Recombinant Human TPH2
- Known as:
- Recombinant Human TPH2
- Catalog number:
- CG32
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human TPH2
Related genes to: Recombinant Human TPH2
- Gene:
- TDO2 NIH gene
- Name:
- tryptophan 2,3-dioxygenase
- Previous symbol:
- -
- Synonyms:
- TDO, TPH2
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-29
- Date modifiied:
- 2016-10-25
- Gene:
- TPH2 NIH gene
- Name:
- tryptophan hydroxylase 2
- Previous symbol:
- -
- Synonyms:
- NTPH, FLJ37295
- Chromosome:
- 12q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-03
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human TPH2
Related articles to: Recombinant Human TPH2
- Squamous cell carcinoma of oropharynx (OPSCC), a head and neck squamous cell carcinoma (HNSCC) subtype, exhibits a remarkably high incidence rate in the North-Eastern regions of India. The development of OPSCC is associated with the exposure to smokeless tobacco with or without consumption of alcohol and smoking tobacco. Despite advanced treatment modalities, OPSCC patients still face a dismal prognosis, necessitating a deeper exploration of the underlying molecular characteristics of the disease. While promoter CpG methylation-driven gene expression alterations in OPSCC have been studied, DNA methylation within gene bodies and its biological significance in this cancer subtype remain largely uncharted. This study represents the first endeavour to investigate gene-body specific DNA methylation-driven transcriptome alterations leading to immune response modulation on a genome-wide scale in OPSCC. - Source: PubMed
Publication date: 2026/03/08
Ghosh SahanaBagchi IndranilMarthong LastbornPatra SubrataShunyu Neizekhotuo BrianGhosh SrimoyeeMaitra Arindam - Temperament plays a critical role in individual susceptibility to mood disorders, particularly in contexts of sleep disruption, through still underexplored mechanisms. This study examined how paradoxical sleep deprivation (PSD) affects behavioral and neurobiological outcomes in high- and low-exploratory (HE and LE) Wistar rats, representing distinct temperament profiles. From a cohort of 80 periadolescent males, 20 HE and 20 LE rats were identified using an open-field test and randomly assigned to PSD or control conditions. Behavioral testing evaluated impulsivity, risk-taking, anxiety-like behavior, anhedonia, despair-like behavior, and memory performance. Biological endpoints included blood uric acid, plasma cytokines, and hippocampal oxidative stress (glutathione and lipid peroxidation), cytokines (interleukin [IL] 1β, IL-6, IL-4), gene expression of circadian regulators (Clock, Bmal1, Per and Cry genes), serotonergic and kynurenine pathway enzymes (Tryptophan Hydroxylase 2, Tph2; Tryptophan 2,3-Dioxygenase,Tdo2; Indoleamine 2,3-Dioxygenase,Ido1), and dopamine D1 (Drd1) and D2 receptor (Drd2) protein levels (measured by Western Blotting). PSD exacerbated risk-taking in HE rats and increased anhedonia and immobility in LE rats. Memory impairments were observed in both groups following PSD. At molecular level, HE rats exposed to PSD showed increased lipid peroxidation, inflammation, upregulation of circadian genes and Tph2, and elevated Drd1 expression. LE rats displayed reduced serotonergic gene expression, increased kynurenine pathway activation, and selective Drd2 upregulation. These findings indicate that temperament shapes behavioral and neurobiological vulnerability to rapid eye movement sleep loss, with distinct profiles associated with mania- and depression-like phenotypes. This supports the relevance of temperament-informed frameworks in understanding mood disorder pathophysiology and guiding personalized treatment strategies. - Source: PubMed
Publication date: 2025/07/10
Lima Camila Nayane Carvalhoda Silva Francisco Eliclécio Rodriguesde Carvalho Michele Albuquerque JalesLima Jose Eduardo de CarvalhoChaves-Filho Adriano José MaiaFries Gabriel RSobreira-Neto Manoel ACosta Deiziane Viana da SilvaFonteles Marta Maria FrançaMacêdo Danielle S - Clinical trials of combined IDO/PD1 blockade in metastatic melanoma (MM) failed to show additional clinical benefit compared to PD1-alone inhibition. We reasoned that a tryptophan-metabolizing pathway other than the kynurenine one is essential. We immunohistochemically stained tissues along the nevus-to-MM progression pathway for tryptophan-metabolizing enzymes (TMEs; TPH1, TPH2, TDO2, IDO1) and the tryptophan transporter, LAT1. We assessed tryptophan and glucose metabolism by performing baseline C11-labeled α-methyl tryptophan (C11-AMT) and fluorodeoxyglucose (FDG) PET imaging of tumor lesions in a prospective clinical trial of pembrolizumab in MM (clinicaltrials.gov, NCT03089606). We found higher protein expression of all TMEs and LAT1 in melanoma cells than tumor-infiltrating lymphocytes (TILs) within MM tumors ( = 68). Melanoma cell-specific TPH1 and LAT1 expressions were significantly anti-correlated with TIL presence in MM. High melanoma cell-specific LAT1 and low IDO1 expression were associated with worse overall survival (OS) in MM. Exploratory optimal cutpoint survival analysis of pretreatment 'high' vs. 