Thyroid gland cDNA
- Known as:
- Thyroid gland complementary Desoxyribonucleic acid
- Catalog number:
- CDR028
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- GeneRiver
- Gene target:
- Thyroid gland cDNA
Ask about this productRelated genes to: Thyroid gland cDNA
- Gene:
- DMBT1 NIH gene
- Name:
- deleted in malignant brain tumors 1
- Previous symbol:
- -
- Synonyms:
- GP340, muclin, SALSA, Gp-340, hensin, vomeroglandin
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2017-02-28
Related products to: Thyroid gland cDNA
0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal10 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal10 days lactation. adult female mammary gland cDNA. RIKEN full-length enriched library. clone D730038M14 product transducer of E - N_A Polyclonal10 days neonate cerebellum cDNA. RIKEN full-length enriched library. clone B930045P16 product hypothetical protein. full insert - N_A Polyclonal10 days neonate cerebellum cDNA. RIKEN full-length enriched library. clone B930045P16 product hypothetical protein. full insert - N_A Polyclonal10. 11 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2810460C24 product RIKEN cDNA 2810460C24 - N_A Polyclonal12 days embryo embryonic body between diaphragm region and neck cDNA. RIKEN full-length enriched library. clone 9430083C07 produ - N_A Polyclonal12 days embryo embryonic body between diaphragm region and neck cDNA. RIKEN full-length enriched library. clone 9430093B05 produ - 0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone15 days embryo head cDNA. RIKEN full-length enriched library. clone D930048N17 product transcription factor AP-4 (activating enh - N_A Polyclonal16 days neonate cerebellum cDNA. RIKEN full-length enriched library. clone 9630004B04 product hypothetical protein. full insert - N_A Polyclonal16.5 kDa submandibular gland glycoprotein,Mouse,Mus musculus,Salivary protein 1,Spt1,Spt-116E1-BP,Homo sapiens,HPV16 E1 protein-binding protein,Human,Human papillomavirus type 16 E1 protein-binding protein,Pachytene checkpoint protein 2 homolog,PCH2,Thyroid hormone receptor interactor 13,T17 days pregnant adult female amnion cDNA. RIKEN full-length enriched library. clone I920028B02 product Hypothetical RNA-binding - N_A Polyclonal Related articles to: Thyroid gland cDNA
- Explore the influence of obesity and Metabolic Syndrome disorders on the plasma proteome and metabolome, through an integrated analysis. - Source: PubMed
da Silva Carlos Vinicius Fda Silva Carlos José FCataldi Thaís RLabate Carlos ASade Youssef BScapin Sandra Mara NThompson Fabiano LThompson CristianeSilva-Boghossian Carina Maciel dade Oliveira Santos Eidy - DMBT1 is a large scavenger receptor cysteine rich (SRCR) B protein that has been reported as a tumor suppressor gene and a co-receptor for HIV-1 infection. Here, we found DMBT1 is a major mucosal protein bound to SARS-CoV-2. Overexpression of DMBT1 in 293T cells may enhanced infection by SARS-CoV-2 in ACE2 dependent manner. Blocking experiments using overlapping peptide library of SRCR domain of DMBT1 showed that peptide 7 (CQGRVEVLYRGSWGTV), which contains bacteria-binding VEVLXXXXW motif, could inhibit SARS-CoV-2 infection. High concentration of peptide 7 can significantly inhibit the replication of SARS-CoV-2 in hamsters. Peptide 7 inhibits SARS-CoV-2 infection by aggregating the spike protein, thereby reducing its binding to and internalization by host cells. The cysteine residue at the N-terminus of peptide 7 is critical for dimerization and antiviral activity. These results indicate that DMBT1 can serve as a candidate target for the development of antiviral drugs. - Source: PubMed
Publication date: 2025/09/03
Zhu ChenxiWang ZiqiaoPan ZhendongMai XinjiaChen YiyunZhang WenZhao PingTang HailinZhang RongZhou Dapeng - The liver is a major target organ for breast cancer metastasis, while the regulatory mechanism of liver colonization by breast cancer remains largely unclear. Neutrophils are known to play important roles in metastatic colonization of cancer cells by the formation of neutrophil extracellular traps (NETs). Here we show the role and mechanism of a subpopulation of Kupffer cells (KCs), the liver resident macrophages, in mediating tumoral induction of NETs and liver metastasis. NETs are activated more abundantly in liver metastases of breast cancer, as compared to metastases to other organs and primary tumors. Liver-tropic tumor cells induce CD62L-expressing KCs by a secretory protein DMBT1, and CD62L KCs activate neutrophils for NETosis via the chemokine CCL8. Inhibition of CCL8 or its receptor on neutrophils, CCR1, impairs NETosis and metastasis. In addition, we identified a KC membrane protein MUC1 that binds to DMBT1 and subsequently activates NF-κB signaling in KCs, leading to CCL8 and CD62L expression. KCs with MUC1 inhibition effectively suppress liver metastasis. Furthermore, a DMBT1 neutralizing antibody was developed with the promise to inhibit tumor-KC interaction and treat metastatic cancer. In conclusion, our work reveals a KC subset that accounts for the liver tropism of breast cancer cells and NETs, and provides potential strategies in metastasis treatment. - Source: PubMed
