AB5423
Anti-Tyrosine Hydroxylase Antibody, phosphoSer31
Chemicon®, from rabbit
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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
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
rat
manufacturer/tradename
Chemicon®
technique(s)
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
phosphorylation (pSer31)
Gene Information
rat ... Th(25085)
Specificity
Tyrosine Hydroxylase, phosphoSer31. The antibody recognizes a protein of 60 kDa corresponding to TH phosphorylated at Ser31 in lysates of PC-12 cells stimulated by okadaic acid.
Immunogen
Epitope: phosphoSer31
Synthetic peptide from the phosphoSer31 of rat Tyrosine Hydroxylase. Available as catalog number AG398
Application
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurotransmitters & Receptors
Neurotransmitters & Receptors
This Anti-Tyrosine Hydroxylase Antibody, phosphoSer31 is validated for use in IC, IH, WB for the detection of Tyrosine Hydroxylase.
Western blot: 1:1,000
Immunocytochemistry: 1:1,000
Immunohistochemistry: 1:1,000
Optimal working dilutions must be determined by the end user.
Immunocytochemistry: 1:1,000
Immunohistochemistry: 1:1,000
Optimal working dilutions must be determined by the end user.
Physical form
Affinity purified immunoglobulin. Liquid in 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 μg/mL BSA and 50% glycerol.
Storage and Stability
Maintain at -20°C in undiluted for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles. Do not store in a self defrosting freezer.
Legal Information
CHEMICON 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 Code
10 - Combustible liquids
WGK
WGK 2
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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Cristina Núñez et al.
Endocrinology, 148(12), 5780-5793 (2007-09-08)
Our previous studies have shown that naloxone-induced morphine withdrawal increases the hypothalamic-pituitary-adrenocortical (HPA) axis activity, which is dependent on a hyperactivity of noradrenergic pathways [nucleus tractus solitarius (NTS) A(2)] innervating the hypothalamic paraventricular nucleus (PVN). Short-term regulation of catecholamine biosynthesis
Rubén García-Cabrerizo et al.
Addiction biology, 24(2), 239-250 (2017-12-29)
While prior studies have established various interacting mechanisms and neural consequences (i.e. monoaminergic nerve terminal damage) that might contribute to the adverse effects caused by methamphetamine administration, the precise mechanisms that mediate relapse during withdrawal remain unknown. This study evaluated
Claire B de La Serre et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 311(5), R930-R939 (2016-11-03)
Increased neuropeptide Y (NPY) gene expression in the dorsomedial hypothalamus (DMH) has been shown to cause hyperphagia, but the pathway underlying this effect remains less clear. Hypothalamic neural systems play a key role in the control of food intake, in
Cristina Núñez et al.
Endocrinology, 150(7), 3118-3127 (2009-01-31)
Chronic opiate exposure induces neurochemical adaptations in the noradrenergic system. Enhanced responsiveness of the hypothalamo-pituitary-adrenal axis after morphine withdrawal has been associated with hyperactivity of ascending noradrenergic input from the nucleus of the solitary tract (NTS-A(2)) cell group to the
P Almela et al.
British journal of pharmacology, 155(1), 73-83 (2008-06-10)
Our previous studies have shown that morphine withdrawal induced hyperactivity of cardiac noradrenergic pathways. The purpose of the present study was to evaluate the effects of morphine withdrawal on site-specific phosphorylation of TH in the heart. Dependence on morphine was
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