Anti-RELA monoclonal antibody, clone FQ3272Z [DyLight® 488]

Name: Anti-RELA monoclonal antibody, clone FQ3272Z [DyLight® 488]
SKU: DCABH-3592
Rating: 5 (1 reviews)

Rabbit anti-Human RELA monoclonal antibody for ICC/IF, FC

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Clone

FQ3272Z

Species Reactivity

Human

Immunogen

Synthetic peptide corresponding to Human NF-kB p65.

Conjugate

Dylight 488

Applications

Application Notes

ICC/IF: 1/100; Flow Cyt: 1/100.

Target

Alternative Names

RELA; v-rel reticuloendotheliosis viral oncogene homolog A (avian); NFKB3, nuclear factor of kappa light polypeptide gene enhancer in B cells 3; transcription factor p65; p65; NF-kappa-B p65delta3; nuclear factor NF-kappa-B p65 subunit; nuclear factor of

Entrez Gene ID

5970

UniProt ID

Q04206

Product Background

Antigen Description

NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1.

Pathway

Activated TLR4 signalling, organism-specific biosystem; Activation of NF-kappaB in B Cells, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adaptive Immune System, organism-specific biosystem; Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem;

Citations

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Documents

pdf COA

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QA & Reviews

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References

Stress responses linked to antimicrobial resistance in Acinetobacter species

APPLIED MICROBIOLOGY AND BIOTECHNOLOGY

Authors: Shin, Bora; Park, Chulwoo; Park, Woojun

Abstract

Since the last 20 years, bacteria of the genus Acinetobacter have been the leading cause of hospital-acquired infections. In addition to the ability of Acinetobacter species to acquire rapid antibiotic resistance, limited knowledge on the mechanisms of multidrug resistance to antibiotics limits the treatment options for such infections. Here, we present a review of cellular processes, including oxidative stress defense, energy metabolism, ppGpp signaling, toxin-antitoxin system, and quorum sensing network in Acinetobacter species and their roles in antimicrobial resistance. Although inhibition of stress responses is an attractive approach to the development of effective antimicrobial therapeutic agents, it is crucial to understand the mechanisms that cause antibiotic resistance in Acinetobacter species, as they are not as well studied as those in other pathogenic bacteria. RelA/SpoT has been shown to be involved in ppGpp synthesis in all 50 genomes of 35 Acinetobacter species. However, toxin-antitoxin (TA) systems are present in less than 30% of the 50 genomes (28/30% of SplT/A; 14/14% of HigB/A; 4/6% of HicA/B), except the RelE/B system (30/78%). These data suggested that ppGpp signaling is conserved in Acinetobacter species, but TA systems are not. This review describes our current knowledge on stress responses with respect to antibiotic resistance or tolerance in pathogenic and non-pathogenic Acinetobacter species.

Identifying the Mechanisms and Molecular Targets of Yizhiqingxin Formula on Alzheimer's Disease: Coupling Network Pharmacology with GEO Database

PHARMACOGENOMICS & PERSONALIZED MEDICINE

Authors: Zhang, Tingting; Pan, Linlin; Cao, Yu; Liu, Nanyang; Wei, Wei; Li, Hao

Abstract

Background: Yizhiqingxin formula (YZQX) is a promising formula for the treatment of Alzheimer's disease (AD) with significant clinical effects. Here, we coupled a network pharmacology approach with the Gene Expression Omnibus (GEO) database to illustrate comprehensive mechanisms and screen for molecular targets of YZQX for AD treatment. Methods: First, active ingredients of YZQX were screened for the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database with the absorption, distribution, metabolism, and excretion (ADME) parameters. Subsequently, putative targets of active ingredients were predicted using the DrugBank database. AD-related targets were retrieved by analyzing published microarray data (accession number GSE5281). Protein-protein interaction (PPI) networks of YZQX putative targets and AD-related targets were constructed visually and merged to identify candidate targets for YZQX against AD using Cytoscape 3.7.2 software. We performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to further clarify the biological functions of the candidate targets. The gene-pathway network was established to filter for key target genes. Results: Forty-three active ingredients were identified, and 193 putative target genes were predicted. Seven hundred and ten targets related to AD were screened with vertical bar log2 FC vertical bar > 1 and P < 0.05. Based on the PPI network, 110 target genes of YZQX against AD were identified. Moreover, 32 related pathways including the PI3K-Akt signaling pathway, MAPK signaling pathway, ubiquitin-mediated proteolysis, apoptosis and the NF-kappa B signaling pathway were significantly enriched. In the gene-pathway network, MAPK1, AKT1, TP53, MDM2, EGFR, RELA, SRC, GRB2, CUL1, and MYC targets are putative core genes for YZQX in AD treatment. Conclusion: YZQX against AD may exert its neuroprotective effect via the PI3K-Akt signaling pathway, MAPK signaling pathway, and ubiquitin-mediated proteolysis. YZQX may be a promising drug that can be used in the treatment of AD.