Anti-Human Nuclear Factor NF-Kappa-B P65 Subunit Antibody (DPAB2627RH)

Rabbit anti-Human Nuclear Factor NF-Kappa-B P65 Subunit Polyclonal antibody for WB


Host Species
Antibody Isotype
Species Reactivity
Synthetic peptide.


Alternative Names
RELA; v-rel reticuloendotheliosis viral oncogene homolog A (avian); nuclear factor NF-kappa-B p65 subunit; nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; transcription factor p65; v-rel avian reticuloendotheliosis viral oncogene hom
Entrez Gene ID
UniProt ID

Product Background

Acute myeloid leukemia; Adipocytokine signaling pathway; B cell receptor signaling pathway; Chemokine signaling pathway; Epithelial cell signaling in Helicobacter pylori infection; Leishmania infection; NOD-like receptor signaling pathway; Pancreatic cancer; RIG-I-like receptor signaling pathway; Small cell lung cancer; T cell receptor signaling pathway; Toll-like receptor signaling pathway; Signalling by NGF


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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STAT3 speeds up progression of osteoarthritis through NF-kappa B signaling pathway


Authors: Wang, Feida; Guo, Zhenye; Yuan, Yinpeng

Osteoarthritis (OA) is the most common motor system disease in the elderly, with a high incidence and a huge social and economic burden. Therefore, it is urgent to study its potential pathogenesis to improve the therapeutic effect of the disease. In this study, we constructed a number of regulator-mediated OA dysfunction modules, and carried out in-depth analysis in order to examine the disease development process. Differential expression analysis, co-expression analysis and enrichment analysis were combined to screen genes related to disease progression. Subsequently, key regulatory factors in the process of OA were identified based on the pivotal regulators that may manipulate important parts of the module subnetwork. A total of 16 OA dysfunction modules were obtained, involving the aggregation of 3,239 module genes. Then, enrichment analysis showed that module genes were significantly involved in apoptosis, inflammation-related functions and signaling pathways. Finally, we revealed a series of regulators, including 842 ncRNA (miR-132-3p, miR-130a-3p and miR-590-3p), 59 transcription factors (NFKB1, RELA and STAT3). We consider that STAT3 is the core transcription factor and promotes the development of OA through the signal of NF-kappa B. Overall, our results provide biologists and pharmacists with a new way of thinking to reveal the disease process of OA, and provide a wider range of candidate targets for follow-up research.

Comprehensive Targeted Sequencing Identifies Monogenic Disorders in Patients With Early-onset Refractory Diarrhea


Authors: Uchida, Takashi; Suzuki, Tasuku; Kikuchi, Atsuo; Kakuta, Fumihiko; Ishige, Takashi; Nakayama, Yoshiko; Kanegane, Hirokazu; Etani, Yuri; Mizuochi, Tatsuki; Fujiwara, Shin-ichi; Nambu, Ryusuke; Suyama, Kazuhide; Tanaka, Masanori; Yoden, Atsushi; Abukawa, Daiki; Sasahara, Yoji; Kure, Shigeo

Objectives: Causes of early-onset refractory diarrhea include exudative diarrhea associated with very early-onset inflammatory bowel diseases, osmotic or secretory diarrhea, and protein-losing enteropathy. Monogenic disorders are included in these diseases, yet a comprehensive genetic analysis has not been fully established. Methods: We established targeted gene panels covering all responsible genes for early-onset diarrhea. In total, 108 patients from 15 institutions were enrolled in this study. We collected clinical data from all patients. Seventy-three patients with exudative diarrhea, 4 with osmotic or secretory diarrhea and 8 with protein-losing enteropathy were subjected to genetic analysis. Results: A total of 15 out of the 108 enrolled patients (13.9%) were identified as monogenic. We identified 1 patient withRELA, 2 withTNFAIP3, 1 withCTLA4, 1 withSLCO2A1, 4 withXIAP, 3 withIL10RA, 1 withHPS1, 1 withFOXP3, and 1 withCYBBgene mutations. We also identified 1 patient withNFKB2and 1 withTERTmutations from the gene panel for primary immunodeficiency syndromes. The patient with refractory diarrhea caused by heterozygous truncated RelA protein expression is the first case identified worldwide, and functional analysis revealed that the mutation affected nuclear factor kappa B signaling. Genotypes were significantly associated with the clinical and pathological findings in each patient. Conclusions: We identified variable monogenic diseases in the patients and found that genes responsible for primary immunodeficiency diseases were frequently involved in molecular pathogenesis. Comprehensive genetic analysis was useful for accurate molecular diagnosis, understanding of underlying pathogenesis, and selecting the optimal treatment for patients with early-onset refractory diarrhea.

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