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
- Microbial short-chain fatty acids (SCFAs) regulate intestinal epithelial homeostasis and immune tolerance. Yet, the specific host effector genes that mediate these responses remain poorly defined, limiting the identification of biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/09/08
Masood ZahraSarwar IqraSanam AyeshaZaidi AmberSadikan Muhammad Zulfiqah - Atopic dermatitis (AD) is driven by complex interactions between keratinocytes and immune cells. In this issue of Cell Chemical Biology, Shao et al. identify that NAT10-dependent ac4C modification stabilizes Relb mRNA in keratinocytes, promoting chemokine production, neutrophil recruitment, and dermatitis progression. - Source: PubMed
Wang Jia-NanMeng Xiao-Ming - 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