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Mouse Anti-NFKB1 Recombinant Antibody (2E6) (CBMAB-N2265-WJ)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
2E6
Antibody Isotype
IgG1, κ
Application
ELISA, IF, WB

Basic Information

Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Nuclear Factor Kappa B Subunit 1
Introduction
This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Alternative splicing results in multiple transcript variants encoding different isoforms, at least one of which is proteolytically processed. [provided by RefSeq, Feb 2016]
Entrez Gene ID
4790
UniProt ID
P19838
Alternative Names
Nuclear Factor Kappa B Subunit 1; Nuclear Factor Of Kappa Light Polypeptide Gene Enhancer In B-Cells 1; DNA-Binding Factor KBF1; EBP-1; Nuclear Factor Kappa-B DNA Binding Subunit; Nuclear Factor NF-Kappa-B P105 Subunit; Nuclear Factor NF-Kappa-B P50 Subunit; NF-Kappabeta; NF-Kappa-B; NF-KappaB;
Function
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 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 RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.
Biological Process
Apoptotic processIEA:UniProtKB-KW
Cellular response to angiotensinManual Assertion Based On ExperimentIMP:BHF-UCL
Cellular response to dsRNAIEA:Ensembl
Cellular response to interleukin-1Manual Assertion Based On ExperimentIEP:BHF-UCL
Cellular response to interleukin-6Manual Assertion Based On ExperimentIMP:BHF-UCL
Cellular response to lipopolysaccharideManual Assertion Based On ExperimentIMP:MGI
Cellular response to mechanical stimulusManual Assertion Based On ExperimentIEP:UniProtKB
Cellular response to nicotineManual Assertion Based On ExperimentIMP:BHF-UCL
Cellular response to tumor necrosis factorIEA:Ensembl
Cellular response to virusIEA:Ensembl
Inflammatory responseManual Assertion Based On ExperimentTAS:UniProtKB
JNK cascadeIEA:Ensembl
Negative regulation of apoptotic processManual Assertion Based On ExperimentTAS:UniProtKB
Negative regulation of calcidiol 1-monooxygenase activityManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of cellular protein metabolic process1 PublicationIC:BHF-UCL
Negative regulation of cholesterol transport1 PublicationIC:BHF-UCL
Negative regulation of gene expressionManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of inflammatory responseIEA:Ensembl
Negative regulation of interleukin-12 productionIEA:Ensembl
Negative regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of vitamin D biosynthetic process1 PublicationIC:BHF-UCL
Positive regulation of canonical Wnt signaling pathwayManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of hyaluronan biosynthetic processManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of lipid storage1 PublicationIC:BHF-UCL
Positive regulation of macrophage derived foam cell differentiation1 PublicationIC:BHF-UCL
Positive regulation of miRNA metabolic processManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:ARUK-UCL
Positive regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Response to muscle stretchIEA:Ensembl
Transcription by RNA polymerase IIManual Assertion Based On ExperimentTAS:UniProtKB
Cellular Location
Nucleus
Cytoplasm
Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).
Involvement in disease
Immunodeficiency, common variable, 12, with autoimmunity (CVID12):
A primary immunodeficiency characterized by hypogammaglobulinemia and recurrent bacterial infections. About half of patients develop autoimmune features, including cytopenia, as well as generalized inflammation and lymphoproliferation manifest as lymphadenopathy or hepatosplenomegaly.
PTM
While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p50 making it an acceptable substrate for the proteasome. This process is known as cotranslational processing. The processed form is active and the unprocessed form acts as an inhibitor (I kappa B-like), being able to form cytosolic complexes with NF-kappa B, trapping it in the cytoplasm. Complete folding of the region downstream of the GRR repeat precludes processing.
Phosphorylation at 'Ser-903' and 'Ser-907' primes p105 for proteolytic processing in response to TNF-alpha stimulation. Phosphorylation at 'Ser-927' and 'Ser-932' are required for BTRC/BTRCP-mediated proteolysis.
Polyubiquitination seems to allow p105 processing.
S-nitrosylation of Cys-61 affects DNA binding.
The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.
More Infomation

Fliegauf, M., Krüger, R., Steiner, S., Hanitsch, L. G., Büchel, S., Wahn, V., ... & Grimbacher, B. (2021). A pathogenic missense variant in NFKB1 causes common variable immunodeficiency due to detrimental protein damage. Frontiers in Immunology, 12, 621503.

Li, J., Lei, W. T., Zhang, P., Rapaport, F., Seeleuthner, Y., Lyu, B., ... & Boisson, B. (2021). Biochemically deleterious human NFKB1 variants underlie an autosomal dominant form of common variable immunodeficiency. Journal of Experimental Medicine, 218(11), e20210566.

Somma, D., Kok, F. O., Kerrigan, D., Wells, C. A., & Carmody, R. J. (2021). Defining the role of nuclear factor (NF)-κB p105 subunit in human macrophage by transcriptomic analysis of NFKB1 knockout THP1 cells. Frontiers in Immunology, 12, 669906.

Mandola, A. B., Sharfe, N., Nagdi, Z., Dadi, H., Vong, L., Merico, D., ... & Roifman, C. M. (2021). Combined immunodeficiency caused by a novel homozygous NFKB1 mutation. Journal of Allergy and Clinical Immunology, 147(2), 727-733.

Lorenzini, T., Fliegauf, M., Klammer, N., Frede, N., Proietti, M., Bulashevska, A., ... & Karim, Y. (2020). Characterization of the clinical and immunologic phenotype and management of 157 individuals with 56 distinct heterozygous NFKB1 mutations. Journal of Allergy and Clinical Immunology, 146(4), 901-911.

Low, J. T., Christie, M., Ernst, M., Dumoutier, L., Preaudet, A., Ni, Y., ... & O’Reilly, L. A. (2020). Loss of NFKB1 results in expression of tumor necrosis factor and activation of signal transducer and activator of transcription 1 to promote gastric tumorigenesis in mice. Gastroenterology, 159(4), 1444-1458.

Best, K. T., Lee, F. K., Knapp, E., Awad, H. A., & Loiselle, A. E. (2019). Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing. Scientific reports, 9(1), 10926.

Coto, E., Reguero, J. R., Avanzas, P., Pascual, I., Martín, M., Hevia, S., ... & Gómez, J. (2019). Gene variants in the NF-KB pathway (NFKB1, NFKBIA, NFKBIZ) and risk for early-onset coronary artery disease. Immunology letters, 208, 39-43.

Li, L., & Zhang, Z. T. (2019). Genetic association between NFKBIA and NFKB1 gene polymorphisms and the susceptibility to head and neck cancer: a meta-analysis. Disease markers, 2019.

Schröder, C., Sogkas, G., Fliegauf, M., Dörk, T., Liu, D., Hanitsch, L. G., ... & Atschekzei, F. (2019). Late-onset antibody deficiency due to monoallelic alterations in NFKB1. Frontiers in Immunology, 10, 2618.

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For research use only. Not intended for any clinical use.

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