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48-602MAG
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Anti-Tryptophan hydroxylase 2 Antibody detects level of Tryptophan hydroxylase 2 & has been published & validated for use in WB, IH(P).
More>>Anti-Tryptophan hydroxylase 2 Antibody detects level of Tryptophan hydroxylase 2 & has been published & validated for use in WB, IH(P). Less<<
Anti-Tryptophan hydroxylase 2 Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
Tryptophan hydroxylase 2 (TPH2) is preferentially expressed in the brain and is thought to play an important role in serotonin synthesis. Recent research has actually associated high levels of TPH2 with risk of suicide. Misfolding of TPH2 may be the cause of a loss of serotonin neuronal function in Parkinson’s disease. Detection and screening of particular mutations in TPH2 has been cited as an approach toward predicting patient sensitivity to potential antidepressant therapies and even the possibility of diagnosis of behavioral disorders.
References
Product Information
Format
Affinity Purified
HS Code
3002 15 90
Control
Rat brain tissue lysate
Presentation
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
CATALYTIC ACTIVITY: L-tryptophan + tetrahydrobiopterin + O2 = 5-hydroxy-L-tryptophan + 4a-hydroxytetrahydrobiopterin. COFACTOR: Fe2+ ion By similarity. PATHWAY: Aromatic compound metabolism; serotonin biosynthesis; serotonin from L-tryptophan: step 1/2. TISSUE SPECIFICITY: Brain specific. INVOLVEMENT IN DISEASE: Genetic variation in TPH2 may influence susceptibility to major depressive disorder (MDD) [MIM:608516]. Defects in TPH2 are the cause of susceptibility to attention deficit-hyperactivity disorder type 7 (ADHD7) [MIM:613003]. ADHD is a neurobehavioral developmental disorder and is primarily characterized by the co-existence of attentional problems and hyperactivity, with each behavior occurring infrequently alone. Note=Naturally occurring variants of TPH2 with impaired enzyme activity could cause deficiency of serotonin production and result in an increased risk of developing behavioral disorders. SEQUENCE SIMILARITIES: Belongs to the biopterin-dependent aromatic amino acid hydroxylase family. Contains 1 ACT domain. BIOPHYSICOHEMICAL PROPERTIES: Kinetic parameters: KM=41.3 µM for L-tryptophan Vmax=833 nmol/min/mg enzyme
Molecular Weight
~56 kDa observed
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blotting in rat brain tissue lysate. Western Blotting Analysis: 0.2 µg/mL of this antibody detected Tryptophan hydroxylase 2 on 10 µg of rat brain tissue lysate.
Usage Statement
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.
Differential postpartum sensitivity to the anxiety-modulating effects of offspring contact is associated with innate anxiety and brainstem levels of dopamine beta-hydroxylase in female laboratory rats. Ragan, CM; Lonstein, JS Neuroscience
256
433-44
2014
In female mammals, the postpartum period involves dramatic shifts in many socioemotional behaviors. This includes a suppression of anxiety-related behaviors that requires recent physical contact with offspring. Factors contributing to differences among females in their susceptibility to the anxiety-modulating effect of offspring contact are unknown, but could include their innate anxiety and brain monoaminergic activity. Anxiety behavior was assessed in a large group of nulliparous female rats and the least-anxious and most-anxious tertiles were mated. Anxiety was assessed again postpartum after females were permitted or prevented from contacting their offspring 4 h before testing. Levels of dopamine β-hydroxylase (DBH, norepinephrine synthesizing enzyme) and tryptophan hydroxylase-2 (TPH2, serotonin synthesizing enzyme) were measured in the brainstem and dorsal raphe, respectively. It was found that anxiety-related behavior in the two groups did not differ when dams were permitted contact with offspring before testing. Removal of the offspring before testing, however, differentially affected anxiety based on dams' innate anxiety. Specifically, dams reverted back to their pre-mating levels of anxiety such that offspring removal slightly increased anxiety in the most-anxious females but greatly lowered anxiety in the least-anxious females. This reduction in anxiety in the least-anxious females after litter removal was associated with lower brainstem DBH. There was no relationship between females' anxiety and dorsal raphe TPH2. Thus, a primary effect of recent contact with offspring on anxiety-related behavior in postpartum rats is to shift females away from their innate anxiety to a more moderate level of responding. This effect is particularly true for females with the lowest anxiety, may be mediated by central noradrenergic systems, and has implications for their ability to attend to their offspring.
Various mutations have occurred during evolution among orthologs, genes in different species that diverged from a common ancestral gene by speciation. Here, we report the remarkable deterioration of a characteristic mammalian maternal behavior, pup retrieval, in nonmammalized mice, in which the transcription factor Pou3f2 was replaced with the Xenopus ortholog lacking all of the homopolymeric amino acid repeats of mammalian POU3F2. Most of the pups born to the nonmammalized mice died within days after birth, depending on the dam genotype alone. Quantitative immunohistochemical analysis revealed decreases in the rate-limiting enzymes of dopamine and serotonin synthesis in various brain structures. Similar results were obtained in knock-in mice in which all of the homopolymeric amino acid repeats of mammalian POU3F2 were removed. Pup retrieval behavior in mammals is thus strongly related to monoamine neurotransmitter levels via the acquisition of homopolymeric amino acid repeats during mammalian evolution.