目录号 | 产品详情 | 靶点 | |
---|---|---|---|
T7281 | 5-HT Receptor | ||
F-15599 是一种高度选择性的 G 蛋白偏向 5-HT1A 受体激动剂,Ki 值为 3.4 nM。 | |||
T22514 | 5-HT Receptor | ||
4F 4PP oxalate 是一种选择性5-HT2A 拮抗剂。 | |||
T12489 | Dopamine Receptor 5-HT Receptor AChR Histamine Receptor | ||
Pimethixene (Calmixen) 是抗组胺和抗血清素剂,用作抗偏头疼剂。它是高效多靶点拮抗剂。 | |||
T0450 | 5-HT Receptor Serotonin Transporter MRP Autophagy | ||
Fluoxetine (LY-110140) 是一种高度特异性的血清素摄取抑制剂,是选择性 5-羟色胺 (5-HT) 再吸收抑制剂。Fluoxetine 具有抗抑郁活性。 | |||
T0031 | Dopamine Receptor 5-HT Receptor Adrenergic Receptor Norepinephrine Histamine Receptor | ||
Ziprasidone hydrochloride monohydrate (CP 88059) 是一种联合 5-HT(5-羟色胺)和多巴胺受体拮抗剂,具有抗精神病活性的强效作用。它也是去甲肾上腺素再摄取抑制剂。 | |||
T6461 | 5-HT Receptor Serotonin Transporter | ||
Dapoxetine hydrochloride (LY-210448 hydrochloride) 是一种具有口服活性的、选择性的血清素再摄取 (serotonin reuptake) 抑制剂 (SSRI),可用于研究早泄 (PE) 。 | |||
T21946 | 5-HT Receptor | ||
BIMU 8 是 5-HT4 的选择性激动剂,对野生型 5HT4 受体、T3.36A 和 W6.48A 突变体 5-HT4 的 EC50 分别为 18 nM、77 nM 和 540 nM。 | |||
T2688 | 5-HT Receptor | ||
LY310762 是 5-HT1D 受体拮抗剂,Ki 为 249 nM。 | |||
TN1032 | 5-HT Receptor | ||
Geissoschizine methyl ether 是从钩藤中发现的一种生物碱,是 Yokukansan 的主要活性成分,具有精神药物作用。它是一种有效的 5-羟色胺 A 受体激动剂,是 Yokukansan 改善攻击性和社交性的候选药物。 | |||
T22987 | 5-HT Receptor | ||
MK 212 monohydrochloride 是一种5-HT1C/5-HT2激动剂。它具有中枢作用,可刺激大脑皮层中的磷酸肌醇水解。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
---|---|---|---|---|---|
TMPH-02099 | AANAT Protein, Human, Recombinant (GST & His) | Human | E. coli | ||
AANAT Protein, Human, Recombinant (GST & His) is expressed in E. coli.
|
|||||
TMPY-01959 | Tryptophan Hydroxylase 1/TPH-1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Tryptophan 5-hydroxylase 1, also known as Tryptophan 5-monooxygenase 1, Tryptophan hydroxylase 1, TPH1, TPH and TPRH, is an enzyme that belongs to the biopterin-dependent aromatic amino acid hydroxylase family. TPH1 contains one ACT domain. Tryptophan hydroxylase catalyzes the biopterin-dependent monooxygenation of tryptophan to 5-hydroxytryptophan (5HT), which is subsequently decarboxylated to form the neurotransmitter serotonin. It is the rate-limiting enzyme in the biosynthesis of serotonin. It is the rate-limiting enzyme in the biosynthesis of serotonin. TPH1 expression is limited to a few specialized tissues: raphe neurons, pinealocytes, mast cells, mononuclear leukocytes, beta-cells of the islets of Langerhans, and intestinal and pancreatic enterochromaffin cells. The tryptophan hydroxylase 1 (TPH1) gene is also reported to be associated with suicidal behavior. Polymorphisms of TPH1 may assist in identifying a subgroup of mood disorder patients that is at higher risk for suicidal behavior.
|
|||||
TMPH-02958 | Tryptophan Hydroxylase 1 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
Oxidizes L-tryptophan to 5-hydroxy-l-tryptophan in the rate-determining step of serotonin biosynthesis. Tryptophan Hydroxylase 1 Protein, Mouse, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 67.3 kDa and the accession number is P17532.
|
|||||
TMPY-03452 | PTS Protein, Human, Recombinant (His) | Human | E. coli | ||
PTS(6-pyruvoyltetrahydropterin synthase) belongs to the PTPS family. It catalyzes the elimination of inorganic triphosphate from dihydroneopterin triphosphate, which is the second and irreversible step in the biosynthesis of tetrahydrobiopterin from GTP. Tetrahydrobiopterin, also known as BH(4), is an essential cofactor and regulator of various enzyme activities, including enzymes involved in serotonin biosynthesis and NO synthase activity. Mutations in this gene result in hyperphenylalaninemia. PTS is involved in the biosynthesis of tetrahydrobiopterin, an essential cofactor of aromatic amino acid hydroxylases. PTS also catalyzes the transformation of 7,8-dihydroneopterin triphosphate into 6-pyruvoyl tetrahydropterin. Defects in PTS are the cause of BH4-deficient hyperphenylalaninemia type A (HPABH4A), also called 6-pyruvoyl-tetrahydropterin synthase deficiency (PTS deficiency) or hyperphenylalaninemia tetrahydrobiopterin-deficient due to PTS deficiency. HPABH4A is an autosomal recessive disorder characterized by depletion of the neurotransmitters dopamine and serotonin, and clinically by severe neurological symptoms unresponsive to the classic phenylalanine-low diet.
|
|||||
TMPH-00862 | HTR1F Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
G-protein coupled receptor for 5-hydroxytryptamine (serotonin). Also functions as a receptor for various alkaloids and psychoactive substances. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase activity. HTR1F Protein, Human, Recombinant (His & SUMO) is expressed in E. coli expression system with N-10xHis-SUMO tag. The predicted molecular weight is 60.2 kDa and the accession number is P30939.
|
|||||
TMPY-02948 | SULT1A3 Protein, Human, Recombinant (His) | Human | E. coli | ||
SULT1A3 belongs to the sulfotransferase 1 family. Sulfotransferase enzymes catalyze the sulfate conjugation of many hormones, neurotransmitters, drugs, and xenobiotic compounds. They are different in their tissue distributions and substrate specificities while their gene structure (number and length of exons) is similar. SULT1A3 gene encodes a phenol sulfotransferase with thermolabile enzyme activity. Four sulfotransferase genes are located on the p arm of chromosome 16; this gene and SULT1A4 arose from a segmental duplication. It is the most centromeric of the four sulfotransferase genes. Exons of this gene overlap with exons of a gene that encodes a protein containing GIY-YIG domains (GIYD1). SULT1A3 is expressed in liver, colon, kidney, lung, brain, spleen, small intestine, placenta and leukocyte. SULT1A3 is a sulfotransferase that utilizes 3'-phospho-5'-adenylyl sulfate (PAPS) as sulfonate donor to catalyze the sulfate conjugation of phenolic monoamines (neurotransmitters such as dopamine, norepinephrine and serotonin) and phenolic and catechol drugs.
|
|||||
TMPH-01248 | ADAR Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication.
|