FYTTD1 siRNA_Lentivectors
- Known as:
- FYTTD1 siRNA_Lentivectors
- Catalog number:
- i008365c
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FYTTD1 siRNA_Lentivectors
Related genes to: FYTTD1 siRNA_Lentivectors
- Gene:
- FYTTD1 NIH gene
- Name:
- forty-two-three domain containing 1
- Previous symbol:
- -
- Synonyms:
- DKFZp761B1514, UIF
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-24
- Date modifiied:
- 2018-08-03
Related products to: FYTTD1 siRNA_Lentivectors
Related articles to: FYTTD1 siRNA_Lentivectors
- Excessive fluoride intake during early tooth development causes dental fluorosis, yet chronic high fluoride exposure may also disrupt gastrointestinal physiology and host-microbe interactions. We profiled the host fecal proteome of school-aged children with severe dental fluorosis (PF; TF 5-9; n = 10) and age-matched controls (CF; TF 0; n = 10) from a fluoride-endemic region of Thailand, with systemic exposure confirmed by elevated 24-h urinary fluoride excretion. LC-MS/MS identified 182 proteins (164 retained after filtering), including 24 proteins detected exclusively in PF samples. Differential protein expression revealed six upregulated (C3, FYTTD1, TRIP11, PRDX4, CDH1, SI) and four downregulated (SIAE, ZG16, MUC5AC, GUSB). Enrichment analyses implicated coordinated alterations in epithelial adhesion and barrier regulation, vesicular trafficking/ER proteostasis, oxidative stress responses, carbohydrate metabolism, and innate immune signaling. Knowledge-based interaction mapping (STRING/IntAct) further nominated cystic fibrosis transmembrane conductance regulator (CFTR)-centered epithelial ion-transport and barrier pathways as a convergent axis linking multiple fluoride-responsive proteins. These findings provide human proteomic evidence that fluorosis associates with intestinal epithelial and immune dysregulation extending beyond enamel pathology, supporting a systems-level view of fluorosis as a multisystem condition. - Source: PubMed
Publication date: 2026/05/27
Pongsapipatana NawapanGavila PatcharapornKhieota ThutchimaJung Han-SungAlinejad-Rokny HamidCho Sung-DaeSriwattanapong KanokwanPorntaveetus Thantrira - Gene function can be described using various measures. We integrated association studies of three types of omics data to provide insights into the pathophysiology of subclinical coronary disease and myocardial infarction (MI). Using multivariable regression models, we associated: (1) single nucleotide polymorphism, (2) DNA methylation, and (3) gene expression with coronary artery calcification (CAC) scores and MI. Among 3106 participants of the Framingham Heart Study, 65 (2.1%) had prevalent MI and 60 (1.9%) had incident MI, median CAC value was 67.8 [IQR 10.8, 274.9], and 1403 (45.2%) had CAC scores > 0 (prevalent CAC). Prevalent CAC was associated with AHRR (linked to smoking) and EXOC3 (affecting platelet function and promoting hemostasis). CAC score was associated with VWA1 (extracellular matrix protein associated with cartilage structure in endomysium). For prevalent MI we identified FYTTD1 (down-regulated in familial hypercholesterolemia) and PINK1 (linked to cardiac tissue homeostasis and ischemia-reperfusion injury). Incident MI was associated with IRX3 (enhancing browning of white adipose tissue) and STXBP3 (controlling trafficking of glucose transporter type 4 to plasma). Using an integrative trans-omics approach, we identified both putatively novel and known candidate genes associated with CAC and MI. Replication of findings is warranted. - Source: PubMed
Publication date: 2023/12/07
Møller Amalie LykkemarkVasan Ramachandran SLevy DanielAndersson CharlotteLin Honghuang