THM Gene thymoma
- Known as:
- THM Gene thymoma
- Catalog number:
- THM
- Category:
- -
- Supplier:
- Transposagen
- Gene target:
- THM Gene thymoma
Ask about this productRelated genes to: THM Gene thymoma
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: THM Gene thymoma
α - Calcitonin Gene Related Peptide, α - CGRP, rat-14 gene protein,Alpha-globin regulatory element-containing gene protein,C16orf35,CGTHBA,Homo sapiens,Human,MARE,Nitrogen permease regulator 3-like protein,NPRL3,Protein CGTHBA10.3 kDa proline-rich protein DAMS,DAMS,Homo sapiens,Human,SMAD5 antisense gene protein 1,SMAD5 antisense RNA 1,SMAD5 opposite strand protein,SMAD5-AS1,SMAD5OS14-3-3 β_α Polyclonal Antibody, Reactivity: H M R, Gene ID: 7529, Synonyms: YWHAB14-3-3 β_α Polyclonal Antibody, Reactivity: H M R, Gene ID: 7529, Synonyms: YWHAB14-3-3 ε Polyclonal Antibody, Reactivity: H M R , Gene ID: 7531, Synonyms: YWHAE14-3-3 ε Polyclonal Antibody, Reactivity: H M R , Gene ID: 7531, Synonyms: YWHAE14-3-3 ζ_δ Polyclonal Antibody, Reactivity: H M R , Gene ID: 7534, Synonyms: YWHAZ14-3-3 ζ_δ Polyclonal Antibody, Reactivity: H M R , Gene ID: 7534, Synonyms: YWHAZ14-3-3 τ Polyclonal Antibody, Reactivity: H M R, Gene ID: 10971, Synonyms: YWHAQ14-3-3 τ Polyclonal Antibody, Reactivity: H M R, Gene ID: 10971, Synonyms: YWHAQ14_3_3_sigma (SFN) Gene Promoter Reporter Vector15-oxoprostaglandin 13-reductase,D3T-inducible gene 1 protein,Dig1,DIG-1,Dithiolethione-inducible gene 1 protein,Ltb4dh,NADP-dependent leukotriene B4 12-hydroxydehydrogenase,PRG-1,Prostaglandin reduct160 kDa nucleoporin,Gene trap locus 1-13 protein,Gtl1-13,GTL-13,Kiaa0197,Mouse,Mus musculus,Nuclear pore complex protein Nup160,Nucleoporin Nup160,Nup16018 kDa Sin3-associated polypeptide,2HOR0202,Cell growth-inhibiting gene 38 protein,GIG38,Histone deacetylase complex subunit SAP18,Homo sapiens,Human,SAP18,Sin3-associated polypeptide p18 Related articles to: THM Gene thymoma
- As a key regulator of intercellular communication, exosomes are essential for tumor cells. In our study, we will explore the mechanisms of exosomes from different sources on lung cancer. We isolated CD8T cells and cancer-associated fibroblasts (CAFs) from venous blood and tumor tissues of lung cancer patients, and isolated exosomes. MiR-2682 was high expression in CD8T-derived exosomes, and lncRNA-FOXD3-AS1 was upregulated in CAF-derived exosomes. Online bioinformatics database analysis showed that RNA Binding Motif Protein 39 (RBM39) was identified as the target of miR-2682, and eukaryotic translation initiation factors 3B (EIF3B) was identified as the RNA binding protein of FOXD3-AS1. CD8T-derived exosomes inhibited the growth of A549 cells and promoted apoptosis, while miR-2682 inhibits reversed these effects of CD8T-derived exosomes. CAF-derived exosomes promoted the growth of A549 cells and inhibited apoptosis, while FOXD3-AS1 siRNA reversed the effect of CAF-derived exosomes. Mechanism studies have found that miR-2682 inhibits the growth of lung cancer cells by inhibiting the expression of RBM39. FOXD3-AS1 promoted the growth of lung cancer cells by binding to EIF3B. In vivo experiments showed that CD8T cell-derived exosome miR-2682 inhibited lung cancer tumor formation, while CAF-derived exosome FOXD3-AS1 promoted lung cancer tumor formation. This study provides mechanistic insights into the role of miR-2682 and FOXD3-AS1 in lung cancer progression and provides new strategies for lung cancer treatment. - Source: PubMed
Publication date: 2024/05/18
