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Invitrogen
Phospho-IkB alpha (Ser32, Ser36) Monoclonal Antibody (H.709.9)
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FIGURE: 1 / 10
Phospho-IkB alpha (Ser32, Ser36) Antibody (MA5-15224) in WB
Western blot analysis of Phospho-I-kappa-B-alpha pSer32/36 in extracts from NIH/3T3 cells, untreated or TNF-alpha-treated (20 ng/mL) for 5 minutes, using Phospho-I-kappa-B-alpha pSer32/36 monoclonal antibody (Product # MA5-15224) (upper) or an I-kappa-B-alpha monoclonal antibody (Amino-terminal Antigen) (lower).
Product Details
MA5-15224
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse,
Non-human primate,
Rat
Published species
Human,
Mouse,
Pig,
Rat
Host/Isotype
Mouse
/ IgG1
Class
Monoclonal
Type
Antibody
Clone
H.709.9
Immunogen
Synthetic phosphopeptide corresponding to residues surrounding pSer32/36 of human IkB alpha
Conjugate
Form
Liquid
Concentration
22 µg/mL
Amount
2.2 µg
Purification
Affinity chromatography
Storage buffer
0.01M HEPES, pH 7.5, with 0.15M NaCl, 100µg/mL BSA, 50% glycerol
Contains
<0.02% sodium azide
Storage conditions
-20°C
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
Product Specific Information
It is not recommended to aliquot this antibody.
Target Information
IkB-alpha is a 40 kDa protein that functions to inhibit NF- kappaB activity. The inhibition occurs via protein-protein interaction between I kappaB proteins and NF- kappaB dimers in the cytosol. The interaction of I kappa B-alpha with NF- kappaB masks the nuclear localization sequence of NF- kappaB, preventing NF- kappaB translocation to the nucleus. A variety of stimuli can activate gene expression by liberating NF- kappaB through the degradation of I kappaB alpha. These stimuli include the proinflammatory cytokines TNF- alpha and IL-1 beta, chemokines, PMA, growth factors, LPS, UV irradiation, viral infection, as well as various chemical and physical stresses. In humans, the gene is located on the q arm of chromosome 14. Activation of NFkB requires that IkB be phosphorylated on specific serine residues, which results in targeted degradation of IkB. IkB kinase alpha (IKK alpha), previously designated CHUK, interacts with IkB-alpha and specifically phosphorylates IkB-alpha on the sites that trigger its degradation Serines 32 and 36. IKK alpha appears to be critical for NFkB activation in response to proinflammatory cytokines. Phosphorylation of IkB by IKK alpha is stimulated by the NFkB inducing kinase (NIK), which itself is a central regulator for NFkB activation in response to TNF and IL-1. The functional IKK complex contains three subunits, IKK alpha, IKK beta and IKK gamma, and each appear to make essential contributions to IkB phosphorylation.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Bioinformatics
Protein Aliases: I(Kappa)B(alpha); I-kappa-B-alpha; I-kappaBalpha; IkappaBalpha; IkB-alpha; IkBa; IKBalpha; Inhibitor of nuclear factor of kappa light chain gene enhancer in B-cells alpha; Inhibitor of nuclear factor of kappa light chain gene enhancer in B-cells, alpha; MAD3; Major histocompatibility complex enhancer-binding protein MAD3; Mutations: 945:OK; NF-kappa-B inhibitor alpha; nuclear factor of kappa light chain gene enhancer in B-cells; nuclear factor of kappa light chain gene enhancer in B-cells inhibitor, alpha; nuclear factor of kappa light polyp gene enhancer in B-cell 1; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; RL/IF-1; unnamed protein product
Gene Aliases: AI462015; EDAID2; IKBA; MAD-3; MAD3; NFKBI; NFKBIA; RL/IF-1
UniProt ID: (Human) P25963, (Rat) Q63746, (Mouse) Q9Z1E3
Entrez Gene ID: (Human) 4792, (Rat) 25493, (Mouse) 18035
protein import into nucleus, translocation
cytoplasmic sequestering of NF-kappaB
regulation of gene expression
negative regulation of macrophage derived foam cell differentiation
positive regulation of cholesterol efflux
negative regulation of lipid storage
lipopolysaccharide-mediated signaling pathway
negative regulation of NF-kappaB transcription factor activity
positive regulation of cellular protein metabolic process
response to muramyl dipeptide
response to lipopolysaccharide
toll-like receptor 4 signaling pathway
response to muscle stretch
regulation of cell proliferation
cytoplasmic sequestering of transcription factor
response to exogenous dsRNA
negative regulation of myeloid cell differentiation
negative regulation of Notch signaling pathway
positive regulation of transcription, DNA-templated
positive regulation of transcription from RNA polymerase II promoter
nucleotide-binding oligomerization domain containing 1 signaling pathway
nucleotide-binding oligomerization domain containing 2 signaling pathway
negative regulation of transcription from RNA polymerase II promoter
immune system process
regulation of transcription from RNA polymerase II promoter
protein import into nucleus
inflammatory response
Notch signaling pathway
I-kappaB kinase/NF-kappaB signaling
signal transduction involved in regulation of gene expression
negative regulation of cholesterol transport
tumor necrosis factor-mediated signaling pathway
NIK/NF-kappaB signaling
negative regulation of protein import into nucleus
negative regulation of I-kappaB kinase/NF-kappaB signaling
positive regulation of inflammatory response
B cell receptor signaling pathway
positive regulation of transcription initiation from RNA polymerase II promoter
cellular response to cold
interleukin-1-mediated signaling pathway
cellular response to cytokine stimulus
cellular response to tumor necrosis factor
negative regulation of cytokine production involved in inflammatory response
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Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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