OP133
Anti-IKKα Mouse mAb (14A231)
liquid, clone 14A231, Calbiochem®
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
14A231, monoclonal
form
liquid
contains
≤0.1% sodium azide as preservative
species reactivity
monkey, human, mouse
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
avoid repeated freeze/thaw cycles
isotype
IgG1
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CHUK(1147)
General description
Immunoaffinity purified mouse monoclonal antibody. Recognizes the ~85 kDa IKKα protein.
Recognizes the ~85 kDa IKKα protein in Daudi cells.
This Anti-IKKα Mouse mAb (14A231) is validated for use in Immunoblotting for the detection of IKKα.
Immunogen
Human
a recombinant protein consisting of full-length human IKKα/IKK1 fused to a His•Tag sequence
Application
Immunoblotting (1-2 g/ml, chemiluminescence)
Packaging
Please refer to vial label for lot-specific concentration.
Warning
Toxicity: Standard Handling (A)
Physical form
In PBS, 0.2% gelatin, pH 7.4.
Reconstitution
Following initial thaw, aliquot and freeze (-20°C).
Analysis Note
Positive Control
Daudi cells
Daudi cells
Other Notes
Antibody should be titrated for optimal results in individual systems.
Zandi, E., et al. 1998 Science281, 1360.
Didonato, J.A., et al. 1997 Nature388, 548.
Lee, F.S., et al. 1997 Cell88, 213.
Mercurio, F., et al. 1997 Science278, 860.
Regnier, C.H., et al. M. 1997 Cell90, 373.
Verma, I. and Stevenson, J.K. 1997 Proc. Nat. Acad. Sci. USA94, 11758.
Verma, I.M., et al. 1995 Genes. Dev.9, 2723.
Didonato, J.A., et al. 1997 Nature388, 548.
Lee, F.S., et al. 1997 Cell88, 213.
Mercurio, F., et al. 1997 Science278, 860.
Regnier, C.H., et al. M. 1997 Cell90, 373.
Verma, I. and Stevenson, J.K. 1997 Proc. Nat. Acad. Sci. USA94, 11758.
Verma, I.M., et al. 1995 Genes. Dev.9, 2723.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
12 - Non Combustible Liquids
WGK
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Faiyaz Ahmad et al.
Scientific reports, 6, 28056-28056 (2016-06-21)
Activation of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, insulin resistance, and metabolic syndrome. The inflammasome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC. Inflammasome activation leads to maturation of
Michael L Kamradt et al.
Cell death & disease, 12(3), 271-271 (2021-03-17)
Cancers, including glioblastoma multiforme (GBM), undergo coordinated reprogramming of metabolic pathways that control glycolysis and oxidative phosphorylation (OXPHOS) to promote tumor growth in diverse tumor microenvironments. Adaptation to limited nutrient availability in the microenvironment is associated with remodeling of mitochondrial
Cristina Aguilera et al.
Proceedings of the National Academy of Sciences of the United States of America, 101(47), 16537-16542 (2004-11-13)
The NF-kappaB pathway plays a pivotal role in proliferation, differentiation, apoptosis, and immune responses in mammals. The NF-kappaB inhibitor, IkappaB, has classically been characterized for its ability to sequester NF-kappaB transcription factors in the cytoplasm. Nevertheless, a nuclear fraction of
Carlota Colomer et al.
Molecular cell, 75(4), 669-682 (2019-07-16)
Phosphorylated IKKα(p45) is a nuclear active form of the IKKα kinase that is induced by the MAP kinases BRAF and TAK1 and promotes tumor growth independent of canonical NF-κB signaling. Insights into the sources of IKKα(p45) activation and its downstream
Jonathan M Starkey et al.
Diabetes, 55(5), 1252-1259 (2006-04-29)
Evidence of diabetes-induced nuclear factor-kappaB (NF-kappaB) activation has been provided with DNA binding assays or nuclear localization with immunohistochemistry, but few studies have explored mechanisms involved. We examined effects of diabetes on proteins comprising NF-kappaB canonical and noncanonical activation pathways
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