GCH1
- Known as:
- GCH1
- Catalog number:
- Y213989
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GCH1
Related genes to: GCH1
- Gene:
- GCH1 NIH gene
- Name:
- GTP cyclohydrolase 1
- Previous symbol:
- GCH, DYT5, DYT14
- Synonyms:
- GTPCH1, DYT5a
- Chromosome:
- 14q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-10-05
Related products to: GCH1
anti-GCH1 (4A12)anti-GCH1 (4A12), Mouse monoclonal to GCH1, Isotype IgG2a, Host Mouseanti-GCH1(4A12)anti-GCH1(4A12) type: Primary antibodies host: MouseAntibodies: GCH1 HOST: Goat Clonality: pAbBovine Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1Bovine Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1Canine Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1Canine Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1Chicken GTP cyclohydrolase 1 (GCH1) ELISA kit, Species Chicken, Sample Type serum, plasmaChicken GTP cyclohydrolase 1(GCH1) ELISA kitChicken GTP cyclohydrolase 1(GCH1) ELISA kit SpeciesChickenChicken Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1Chicken Guanosine 5-triphosphate Cyclohydrolase1 ELISA , GCH1ELISA Kit FOR GTP cyclohydrolase 1; organism: Mouse; gene name: Gch1 Related articles to: GCH1
- In inflammatory tissue niches, macrophages encounter intense oxidative stress due to their own production of reactive oxygen and nitrogen species as part of antimicrobial defense. Our findings reveal that inflammatory macrophages deploy distinct, context-dependent redox-protective mechanisms to survive this self-inflicted stress, thereby avoiding ferroptotic cell death. Specifically, LPS-activated macrophages, M(LPS), rely on the GTP cyclohydrolase 1 (GCH1)-tetrahydrobiopterin (BH4) pathway for ferroptosis resistance, whereas LPS + IFN-γ-activated macrophages, M(LPS-IFN-γ), depend primarily on nitric oxide produced by inducible nitric oxide synthase (iNOS)-with the BH4 pathway suppressing cell death in the absence of nitric oxide. These distinct adaptations highlight a novel GCH1-BH4-iNOS axis that governs macrophage ferroptosis susceptibility. In both the LPS or the LPS + IFN-γ-activated settings, the redox-protective phenotype is reversible: Removal of inflammatory stimuli abolishes the protection, indicating that this metabolic programming requires continuous stimulation and is not a permanently fixed state. These findings uncover redox metabolism-guided metabolic distinctions between inflammatory macrophages and reveal how they preserve viability over prolonged inflammatory activation. Ultimately, our findings establish the GCH1-BH4-iNOS axis as a central, targetable mechanism to manipulate macrophage ferroptosis resistance for therapeutic purposes. - Source: PubMed
Sauer JuliaOgger Patricia PDukic JasminaNessensohn AlinaGabler SvenjaSchwenzer Ann-KatrinUnsöld Julia KirstinCortès Birgit MariaSteigenberger BarbaraFernandez Perez NuriaStrasser AlexanderDias Requiao RodrigoSchleicher UlrikeGriesser EvaBretschneider TomGantner FlorianThomas Matthew JamesWatson Carolin KirstinEl Kasmi Karim ChristianMurray Peter J - Childhood-onset dystonia (COD) encompasses a clinically and etiologically heterogeneous group of disorders, often with overlapping features. Genetic testing plays a pivotal role in uncovering underlying causes, identifying treatable subtypes, and informing individualized management strategies. - Source: PubMed
Publication date: 2026/06/16