Publication date: 2025/08/12
Tian PuWu QiuyaoHe DasaZhao WenjingLuo LichaoJia ZhenchangLuo WenqianLv XianzheLiu YananWang YuanWang QianZhang PeiyuanLiang YajunYang QifengHu Guohong - The upper respiratory tract, spanning the pharyngolaryngeal to tracheobronchial regions, enables breathing, vocalization, and frontline defense against airborne insults. We generated a cellular and molecular atlas of the mouse upper respiratory epithelium from pharynx/larynx to tracheobronchial carina by combining single-cell RNA sequencing with spatial validation. Our analysis revealed 18 epithelial cell types, organized into three spatially distinct compartments: + pharyngolaryngeal, + tracheobronchial, and + submucosal glands. Stratified squamous pharyngolaryngeal zones displayed extensive and region-specific Keratin codes. Within the pseudostratified tracheobronchial epithelium, diverse luminal cells, including multiple varieties of club cells, exhibit marker-expression gradients along the proximal-distal axes. Lastly, analysis of the submucosal gland epithelium -which contains various cell types, including distinctive myoepithelial cells- revealed extensive diversity both among and within its cellular populations. This spatially resolved transcriptomic atlas elucidates how epithelial identity varies along the upper respiratory axes and will guide investigations into cellular dynamics in health and disease. - Source: PubMed
Publication date: 2025/06/07
Foote Alexander GSun Xin - Nasopharyngeal carcinoma (NPC) is prevalent in Southeast Asia, particularly in Indonesia. Despite advances in treatment, patients with advanced NPC face poor outcomes. Examining the NPC mutational landscape is crucial for understanding its biology and enable potential new therapeutic strategy. To characterize the landscape of single nucleotide variants (SNVs), structural variants (SVs), copy number variations (CNVs), and short tandem repeats (STRs) in locally advanced to advanced NPC within an Indonesian cohort using long-read sequencing. Six fresh-frozen nasopharyngeal biopsy samples were collected from the NPC biobank. DNA was extracted and sequenced using Oxford Nanopore's Promethion 2 Solo long-read sequencer. Structural and small variants were identified and annotated. The SNVs, SVs, and CNVs were categorized based on predicted effects, and key findings were validated using external RNA-seq data. Copy number loss genes were checked against the Tumour Suppressor Gene database (TSGene v2.0). Genetic findings were correlated with patient clinical histories. Approximately 4.4 to 5.1 million SNVs were identified per sample, with 0.023% categorized as high consequence. Notable tumour suppressor genes, such as LIMD1 and CNDP2, were frequently mutated. Around 30,000 to 41,599 SVs were detected per sample. High-consequence tumour suppressor gene SVs were identified in EPHA3, CASP8, DMBT1, ZFHX3, and IRF5 gene. Common copy number tumour suppressor gene loss observed in RNH1, H19, CDKN1C, and others, suggesting their role in NPC carcinogenesis. Copy number gains were found in potential oncogenes such as Y RNA, LTO1, and FADD. Pathogenic short tandem repeats (STRs) in PABPN1 and RFC1 were identified in three samples, presenting a novel association with NPC. NPC sample which exhibited significant genomic instability had the shortest survival, potentially linked to multiple defective DNA repair genes. This study utilized long-read sequencing to identify a complex spectrum of genetic alterations, including numerous SVs and potentially pathogenic STRs, in Indonesian NPC. Extensive DNA repair gene defects, primarily complex SVs detectable by long reads, were observed and highly possibly associated with poor survival. These findings underscore the potential of long-read sequencing for uncovering clinically relevant mutations in NPC. - Source: PubMed
Publication date: 2025/07/01
Handoko Adham MarlindaRachmadi LisnawatiTobing Demak LumbanAsmarinah Fadilah Dai WeiLee Anne Wing MuiGondhowiardjo Soehartati A