NF-kB p65 Antibody from ANTIBODIES-ONLINE GmbH

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Antigenic SpecificityNF-kB p65
Clonepolyclonal
Host SpeciesRabbit
Reactive Specieshuman
Isotypen/a
Formatunconjugated
Size100 µg
Concentration1.0 mg/mL
ApplicationsELISA, Immunohistochemistry, Western Blotting
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DescriptionThis antibody is designed, produced, and is suitable for Cancer, Immunology and Nuclear Signaling research. NFkB was originally identified as a factor that binds to the immunoglobulin kappa light chain enhancer in B cells. It was subsequently found in non-B cells in an inactive cytoplasmic form consisting of NFkB bound to IkB. NFkB was originally identified as a heterodimeric DNA binding protein complex consisting of p65 (RelA) and p50 (NFKB1) subunits. Other identified subunits include p52 (NFKB2), cRel, and RelB. The p65, cRel, and RelB subunits are responsible for transactivation. The p50 and p52 subunits possess DNA binding activity but limited ability to transactivate. p52 has been reported to form transcriptionally active heterodimers with the NFkB subunit p65, similar to p50/p65 heterodimers. Lowlevels of p52 and p50 homodimers can also exist in cells. The heterodimers of p52/p65 and p50/p65 are regulated by physical inactivation in the cytoplasm by IkB-a. IkB-a binds to the p65 subunit, preventing nuclear localization, and DNA binding. Activators mediate a rapid phosphorylation of IkB by IkB kinase (IKK), which results in subsequent ubiquitination and proteolytic degradation. NFkB is then transported to the nucleus, where it activates transcription of target genes through binding to NFkB target sequences within the promoter. The HTLV-I protein Tax can induce constitutive NFkB activation through phosphorylation of both IκB-α and IκB-β. The transforming protein Tax inhibits p53 transcriptional activity through the NFkB signaling pathway, specifically via the p65 (RelA) subunit. The inhibition of p53 activity is dependent upon phosphorylation of p65 (RelA) at S536 by the upstream kinase IKKβ.Target Information: NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor, NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene, RELA. Four transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2011].
ImmunogenThis affinity purified antibody was prepared from whole rabbit serum produced by repeated immunizations with a synthetic peptide corresponding to residues surrounding S536 of human p65 (RelA) protein.
Other NamesC-Rel|C-Rel proto-oncogene protein|oncogene REL|avian reticuloendotheliosis|proto-oncogene c-Rel|v-rel reticuloendotheliosis viral oncogene homolog|REL proto-oncogene, NF-kB subunit|REL|Nuclear Factor-kB p65|NFkBP65|NF-kB p65|NFKB3|p65|NF-kappa-B p65delta3|nuclear factor NF-kappa-B p65 subunit|nuclear factor of kappa light polypeptide gene enhancer in B-cells 3|transcription factor p65|v-rel reticuloendotheliosis viral oncogene homolog A|RELA proto-oncogene, NF-kB subunit|RELA|C-Rel protein|p68|NF-kappaB transcription factor p65 subunit|NFkB|nuclear factor kappa B subunit p65|avian reticuloendotheliosis viral (v-rel) oncogene homolog A|p65 NF kappaB|p65 NF-kappa B|p65 NFkB|v-rel reticuloendotheliosis viral oncogene homolog A (avian)|NF-kB p65 subunit|reticuloendotheliosis oncogene|v-rel avian reticuloendotheliosis viral oncogene homolog|LOW QUALITY PROTEIN: proto-oncogene c-Rel|zgc:100833|Xrel2|Xrel3|rel-A|rel2|rel3|v-rel|xrel|v-rel avian reticuloendotheliosis viral oncogene homolog L homeolog|rel.L
Gene, Accession #Gene ID: 5966
Catalog #ABIN129575
Price$537
Order / More InfoNF-kB p65 Antibody from ANTIBODIES-ONLINE GmbH
Product Specific Referencesn/a
ANTIBODIES-ONLINE GmbH
ANTIBODIES-ONLINE GmbH
ANTIBODIES-ONLINE GmbH
Schloss-Rahe-Str. 15
52072 Aachen GERMANY
P: +49 (0)241 95 163 153
F: +49 (0)241 95 163 155

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