Ask about this productRelated genes to: TTYH3 Blocking Peptide
- Gene:
- TTYH3 NIH gene
- Name:
- tweety family member 3
- Previous symbol:
- -
- Synonyms:
- KIAA1691
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-10
- Date modifiied:
- 2018-11-22
Related products to: TTYH3 Blocking Peptide
Related articles to: TTYH3 Blocking Peptide
- Tyrosine sulfation is a widespread posttranslational modification in mammals and is known to influence protein function and signaling. However, its functional significance during porcine preimplantation development remains poorly understood. - Source: PubMed
Publication date: 2026/01/22
Gao JiazeWang ChengpengXie HongshuangYang GuangYang QingboHuang ChengLi ShijieLiu ZhonghuaHe TianyaoYin ZhiJin Jun-XueWang Jiaqiang - Small extracellular vesicles (sEVs), lipid-bilayer delimited particles (50-200 nm) released by cells, are emerging as a promising class of liquid biopsy biomarkers for elusive cancers, such as high-grade serous ovarian cancer (HGSOC). HGSOC originates from the fallopian tube (FT), progressing from p53 signatures to a precursor lesion known as serous tubal intraepithelial carcinoma (STIC). We hypothesize that sEVs contribute to ovarian cancer pathogenesis, carry cargo reflective of their site of origin, and serve as diagnostic biomarkers for early detection. To test this, we established a case-control cohort using archival plasma samples from 30 HGSOC patients (10 early stage [ES] and 20 late stage [LS]) and 40 healthy controls (HC). sEVs were enriched by size-exclusion chromatography and profiled by LC-MS/MS. Across all samples, 1078 EV-associated proteins (exoproteins) were identified, including 52 upregulated in ES HGSOC versus HC and 59 upregulated in LS HGSOC versus HCs (log fold change >1, p < 0.05). Upregulated EV proteins were prioritized based on FT origin and tissue expression in STIC lesions. Seven candidate biomarkers (MYL6, GSTP1, TTYH3, PRDX6, MUC1, MYH14, and PTGS1) were validated by immunohistochemistry in FT tissue harboring STIC lesions and in HGSOC tissues, as well as by Western blotting in FT/HGSOC cell-derived EVs. These findings suggest that circulating exoproteins upregulated in ES cancer disease reflect precursor lesions. A four-protein combinatorial panel (MUC1, MYL6, TTYH3, and GSTP1), selected using Akaike Information Criterion, yielded an area under the curve (AUC) of 0.975 and 90% sensitivity at 95% specificity for distinguishing ES HGSOC versus HC. In addition, increased MUC1 levels in circulating sEVs were confirmed by immunoassay (AUC = 0.840 for ES HGSOC versus HC; AUC = 0.860 for LS HGSOC versus HC, p < 0.05). In summary, our sEV proteomic analysis of ES HGSOC reveals exobiomarkers associated with early FT lesions, offering a promising avenue for detecting disease while it remains confined to the FT. - Source: PubMed
Publication date: 2026/01/08
Rayamajhi SagarSipes JaredNgala BidiiMitra AmritaLi MeizhangTrinidad Camille VCui WeiRahman Mohammod MahmudurAhmmed FoyezBantis Leonidas ESardiu Mihaela EProvince Dennis WPathak Harsh BGodwin Andrew K - Histopathologic diagnosis of thin, invasive cutaneous melanoma (CM) is only 34-62% accurate. Therefore, we sought to develop a transcriptomic biomarker to distinguish benign from malignant melanocytic neoplasms. We generated a targeted RNA-Sequencing dataset (TempO-Seq) of benign nevi (BN; n = 50) and CM (Breslow depth ≤ 1.0 mm; n = 51) and demonstrated enrichment of immune-related pathways among the 450 differentially expressed genes. Next, we trained a putative transcriptomic biomarker in two datasets, including BN and CM, and one dataset with CM in association with a nevus, macrodissected into CM and nevus regions. We refer to the nevus portion of CM in association with a nevus as progressing nevi (PN), since these nevi progressed to CM. Principal component analysis showed that PN samples clustered in a component intermediate to BN and CM. Ordinal regularized regression selected PYGL, AP000845.1, PHYHIP, WSCD1, FBXO7, TRPM1, SLC4A4, NALCN, FRMD4B, HHATL, COL1A1, CRYM, EPOP, RGS1, KRT6C, IGHG1, CNTN1, MMP11, GZMM, AP001880.1, TTYH3, TMEM132A, and PRAME; these genes were consistently selected in 1000 models