FLJ33706 Blocking Peptide
- Known as:
- FLJ33706 Blocking Peptide
- Catalog number:
- 33r-8062
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- FLJ33706 Blocking Peptide
Related genes to: FLJ33706 Blocking Peptide
- Gene:
- C20orf203 NIH gene
- Name:
- chromosome 20 open reading frame 203
- Previous symbol:
- -
- Synonyms:
- FLJ33706
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2010-04-01
- Date modifiied:
- 2017-03-07
Related products to: FLJ33706 Blocking Peptide
Related articles to: FLJ33706 Blocking Peptide
- The objective of this study was to screen lymphoma radiotherapy-resistant genes using CRISPR activation (CRISPRa). - Source: PubMed
Publication date: 2023/01/30
Luo Bi-HuaHuang Jian-QingHuang Chun-YuTian PanChen Ai-ZhenWu Wei-HaoMa Xiao-MeiYuan Yue-XingYu Lian - Epidemiological studies have reported a comorbid relationship between headache and thyroid traits; however, little is known about the shared genetics and causality that contributes to this association. We investigated the genetic overlap and associations between headache and thyroid function traits using genome-wide association study (GWAS) data. We found a significant genetic correlation (rg) with headache and hypothyroidism (rg = 0.09, p = 2.00 × 10−4), free thyroxine (fT4) (rg = 0.08, p = 5.50 × 10−3), and hyperthyroidism (rg = −0.14, p = 1.80 × 10−3), a near significant genetic correlation with secondary hypothyroidism (rg = 0.20, p = 5.24 × 10−2), but not with thyroid stimulating hormone (TSH). Pairwise-GWAS analysis revealed six, 14, four and five shared (pleiotropic) loci with headache and hypothyroidism, hyperthyroidism, secondary hypothyroidism, and fT4, respectively. Cross-trait GWAS meta-analysis identified novel genome-wide significant loci for headache: five with hypothyroidism, three with secondary hypothyroidism, 12 with TSH, and nine with fT4. Of the genes at these loci, six (FAF1, TMX2-CTNND1, AARSD1, PLCD3, ZNF652, and C20orf203; headache-TSH) and six (HMGB1P45, RPL30P1, ZNF462, TMX2-CTNND1, ITPK1, SECISBP2L; headache-fT4) were significant in our gene-based analysis (pFisher’s combined p-value < 2.09 × 10−6). Our causal analysis suggested a positive causal relationship between headache and secondary hypothyroidism (p = 3.64 × 10−4). The results also suggest a positive causal relationship between hypothyroidism and headache (p = 2.45 × 10−3) and a negative causal relationship between hyperthyroidism and headache (p = 1.16 × 10−13). These findings suggest a strong evidence base for a genetic correlation and complex causal relationships between headache and thyroid traits. - Source: PubMed
Publication date: 2022/12/21
Tasnim SanaWilson Scott GWalsh John PNyholt Dale R - To investigate the regulatory network of long non-coding RNA (lncRNA) as competing endogenous RNAs (ceRNAs) in osteonecrosis of the femoral head (ONFH). - Source: PubMed
Publication date: 2021/03/21
Han NingLi Zengchun - Osteoarthritis (OA) is a chronic degenerative joint disease. Early studies have indicated that genetic and environmental factors contribute to the risk of OA. However, the etiology of OA remains unknown. Our study aimed to evaluate the association of DNMT3B gene with the risk of hip OA in Han Chinese individuals. - Source: PubMed
Publication date: 2020/08/10
Wang BaohuiSun YindiLiu HongliangCao YiLei Tao - To understand whether any human-specific new genes may be associated with human brain functions, we computationally screened the genetic vulnerable factors identified through Genome-Wide Association Studies and linkage analyses of nicotine addiction and found one human-specific de novo protein-coding gene, FLJ33706 (alternative gene symbol C20orf203). Cross-species analysis revealed interesting evolutionary paths of how this gene had originated from noncoding DNA sequences: insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids. We experimentally verified FLJ33706's mRNA and protein expression in the brain. Real-Time PCR in multiple tissues demonstrated that FLJ33706 was most abundantly expressed in brain. Human polymorphism data suggested that FLJ33706 encodes a protein under purifying selection. A specifically designed antibody detected its protein expression across human cortex, cerebellum and midbrain. Immunohistochemistry study in normal human brain cortex revealed the localization of FLJ33706 protein in neurons. Elevated expressions of FLJ33706 were detected in Alzheimer's brain samples, suggesting the role of this novel gene in human-specific pathogenesis of Alzheimer's disease. FLJ33706 provided the strongest evidence so far that human-specific de novo genes can have protein-coding potential and differential protein expression, and be involved in human brain functions. - Source: PubMed
Publication date: 2010/03/26
Li Chuan-YunZhang YongWang ZhanboZhang YanCao ChunmeiZhang Ping-WuLu Shu-JuanLi Xiao-MoYu QuanZheng XiaofengDu QuanUhl George RLiu Qing-RongWei Liping