Product nameAnti-IKK gamma/NEMO (phospho S85) antibody
See all IKK gamma/NEMO primary antibodies
DescriptionRabbit polyclonal to IKK gamma/NEMO (phospho S85)
Detects endogenous levels of IKK gamma/NEMO only when phosphorylated at serine 85.
Tested applicationsSuitable for: ELISA, WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse
- Extracts from HepG2 cells
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol, 0.87% Sodium chloride
Without Mg2+ and Ca2+
Concentration information loading...
PurityImmunogen affinity purified
Purification notesThe antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
Our Abpromise guarantee covers the use of ab63551 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/1000. Detects a band of approximately 47 kDa (predicted molecular weight: 47 kDa).|
FunctionRegulatory subunit of the IKK core complex which phosphorylates inhibitors of NF-kappa-B thus leading to the dissociation of the inhibitor/NF-kappa-B complex and ultimately the degradation of the inhibitor. Also considered to be a mediator for TAX activation of NF-kappa-B. Could be implicated in NF-kappa-B-mediated protection from cytokine toxicity (By similarity). Essential for viral activation of IRF3.
Tissue specificityHeart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas.
Involvement in diseaseDefects in IKBKG are the cause of ectodermal dysplasia anhidrotic with immunodeficiency X-linked (EDAID) [MIM:300291]; also known as hypohidrotic ectodermal dysplasia with immunodeficiency (HED-ID). Is a form of ectoderma dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. Characterized by absence of sweat glands, sparse scalp hair, rare conical teeth and immunological abnormalities resulting in severe infectious diseases.
Defects in IKBKG are the cause of ectodermal dysplasia anhidrotic with immunodeficiency-osteopetrosis-lymphedema (OLEDAID) [MIM:300301].
Defects in IKBKG are a cause of immunodeficiency NEMO-related without anhidrotic ectodermal dysplasia (NEMOID) [MIM:300584]; also called immunodeficiency without anhidrotic ectodermal dysplasia, isolated immunodeficiency or pure immunodeficiency. Patients manifest immunodeficiency not associated with other abnormalities, and resulting in increased infection susceptibility. Patients suffer from multiple episodes of infectious diseases.
Defects in IKBKG are the cause of susceptibility to X-linked familial atypical micobacteriosis type 1 (AMCBX1) [MIM:300636]; also known as X-linked disseminated atypical mycobacterial infection type 1 or X-linked susceptibility to mycobacterial disease type 1. AMCBX1 is the X-linked recessive form of mendelian susceptibility to mycobacterial disease (MSMD). MSMD is a congenital syndrome resulting in predisposition to clinical disease caused by weakly virulent mycobacterial species, such as bacillus Calmette-Guerin vaccines and non-tuberculous, environmental mycobacteria. Patients are also susceptible to the more virulent species Mycobacterium tuberculosis.
Defects in IKBKG are the cause of recurrent isolated invasive pneumococcal disease type 2 (IPD2) [MIM:300640]. Recurrent invasive pneumococcal disease (IPD) is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD.
Defects in IKBKG are the cause of incontinentia pigmenti (IP) [MIM:308300]; formerly designed familial incontinentia pigmenti type II (IP2). IP is a genodermatosis usually prenatally lethal in males. In affected females, it causes abnormalities of the skin, hair, eyes, nails, teeth, skeleton, heart, and central nervous system. The prominent skin signs occur in four classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation and dermal scarring.
Sequence similaritiesContains 1 C2HC-type zinc finger.
DomainThe leucine-zipper domain and the C2HC-type zinc-finger are essential for polyubiquitin binding and for the activation of IRF3.
modificationsPhosphorylation at Ser-68 attenuates aminoterminal homodimerization.
Polyubiquitinated on Lys-285 through 'Lys-63'; the ubiquitination is mediated by NOD2 and RIPK2 and probably plays a role in signaling by facilitating interactions with ubiquitin domain-containing proteins and activates the NF-kappa-B pathway. Polyubiquitinated on Lys-399 through 'Lys-63'; the ubiquitination is mediated by BCL10, MALT1 and TRAF6 and probably plays a role in signaling by facilitating interactions with ubiquitin domain-containing proteins and activates the NF-kappa-B pathway. Monoubiquitinated on Lys-277 and Lys-309; promotes nuclear export. Linear polyubiquitinated on Lys-285; the head-to-tail polyubiquitination is mediated by the LUBAC complex. Linear polyubiquitinated on Lys-309; the head-to-tail polyubiquitination is mediated by the LUBAC complex.
Sumoylated on Lys-277 and Lys-309 by SUMO1; the modification results in phosphorylation of Ser-85 by ATM leading to a replacement of the sumoylation by mono-ubiquitination on these residues.
Cellular localizationCytoplasm. Nucleus. Sumoylated NEMO accumulates in the nucleus in response to genotoxic stress.
- Information by UniProt
- IkB kinase associated protein 1 antibody
- IkB kinase subunit gamma antibody
- Inhibitor of nuclear factor kappa B kinase subunit gamma antibody
All lanes : Anti-IKK gamma/NEMO (phospho S85) antibody (ab63551) at 1/500 dilution
Lane 1 : extracts from HepG2 cells,
treated with Anisomycin (0.5uM, 5hours)
Lane 2 : extracts from HepG2 cells,
treated with Anisomycin (0.5uM, 5hours) with immunizing peptide at 10 µg
Lysates/proteins at 30 µg per lane.
Predicted band size: 47 kDa
Observed band size: 47 kDa
This product has been referenced in:
- Chen WT et al. ATM regulation of IL-8 links oxidative stress to cancer cell migration and invasion. Elife 4:N/A (2015). WB ; Human . Read more (PubMed: 26030852) »
- Wu Z et al. An LRP16-containing preassembly complex contributes to NF-?B activation induced by DNA double-strand breaks. Nucleic Acids Res 43:3167-79 (2015). Read more (PubMed: 25735744) »