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Merck
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Key Documents

07-210

Sigma-Aldrich

Anti-AKAP 150 Antibody

serum, Upstate®

Sinónimos:

Anti-Anti-AKAP75, Anti-Anti-AKAP79, Anti-Anti-H21

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

rat

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... AKAP1(8165)

Specificity

AKAP 150

Immunogen

peptide corresponding to amino acids 428-449 of rat AKAP 150 (C-TTVGQAEEATVGQAEEATVGQA)

Application

Anti-AKAP 150 Antibody is an antibody against AKAP 150 for use in WB.
Research Category
Signaling
Research Sub Category
Kinases & Phosphatases

RNA Binding Protein (RBP)

Quality

routinely evaluated by immunoblot on a rat brain cytosolic preparation

Target description

150kDa

Physical form

0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
Antiserum

Storage and Stability

2 years at -20°C

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


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Matthew A Nystoriak et al.
Science signaling, 10(463) (2017-01-26)
Hypercontractility of arterial myocytes and enhanced vascular tone during diabetes are, in part, attributed to the effects of increased glucose (hyperglycemia) on L-type CaV1.2 channels. In murine arterial myocytes, kinase-dependent mechanisms mediate the increase in CaV1.2 activity in response to
AKAP signaling in reinstated cocaine seeking revealed by iTRAQ proteomic analysis.
Reissner, KJ; Uys, JD; Schwacke, JH; Comte-Walters, S; Rutherford-Bethard, JL; Dunn et al.
The Journal of Neuroscience null
Bo Chen et al.
Journal of neuroinflammation, 19(1), 181-181 (2022-07-14)
Perioperative neurocognitive disorders (PNDs) are considered the most common postoperative complication in geriatric patients. However, its pathogenesis is not fully understood. Surgery-triggered neuroinflammation is a major contributor to the development of PNDs. Neuroinflammation can influence N-methyl-D-aspartate receptor (NMDAR) expression or
Aleksandra Polishchuk et al.
Cell communication and signaling : CCS, 22(1), 371-371 (2024-07-24)
Protein kinase A (PKA) enhances neurotransmission at the neuromuscular junction (NMJ), which is retrogradely regulated by nerve-induced muscle contraction to promote Acetylcholine (ACh) release through the phosphorylation of molecules involved in synaptic vesicle exocytosis (SNAP-25 and Synapsin-1). However, the molecular
Christopher H Bohrer et al.
Nature methods, 18(6), 669-677 (2021-06-02)
Single-molecule localization microscopy (SMLM) relies on the blinking behavior of a fluorophore, which is the stochastic switching between fluorescent and dark states. Blinking creates multiple localizations belonging to the same fluorophore, confounding quantitative analyses and interpretations. Here we present a

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