Mao GuangxianLiu Jixian - Amyotrophic lateral sclerosis (ALS) is one of the most common neurodegenerative diseases, yet effective treatment is lacking. Moreover, the underlying pathomechanisms of ALS remain unclear, with impaired mitophagy function being increasingly recognized as a contributing factor. FUN14 domain-containing protein 1 (FUNDC1) is an autophagy receptor localized to the outer mitochondrial membrane and a mitochondrial membrane protein that mediates mitophagy and therefore considered as important factor in neurodegenerative diseases. However, its specific role in ALS is not yet clear. Therefore, this study aimed to investigate the regulatory role of FUNDC1 in ALS and determine its regulatory mechanisms. ALS transgenic mice were obtained and maintained under standard conditions. Cell lines were generated by stable transfection with hSOD1 or control vectors. Mice received intrathecal injections of AAV9 vectors expressing FUNDC1 or EGFP. Motor function was assessed through behavioral tests, and histological and immunostaining analyses were performed. Colocalization analysis was conducted in transfected cells, and protein expression was evaluated via western blotting. For the first time, we observed that FUNDC1 was significantly downregulated in the spinal cord tissues of SOD1 mice. FUNDC1 overexpression considerably improved locomotor activity and prolonged survival time in SOD1 mice. Mechanistically, reduced expression of FUNDC1 resulted in decreased mitophagy, as indicated by decreased recruitment through LC3 in SOD1 mice and cellular models. Consequently, this led to increased mitochondrial accumulation and cell apoptosis, exacerbating the ALS phenotype. Furthermore, we identified transcription factor FOXD3 as an essential upstream factor of FUNDC1, resulting in reduced transcription of FUNDC1 in ALS lesions. This study suggests a novel strategy of targeting FUNDC1-mediated mitophagy for developing therapeutic interventions to mitigate disease progression and improve outcomes for ALS patients. - Source: PubMed
Publication date: 2024/05/15
Guo XiaZhang ZhuoGu JuanKe PingYangLiu JingMeng YuanZheng WeiQue WenJunFan RuiLuo JingXiao Fei - Carcass traits are crucial indicators of meat production efficiency. However, the molecular regulatory mechanisms associated with these traits remain unclear. - Source: PubMed
Publication date: 2024/05/11
Zhao DiLiu RanranTan XiaodongKang HuiminWang JieMa ZhengZhao HaiquanXiang HaiZhang ZhengfenLi HuaZhao Guiping - A lot of people are dying from pancreatic cancer (PC) annually. The early detection of this cancer is particularly challenging due to the fact that symptoms tend to appear in advanced stages. It has been suggested that oxidative stress may play a role in the development of PC. Several genes regulate this process, including long noncoding RNAs (lncRNAs). There is no comprehensive study on the expression pattern of lncRNAs related to oxidative stress in PC patients. In the present case-control study, we quantified levels of oxidative stress-associated lncRNAs in PC patients versus healthy controls. - Source: PubMed
Publication date: 2024/04/25
Baradaran-Bagherian SetayeshMehrab Mohseni MahdiehSharifi RoyaAmirinejad RoyaShirvani-Farsani Zeinab - Hyperglycemia in pregnancy can increase the risk of congenital disorders, but little is known about craniofacial skeleton malformation and its corresponding medication. Our study first used meta-analysis to review the previous findings. Second, baicalin, an antioxidant, was chosen to counteract high glucose-induced craniofacial skeleton malformation. Its effectiveness was then tested by exposing chicken embryos to a combination of high glucose (HG, 50 mM) and 6 μM baicalin. Third, whole-mount immunofluorescence staining and hybridization revealed that baicalin administration could reverse HG-inhibited neural crest cells (NCC) delamination and migration through upregulating the expression of Pax7 and Foxd3, and mitigate the disordered epithelial-mesenchymal transition (EMT) process by regulating corresponding adhesion molecules and transcription factors (i.e., E-cadherin, N-cadherin, Cadherin 6B, Slug and Msx1). Finally, through bioinformatic analysis and cellular thermal shift assay, we identified the AKR1B1 gene as a potential target. In summary, these findings suggest that baicalin could be used as a therapeutic agent for high glucose-induced craniofacial skeleton malformation. - Source: PubMed
Publication date: 2024/03/07
Lu Jia-QiLuo Zhi-YanSun ChengyangWang Si-MiaoSun DixiangHuang Ruo-JingYang XuesongDing YongWang Guang