Ask about this productRelated genes to: TBC1D14 antibody
- Gene:
- TBC1D14 NIH gene
- Name:
- TBC1 domain family member 14
- Previous symbol:
- -
- Synonyms:
- KIAA1322
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-30
- Date modifiied:
- 2016-02-22
Related products to: TBC1D14 antibody
Related articles to: TBC1D14 antibody
- Luffa cylindrica flower has been used to treat haemorrhoids and breast hyperplasia, but the mechanism is unclear. - Source: PubMed
Liu ChangYuan JunZou DengJiang XiaojieLi JunZhang HaijunSun Yuxuan - Head and neck squamous cell carcinoma (HNSCC) has great aggressiveness and a high early lymph node metastasis rate. Ribosome biogenesis (RiBi) is frequently hyperactivated in tumors and is strongly associated with oncogenesis. However, its function in HNSCC lymph node metastasis is poorly characterized. Here, we found TBC1D14 expression was downregulated in lymph node-metastatic HNSCC and inversely correlated with Pol I expression. TBC1D14 suppressed RiBi in HNSCC by bioinformatics mining and in vitro experiments. And inhibiting RiBi effectively reduced the proliferation, invasion, and migration capacities of HNSCC cells in vitro. In addition, inhibiting RiBi within TBC1D14-knockdown HNSCC cells suppressed epithelial-mesenchymal transition (EMT). Further in vivo experimentation substantiated that suppression of RiBi in HNSCC effectively attenuated TBC1D14 silencing-induced augmentation of tumor progression and lymph node metastasis. Analysis of our previous proteomic profiling data revealed that DDX31 was significantly downregulated in TBC1D14-overexpressing cells. Further investigations revealed that TBC1D14 inhibited RiBi by promoting the degradation of DDX31 via the ubiquitination pathway. Finally, we found that DDX31 underwent ubiquitination-dependent degradation via the TRIM25-mediated and K63-linked polyubiquitination pathway. Overall, our study demonstrates that TBC1D14 suppresses lymph node metastasis in HNSCC by promoting the ubiquitin-mediated degradation of DDX31 and subsequently inhibiting RiBi, consequently attenuating EMT. These findings revealed novel therapeutic targets for TBC1D14-deficient HNSCC. - Source: PubMed
Publication date: 2025/08/08
Liu YuhongWang MengnaLi YanshiLu TaoWang MinZhan WanyiChen LinHu GuohuaPan Min - This study aimed to investigate the correlation between chromosomal abnormalities in spontaneous abortion with clinical features and seek copy number variations (CNVs) and genes that might be connected to spontaneous abortion. - Source: PubMed
Publication date: 2024/04/26
Qin YuTouch KoksearSha MenghanSun YananZhang ShunranWu JianliWu YuanyuanFeng LingChen SuhuaXiao Juan - Although previous studies reported structural changes associated with electroconvulsive therapy (ECT) in major depressive disorder (MDD), the underlying molecular basis of ECT remains largely unknown. Here, we combined two independent structural MRI datasets of MDD patients receiving ECT and transcriptomic gene expression data from Allen Human Brain Atlas to reveal the molecular basis of ECT for MDD. We performed partial least square regression to explore whether/how gray matter volume (GMV) alterations were associated with gene expression level. Functional enrichment analysis was conducted using Metascape to explore ontological pathways of the associated genes. Finally, these genes were further assigned to seven cell types to determine which cell types contribute most to the structural changes in MDD patients after ECT. We found significantly increased GMV in bilateral hippocampus in MDD patients after ECT. Transcriptome-neuroimaging association analyses showed that expression levels of 726 genes were positively correlated with the increased GMV in MDD after ECT. These genes were mainly involved in synaptic signaling, calcium ion binding and cell-cell signaling, and mostly belonged to excitatory and inhibitory neurons. Moreover, we found that the MDD risk genes of CNR1, HTR1A, MAOA, PDE1A, and SST as well as ECT related genes of BDNF, DRD2, APOE, P2RX7, and TBC1D14 showed significantly positive associations with increased GMV. Overall, our findings provide biological and molecular mechanisms underlying structural plasticity induced by ECT in MDD and the identified genes may facilitate future therapy for MDD. - Source: PubMed
Publication date: 2024/04/26
Sun HuiBai TongjianZhang XiaodongFan XinxinZhang KaiZhang JiangHu QingmaoXu JinpingTian YanghuaWang Kai - Oral cholera vaccine is one of the key interventions used in our fight to end the longest pandemic of our time, cholera. The immune response conferred by the currently available cholera vaccines, as measured by serum antibody levels, is variable amongst its recipients. We undertook a genome wide association study (GWAS) on antibody response to the cholera vaccine; globally, the first GWAS on cholera vaccine response. We identified three clusters of bi-allelic SNPs, in high within-cluster linkage disequilibrium that were moderately (p < 5 × 10) associated with antibody response to the cholera vaccine and mapped to chromosomal regions 4p14, 4p16.1 and 6q23.3. Intronic SNPs of TBC1D1 comprised the cluster on 4p14, intronic SNPs of TBC1D14 comprised that on 4p16.1 and SNPs upstream of TNFAIP3 formed the cluster on 6q23.3. SNPs within and around these clusters have been implicated in immune cell function and immunological aspects of autoimmune or infectious diseases (e.g., diseases caused by Helicobacter pylori and malarial parasite). 6q23.3 is a prominent region harbouring many loci associated with immune related diseases, including multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus, as well as IL2 and INFα response to a smallpox vaccine. The gene clusters identified in this study play roles in vesicle-mediated pathway, autophagy and NF-κB signaling. No significant effect of O blood group on antibody response to the cholera vaccine was observed in this study. - Source: PubMed
Publication date: 2023/09/10
Roy Vijay LaxmiMajumder Partha P