RelB
- Known as:
- RelB
- Catalog number:
- 000125A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- RelB
Related genes to: RelB
- 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
Related articles to: RelB
- 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 - The Nuclear Factor Kappa B (NF-kB) signalling pathway is essential for regulating inflammation, cell survival, and adaptive immune responses through its canonical (NF-κB1-associated) and noncanonical (NF-κB2-associated) branches. The canonical pathway mediates rapid and broad reactions to immune stimuli, whereas the noncanonical pathway is activated by specific signals and contributes to lymphoid organ development, B-cell maturation including germinal centre activity, T-cell differentiation, thymic selection and antiviral defence. NF-κB transcription factors consist of five subunits: NF-kB1 (p105/p50), NF-kB2 (p100/p52), RelA, RelB and c-Rel-and heterozygous variants in NFKB1 or NFKB2 genes result in a wide range of immune dysregulation. NFKB1 mutations have been associated with common variable immunodeficiency, autoinflammatory or rheumatologic manifestations, Epstein-Barr virus-related lymphoproliferation, gastrointestinal involvement and susceptibility to recurrent or opportunistic infections. Clinical features of NFKB2 deficiency show considerable variability depending on mutation location, but recurrent infections and hypogammaglobulinemia remain the most frequently reported findings. Despite growing recognition of NF-κB-related inborn errors of immunity, the phenotypic spectrum continues to expand and genotype-phenotype correlations remain challenging. In this study, we describe seven individuals from five families with NFKB1 or NFKB2 variants and demonstrate considerable clinical and immunological heterogeneity, including marked intrafamilial variability. - Source: PubMed
Sevinç Selinİslamoğlu CandanHaskoloğlu ŞuleÖztürk GökcanBal Sevgi KöstelAslan Ayşen DurakŞahap Seda KaynakErsöz Cevriye CansızKendirli TanılDoğu Figenİkincioğulları Aydan - PIWILs are RNA-binding proteins whose role in ischemic stroke remains poorly defined. Here, we investigated the contribution of PIWILs to post-ischemic neuroinflammation by using a mouse model of 1 h transient middle cerebral artery occlusion (tMCAo), followed by 6 or 24 h of reperfusion. Brain tissues, blood, and peripheral organs were collected to assess PIWIL expression, inflammatory responses, and brain damage. PIWIL1 and PIWIL2 were significantly upregulated in the cortex and striatum at 24 h post-ischemia, with PIWIL2 also increased in blood and peripheral tissues. Immunofluorescence analyses revealed cell-type-specific localization of PIWILs in neurons, astrocytes, and endothelial cells. Notably, siRNA-mediated silencing of PIWIL2 significantly reduced infarct volume. PIWIL2 silencing also attenuated NF-κB-p65 and phospho-IκBα levels in the peri-infarct cortex but not in the striatum, indicating region-specific modulation of NF-κB signaling and differentially reprogrammed systemic chemokine profiles, with selective upregulation of CCL3, CCL5, and CXCL13 and downregulation of CCL2, CCL17, CCL20, and CXCL1. Mechanistically, PIWIL2 interacted with IKKα and promoted activation of the NF-κB pathway, leading to RelA- and RelB-dependent transcriptional regulation of pro-inflammatory chemokines. Together, these findings identify PIWIL2 as an upstream regulator of NF-κB-dependent neuroinflammation that exacerbates ischemic brain injury and suggest PIWIL2 as a promising therapeutic target targeting post-stroke inflammatory damage. - Source: PubMed
Publication date: 2026/07/24
Patil Rohan MaheshLaudati GiusyGuida NatasciaRuggiero SilviaDi Muraglia NoemiAnzilotti SerenellaLanthaler JulianCoppola LuigiFormisano LuigiAnnunziato LucioEsposito ElgaPignataro Giuseppe