'low' C11-AMT SUV of the hottest tumor lesion per patient revealed that the 'low' C11-AMT SUV was associated with longer progression-free survival in our clinical trial ( = 26). We saw no such trends with pretreatment FDG PET SUV. Treatment of melanoma cell lines with telotristat, a TPH1 inhibitor, increased IDO expression and kynurenine production in addition to suppression of serotonin production. High melanoma tryptophan metabolism is a poor predictor of pembrolizumab response and an adverse prognostic factor. Serotoninergic but not kynurenine pathway activation may be significant. Melanoma cells outcompete adjacent TILs, eventually depriving the latter of an essential amino acid. - Source: PubMed
Publication date: 2023/04/26
Oldan Jorge DGiglio Benjamin CSmith EricZhao WeilingBouchard Deeanna MIvanovic MarijaLee Yueh ZCollichio Frances AMeyers Michael OWallack Diana EAbernethy-Leinwand AmberLong Patricia KTrembath Dimitri GGooge Paul BKowalski Madeline HIvanova AnastasiaEzzell Jennifer ANikolaishvili-Feinberg NanaThomas Nancy EWong Terence ZOllila David WLi ZiboMoschos Stergios J - TDO2 is a key enzyme in the kynurenine metabolic pathway, which is the most important pathway of tryptophan metabolism. It has been shown that miRNAs are involved in cell metastasis through interaction with target mRNAs. In this study, we found 645 miRNAs that could be immunoprecipitated with TDO2 through the RNA-immunoprecipitation experiment. miR-126-5p was selected as the research target, which was also confirmed by dual-luciferase reporter assay. Through qRT-PCR analysis, it was verified that the overexpression of miR-126-5p promoted the expression of TDO2, PI3K/AKT and WNT1. Meanwhile, it was verified that overexpression of miR-126-5p can promote intracellular tryptophan metabolism by HPLC. We also verified the effects of miR-126-5p on cell proliferation, migration, and invasion by cck-8, cell colony formation and trans-well assay in both HCCLM3 cells and HepG2 cells. In vivo experiments were also conducted to verify that miR-126-5p promoted tumor formation and growth via immunohistochemical detection of cell infiltration and proliferation to generate markers Ki-67, BAX, and VEGF. In conclusion, our results suggest that miR-126-5p is a biomarker and a potential new treatment target in the progression of HCC via promoting the expression of TDO2. - Source: PubMed
Publication date: 2022/01/10
Ai YangLuo SangWang BenXiao ShuaiWang Yefu - Depression is the serious mental disorder. Previous studies suggest that the development mechanism of depression may be associated with disorders of the tryptophan catabolic pathway (TRYCAT). Thus, this study investigates the effect of agomelatine treatment on the expression and methylation status of genes involved in TRYCAT in the brain and blood of rats exposed to a chronic mild stress (CMS). Separate groups of rats were exposed to CMS for two or seven weeks; the second group received vehicle or agomelatine for five weeks. After completion of both stress conditions and treatment, the expression levels of messenger RNA (mRNA) and protein, as well as the methylation status of promoters, were measured in peripheral blood mononuclear cells (PBMCs) and in brain structures with the use of TaqMan Gene Expression Assay, Western blot, and methylation-sensitive high-resolution melting techniques. In PBMCs, mRNA expression increased in the group after CMS, while this effect was normalized by agomelatine therapy. In brain, and expression changed following CMS exposure. Moreover, CMS decreased the methylation status of the second promoter in the amygdala. Protein expression of Tph1, Tph2, Ido1, and KatII changed in the group after CMS and agomelatine administration, most prominently in the basal ganglia, cerebral cortex, hippocampus, and amygdala. The results indicate that CMS and agomelatine affect the mRNA and protein expression, as well as the methylation of promoters of genes involved in the tryptophan catabolic pathway. - Source: PubMed
Publication date: 2020/09/18
Wigner PaulinaSynowiec EwelinaJóźwiak PawełCzarny PiotrBiałek KatarzynaBijak MichalSzemraj JanuszGruca PiotrPapp MariuszSliwinski Tomasz