines and growth factors that may contribute to the proliferation of tumor cells. Unless exposed to inflammatory cytokines, resting endothelial cells usually do not express adhesion molecules. Here, we demonstrate that KSHV-infected latent endothelial cells induce the expression of vascular cell adhesion molecule, which promotes leukocyte adhesion and transendothelial migration. - Source: PubMed
Publication date: 2026/09/08
Zhang ZhigangHost Kurtis MWong JasonAnders PennyDamania Blossom - Pectolinarigenin (PEC) is a natural flavonoid compound derived from Chinese herbal medicines. Previous studies have demonstrated its significant inhibitory effects against various malignancies. However, the effect and molecular mechanism of PEC in esophageal squamous cell carcinoma (ESCC) as well as its potential for combination with clinical chemotherapeutics for ESCC treatment is still obscure. Here, we systematically explored the anti-ESCC effects of PEC, elucidated its molecular mechanism, and evaluated its synergistic therapeutic potential with paclitaxel (PTX), a first-line chemotherapeutic agent for ESCC. The results showed that PEC obviously restrained proliferation and migration, and induced apoptosis of ESCC cells. Mechanistically, we found that PEC targets the non-canonical pathway of NF-κB, specifically preventing nuclear translocation of p52 and RELB, thus suppressing the transcriptional activity of this pathway. Moreover, we confirmed that PEC markedly inhibited tumor growth and exhibited a strong synergistic effect on the progression of ESCC when combined with PTX using a xenograft model of nude mice. Our research results have revealed a new molecular mechanism for the anti-ESCC efficiency of PEC. This study highlights PEC potential as a promising candidate for ESCC monotherapy or combination therapy with PTX and points out a new strategy for the clinical treatment of natural flavonoids to ESCC. - Source: PubMed
Li ErlingWang LipengHu WenxuZhu MenglinShi ZixuanXu PeirongFan TianliHou Guiqin - Huanglian ointment, recorded in the 'Medical Canon of the Golden Mirror', is traditionally used to treat nasal sores and damp-heat conditions. Allergic rhinitis (AR) is a common immune-mediated disease. However, the mechanism by which the supercritical extract of Huanglian ointment (HLGSE) relieves AR remains unclear. - Source: PubMed
Publication date: 2026/08/28
Bai XueyuanShang LiyingZhang LequnWang XinXu YananZhao DaqingZhang HeZhang Wei - As a master of host-cell reprogramming, () tachyzoites manipulate diverse signaling networks to establish a niche permissive for long-term infection. While the parasite's subversion of canonical NF-κB signaling (p65/p50) is well established, how infection impacts the non-canonical NF-κB pathway has been largely unexplored. Here, we report that infection induces nuclear accumulation of the non-canonical NF-κB subunits RelB and p52 in both human and murine fibroblasts. This response is conserved across both type I and type II parasite genetic backgrounds. We demonstrate that this reprogramming is dependent on the MYR1-mediated export of dense granule effectors. Mechanistically, infection drives the depletion of the negative regulator TRAF3, leading to the stabilization of NF-κB-inducing kinase (NIK), phosphorylation of p100, and its subsequent processing into p52. Utilizing a panel of combinatorial knockout parasites, we reveal that no single effector is responsible for this phenotype. Instead, a suite of eight MYR1-dependent effectors, IST, NSM, HCE1/TEEGR, GRA16, GRA18, GRA24, GRA28, and GRA84, functions through a collaborative, additive network to drive most of the non-canonical response. These findings highlight a distributed regulatory strategy used by the parasite to overcome host transcriptional robustness and shape host signaling. - Source: PubMed
Publication date: 2026/08/28
Berg KennaPanas Michael WKurup Samarchith PBoothroyd John CRosenberg Alex - Ischemic brain injury is a major contributor to global mortality and disability. Despite extensive pathological characterization, systematic integration of rodent transcriptomic data remains limited. This study investigates orthologous transcription factors (TFs) in cerebral ischemia models and their roles in regulating neuroinflammation to develop novel diagnostic and/or predictive biomarkers. - Source: PubMed
Publication date: 2026/08/11
Xu HuiHuang XuHong Ming-YangXu JianYang Tao-TaoShi Rui-RuiGu Jin-Hua