07-1387
Anti-oxidized-CaM Kinase II (Met281/282) Antibody
serum, from rabbit
Synonym(s):
CAMKK beta protein, CaM-KK beta, CaM-kinase kinase beta, CaMKK beta, Calcium/calmodulin-dependent protein kinase kinase beta, calcium/calmodulin-dependent protein kinase beta, calcium/calmodulin-dependent protein kinase kinase 2 beta, calcium/calmodulin-
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
serum
antibody product type
primary antibodies
clone
polyclonal
species reactivity
mouse, rat, human
technique(s)
immunocytochemistry: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... CAMK2D(817)
General description
The Ca2+/Calmodulin-Dependent Kinase family includes CaM Kinases I through IV, Phosphorylase Kinase, and MLCK. The CaM Kinases are inactive in the absence of stimuli; binding to Ca2+/Calmodulin induces conformational changes and activation. CaM Kinases have broad substrate specificity, with many cellular functions.
Specificity
Expected to cross-react on Mouse and Rat based on 100% homology with immunogen sequence.
This antibody recognizes CaM Kinase II when oxidized on Met281/282.
Immunogen
Epitope: Oxidized Met281/282
Synthetic peptide encompassing and including oxidized Met281/282.
Application
An independent lab validated this antibody to work in immunocytochemistry in heart sections from mice treated with saline, AngII,or Iso (Erickson, J.R., 2008).
This Anti-oxidized-CaM Kinase II (Met281/282) Antibody is validated for use in WB, IC for the detection of oxidized-CaM Kinase II (Met281/282).
Quality
Evaluated by western blot on untreated and H2O2-treated mouse heart cell lysate.
Western Blot Analysis: 1:1,000 dilution of this antibody was used to detect oxidized CaM Kinase II in mouse heart cell lysates.
Western Blot Analysis: 1:1,000 dilution of this antibody was used to detect oxidized CaM Kinase II in mouse heart cell lysates.
Target description
60 kDa
Linkage
Replaces: 04-1079
Storage and Stability
Stable for 1 years at -20°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.
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Ichiro Matsuo et al.
PloS one, 17(6), e0258823-e0258823 (2022-06-02)
Oral infections, particularly periodontitis, are a well-established risk factor for cardiovascular diseases, although the molecular mechanisms involved remain elusive. The aims of the present study were to investigate the effects of lipopolysaccharide derived from Porphyromonas gingivalis (PG-LPS) on cardiac function
Shuo Geng et al.
Science advances, 5(2), eaav2309-eaav2309 (2019-02-19)
Nonresolving inflammation perpetuated by innate leukocytes is involved in the pathogenesis of unstable atherosclerosis. However, the role and regulation of neutrophils related to nonresolving inflammation and atherosclerosis are poorly understood. We report herein that chronic subclinical endotoxemia, a risk factor
Gabrielle Fredman et al.
Nature communications, 7, 12859-12859 (2016-09-24)
Chronic unresolved inflammation plays a causal role in the development of advanced atherosclerosis, but the mechanisms that prevent resolution in atherosclerosis remain unclear. Here, we use targeted mass spectrometry to identify specialized pro-resolving lipid mediators (SPM) in histologically-defined stable and
Patricia Rouet-Benzineb et al.
Physiological reports, 6(21), e13912-e13912 (2018-11-16)
We investigated the potential adverse effects of hyperaldosteronism and/or hypoestrogenism on cardiac phenotype, and examined their combined effects in female mice overexpressing cardiac aldosterone synthase (AS). We focused on some signaling cascades challenging defensive responses to adapt and/or to survive
Rohan Varshney et al.
International journal of molecular sciences, 22(4) (2021-03-07)
Free radicals, or reactive oxygen species, have been implicated as one of the primary causes of myocardial pathologies elicited by chronic diseases and age. The imbalance between pro-oxidants and antioxidants, termed "oxidative stress", involves several pathological changes in mouse hearts
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