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AB190205

重组Alexa Fluor® 488荧光Anti-NF-kB p65抗体[E379]

Alexa Fluor® 488 Anti-NF-kB p65 antibody [E379]

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(4 Publications)

Rabbit Recombinant Monoclonal NF-kB p65 antibody - conjugated to Alexa Fluor® 488. Suitable for ICC/IF and reacts with Human samples. Cited in 4 publications.

查看别名

NFKB3, RELA, Transcription factor p65, Nuclear factor NF-kappa-B p65 subunit, Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3

1 Images
Immunocytochemistry/ Immunofluorescence - Alexa Fluor® 488 Anti-NF-kB p65 antibody [E379] (AB190205)
  • ICC/IF

Lab

Immunocytochemistry/ Immunofluorescence - Alexa Fluor® 488 Anti-NF-kB p65 antibody [E379] (AB190205)

ab190205 staining NF-kB p65 in HeLa cells. The cells were fixed with 100% methanol (5 min), permeabilized in 0.1% Triton X-100 for 5 minutes and then blocked in 1% BSA/10% normal goat serum/0.3M glycine in 0.1%PBS-Tween for 1h. The cells were then incubated with ab190205 at a working dilution of 1 in 50 (shown in green) and ab195889, Mouse monoclonal [DM1A] to alpha Tubulin (Alexa Fluor® 594, shown in red) at a dilution of 1 in 250 overnight at +4°C. Nuclear DNA was labelled in blue with DAPI.

This product also gave a positive signal in 4% formaldehyde (10 min) fixed HeLa cells under the same testing conditions.

Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).

不同偶联物与剂型 (4)

  • Biotin

    Biotin Anti-NF-kB p65 antibody [E379]

  • 578 PE

    PE Anti-NF-kB p65 antibody [E379]

  • 617 Alexa Fluor® 594

    Alexa Fluor® 594 Anti-NF-kB p65 antibody [E379]

  • 665 Alexa Fluor® 647

    Alexa Fluor® 647 Anti-NF-kB p65 antibody [E379]

关键信息

宿主种属

Rabbit

克隆

Monoclonal

克隆号

E379

亚型

IgG

偶联物

Alexa Fluor® 488

激发波长/发射波长

Ex: 495nm, Em: 519nm

不含载体蛋白

No

反应种属

Human

应用

ICC/IF

applications

免疫原

The exact immunogen used to generate this antibody is proprietary information.

反应性数据

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "ICCIF" : {"fullname" : "Immunocytochemistry/ Immunofluorescence", "shortname":"ICC/IF"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "ICCIF-species-checked": "testedAndGuaranteed", "ICCIF-species-dilution-info": "1/50", "ICCIF-species-notes": "<p>Signal can be observed in cells fixed with MeOH or PFA.</p>" } } }

产品详情

Patented technology
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.

Alexa Fluor® is a registered trademark of Molecular Probes, Inc, a Thermo Fisher Scientific Company. The Alexa Fluor® dye included in this product is provided under an intellectual property license from Life Technologies Corporation. As this product contains the Alexa Fluor® dye, the purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). As this product contains the Alexa Fluor® dye the sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: in manufacturing; (ii) to provide a service, information, or data in return for payment (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are sold for use in research. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, 5781 Van Allen Way, Carlsbad, CA 92008 USA or outlicensing@thermofisher.com.

性能和储存信息

形式
Liquid
纯化工艺
Affinity purification Protein A
存储溶液
pH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
运输条件
Blue Ice
推荐的短期储存时间
1-2 weeks
推荐的短期储存条件
+4°C
推荐的长期储存条件
-20°C
分装信息
Upon delivery aliquot
储存信息
Avoid freeze / thaw cycle|Store in the dark

补充信息

This supplementary information is collated from multiple sources and compiled automatically.

NF-kB p65 also known as RelA is a significant component of the NF-kB protein complex. This complex usually involves a molecular weight for p65 of approximately 65 kDa. NF-kB p65 is mechanistically a transcription factor that regulates genes involved in inflammation cell survival and immune response. Expression of p65 is widely seen in various cell types including immune cells and epithelial cells suggesting its role in numerous physiological processes.
Biological function summary

NF-kB p65 acts as part of the larger NF-kB complex usually forming a heterodimer with other family members like p50. This complex translocates to the nucleus upon activation where it binds specific DNA sequences to regulate gene expression. The p65 subunit is essential for transactivating target genes involved in immune and inflammatory responses. Its regulation is important for proper cellular functioning especially in the maintenance of immune homeostasis and inflammatory response.

Pathways

NF-kB p65 participates in critical pathways like the NF-kB signaling and Toll-like receptor pathways. These pathways are fundamental for initiating immune responses and contribute to the regulation of apoptosis and cellular stress responses. In the context of these pathways the IKK complex plays a pivotal role in NF-kB activation leading to the phosphorylation and subsequent degradation of inhibitors that retain NF-kB p65 in the cytoplasm therefore allowing its movement to the nucleus.

NF-kB p65 is implicated in conditions such as cancer and autoimmune diseases. Its dysregulation can lead to persistent activation of inflammatory pathways contributing to tumorigenesis and chronic inflammation. In the context of these diseases proteins such as the p50 subunit and the IKK complex are often involved reflecting the importance of tight regulation of NF-kB signaling in preventing pathological conditions.

产品实验方案

For this product, it's our understanding that no specific protocols are required. You can visit:

靶点信息

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes 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. The heterodimeric RELA-NFKB1 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. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. 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. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells (PubMed : 15790681). The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression. Key transcription factor regulating the IFN response during SARS-CoV-2 infection (PubMed : 33440148).
See full target information RELA

文献 (4)

Recent publications for all applications. Explore the full list and refine your search

STAR protocols 3:101374 PubMed35586313

2022

ChipCytometry for multiplexed detection of protein and mRNA markers on human FFPE tissue samples.

Applications

Unspecified application

Species

Unspecified reactive species

Sebastian Jarosch,Jan Köhlen,Sabrina Wagner,Elvira D'Ippolito,Dirk H Busch

Cell reports methods 1:100104 PubMed35475000

2021

Multiplexed imaging and automated signal quantification in formalin-fixed paraffin-embedded tissues by ChipCytometry.

Applications

Unspecified application

Species

Unspecified reactive species

Sebastian Jarosch,Jan Köhlen,Rim S J Sarker,Katja Steiger,Klaus-Peter Janssen,Arne Christians,Christian Hennig,Ernst Holler,Elvira D'Ippolito,Dirk H Busch

Molecular carcinogenesis 60:567-581 PubMed34101920

2021

Anticancer activities of parthenolide in primary effusion lymphoma preclinical models.

Applications

Unspecified application

Species

Unspecified reactive species

Louna Karam,Soumaiah Abou Staiteieh,Rady Chaaban,Berthe Hayar,Bassel Ismail,Frank Neipel,Nadine Darwiche,Raghida Abou Merhi

Eye (London, England) 30:877-87 PubMed26987588

2016

Silencing of S100A4, a metastasis-associated protein, inhibits retinal neovascularization via the downregulation of BDNF in oxygen-induced ischaemic retinopathy.

Applications

Unspecified application

Species

Unspecified reactive species

G Cheng,T He,Y Xing
View all publications

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