Yilmaz SanemSerdaroglu EsraSimsek ErdemKara BulentTurkdogan DilsadYis UlucErol IlknurYuksel DenizKanmaz SedaEroglu ArzuCanpolat MehmetKomur MustafaCıtak Kurt NeseSakarya Gunes AyferSoydemir DidemBesen SeydaBektas OmerKirik SerkanAtalay Celik HaleArdicli DidemAksoy AyseYarar CoskunCerci Kubur CisilOlgac Dundar NihalGungor OlcayKamasak TulayOlculu Cemile BusraGumus HakanYildirim MiracIsik EsraAtik TahirCogulu OzgurBasak Ayse NazliSunnetci Akkoyunlu DenizÖzbakır Derya HazalKayhan GülsümGerik Çelebi Hamide BetulKaraer KadriDundar MunisKaiyrzhanov RauanCeylaner SerdarPer HuseyinHiz Ayse SemraCansu AliOkuyaz CetinAnlar BanuTekgul Hasan - The present study engineered a bioactive seed coating based on molecularly optimized chitosan-salicylic acid (SA-CS) networks to fortify folate biosynthesis in wheat seedlings. Among tested phytohormones, salicylic acid (SA) promoted seedling growth, folate accumulation, and antioxidant capacity. Composite coatings were fabricated using chitosan of varying molecular weights; films formulated with 0.3% medium molecular weight chitosan and 0.1% SA (SA-MCS) exhibited moderate water vapor permeability and sustained release, creating a favorable microenvironment for germination. SA-MCS coatings significantly increased total folates from 569.87 to 702.75 μg 100 g DW. Mechanistically, controlled SA delivery upregulated GTP cyclohydrolase 1 (GCH1) and aminodeoxychorismate synthase (ADCS), accelerating metabolic flux into the pterin and -aminobenzoic acid (ABA) branches. Multiomics analysis revealed coordinated mobilization of carbon units from histidine catabolism and glutamate into one-carbon metabolism, providing structural backbones and methyl groups for folate enrichment. These findings demonstrate SA-CS coatings as an efficient, biodegradable seed delivery platform for eco-friendly folate biofortification. - Source: PubMed
Publication date: 2026/06/16
Bilal MuhammadQin BowenWu YiweiLi DandanXie ChongYang RunqiangJiang DongWang Pei - Ferroptosis, an iron-dependent and lipid peroxidation-driven form of regulated cell death, has emerged as a "versatile player" in oncology. It exerts a dual, context-dependent role in cancer, acting as both a potent tumor suppressor and a facilitator of tumor progression and therapeutic resistance. This review systematically delineates the core molecular regulatory networks of ferroptosis, highlighting the intricate balance between its execution mechanisms-driven by polyunsaturated fatty acid (PUFA) oxidation, iron catalysis, and mitochondrial dysfunction-and the robust endogenous defense systems, including the GSH-GPX4, FSP1/DHODH-CoQ10, and GCH1-BH4 axes. We deeply explore the dichotomous nature of ferroptosis in tumorigenesis: while classical tumor suppressors like p53 and CDKN2A harness ferroptosis to halt tumor growth, cancer cells can hijack lipid metabolic reprogramming and specific enzymes (e.g., iPLA2β) to evade cell death and promote distant metastasis. Furthermore, we dissect the multidimensional crosstalk between ferroptosis and the tumor microenvironment (TME), emphasizing its bidirectional immunoregulatory effects. Although CD8+ T cell-derived IFN-γ can sensitize tumor cells to ferroptosis and amplify anti-tumor immunity, aberrant ferroptotic activation can paradoxically foster an immunosuppressive niche. Finally, we summarize the latest translational strategies using small-molecule inducers and synergistic combination therapies, emphasizing that biomarker-guided patient stratification remains the ultimate paradigm for overcoming resistance and realizing precision ferroptosis-targeted cancer therapy. - Source: PubMed
Publication date: 2026/06/03
Zhu YuChen MeijiaChen JianglongWang JunjieZhou RujieCui YunfeiLi Guang - Young-onset Parkinson's disease (YOPD), defined by symptom onset at or before 50 years of age, has a strong genetic component. The mutation spectra vary markedly across ethnic groups. However, YOPD among the Hakka, a subgroup of the Han Chinese ethnicity, remains uncharacterized. We investigated the genetic and clinical profiles of YOPD in the Hakka population of western Fujian. - Source: PubMed
Pan Li-YingGuo FangZheng ChongHu Xiao-HongChen Yan-GuiLin Rong-Rong