using data from bootstrap resamples and had a single model predictive accuracy of at least 0.90 (area under the receiver operator characteristics curve). Linear regression models fit with these 23 genes in the TempO-Seq data, and publicly available microarray datasets from BN, dysplastic nevi, and CM, showed high consistency in the magnitude and directionality of gene expression differences between nevi and CM. Furthermore, immunohistochemical staining showed consistent protein-level changes in MMP11 and PYGL. These results illuminate the potential for a transcriptomic biomarker to differentiate benign from malignant melanocytic neoplasms and improve the accuracy of melanoma diagnosis. - Source: PubMed
Publication date: 2025/10/03
Borden Elizabeth SHastings Colin TPrakash NithishKuo TylerTapia EdgarYozwiak MichaelSagerman PaulVargas de Stefano DanielleBuetow Kenneth HWilson Melissa ACuriel-Lewandrowski ClaraChow Hsiao-Hui SherryLaFleur Bonnie JHastings Karen Taraszka - Cattle body size measurements constitute the conformation traits that facilitate their production, fertility, and longevity status. Prioritizing functional variants and causal genes of conformation traits is essential for understanding their genetic basis. In this study, we conducted single-trait and multitrait GWAS for 20 body conformation traits using imputed sequence data in 7,674 Chinese Holstein individuals and identified 27 QTL regions. Leveraging these QTL regions, we performed multitrait Bayesian fine-mapping to identify 30 independent credible sets of putative causal variants. Incorporating GWAS and cis-acting expression QTL data, Mendelian randomization was used to infer 153 putative causal gene-trait relationships. The previously reported genes, such as CCND2, TMTC2, and NRG3, were confirmed in our study. Of note, several novel candidate causal genes were also identified, such as C1R, RIMS1, SERPINB8, NETO2, TTYH3, TTC3, ANAPC4, and PSMD13. Our results provide new insights into the regulatory mechanisms of body conformation traits in cattle. - Source: PubMed
Publication date: 2025/05/16
Teng JunDuan ChongweiZhang XinyiChen ZhujunNing ChaoLi RonglingGao YundongGao HongdingLiu HuimingLi JianbinWang XiaoZhang Qin - Metastasis is the predominant culprit of cancer-associated mortality in non-small cell lung cancer (NSCLC). Tweety homolog 3 (TTYH3) reportedly functions vitally in the development of diverse cancers, including NSCLC; nevertheless, its role in NSCLC metastasis remains ambiguous. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were initially employed to detect TTYH3 expression in NSCLC and normal lung epithelial cells. Subsequently, A549 and NCI-H1650 cells were chosen as NSCLC models in vitro and transfected with short hairpin RNAs (sh-TTYH3, sh-LUCAT1, and sh-ALYREF) or overexpression plasmids (oe-ALYREF and oe-TTYH3). Transwell assays were used for migrative and invasive tests. Epithelial mesenchymal transformation (EMT)-related proteins (E-cadherin, N-cadherin, Vimentin, and Snail) were measured by western blot. A mouse lung metastasis model was built to define the function of TTYH3 in NSCLC metastasis, followed by hematoxylin-eosin staining. RNA pull-down, RNA immunoprecipitation, qRT-PCR, western blot, and actinomycin D assays were adopted to determine the relationships among LUCAT1, ALYREF, and TTYH3. TTYH3 was highly expressed in NSCLC cells relative to normal lung cells. Functionally, TTYH3 knockdown restrained NSCLC migration, invasion, EMT, and metastasis. Mechanistic experiments demonstrated that LUCAT1 bound to ALYREF. After LUCAT1 knockdown, TTYH3 expression and mRNA stability were reduced, which was reversed by ALYREF overexpression. Furthermore, ALYREF overexpression counteracted the inhibitory effects of LUCAT1 knockdown on NSCLC cell migration, invasion, and EMT. TTYH3 overexpression eliminated the suppressive functions of ALYREF downregulation in NSCLC progression. LUCAT1 promotes TTYH3 expression via interacting with ALYREF, thereby facilitating NSCLC migration, invasion, and EMT. - Source: PubMed
Publication date: 2025/02/10
Fang FangZhao MeiMeng JinmingHe JiaqiYang ChunleiWang ChanghongWang JiaxiaoXie ShengJin XiaoweiShi Wei