ANKRD18A
- Known as:
- ANKRD18A
- Catalog number:
- 001611A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKRD18A
Related genes to: ANKRD18A
- Gene:
- ANKRD18A NIH gene
- Name:
- ankyrin repeat domain 18A
- Previous symbol:
- -
- Synonyms:
- KIAA2015, FLJ35740
- Chromosome:
- 9p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-28
- Date modifiied:
- 2014-11-18
Related products to: ANKRD18A
Related articles to: ANKRD18A
- Sorafenib, a multikinase inhibitor, is currently the standard treatment for advanced liver cancer. However, its application has become limited by the development of drug resistance. We intended to explore the mechanisms underlying the development of sorafenib resistance, therefore identifying an effective strategy to overcome sorafenib resistance remain challenges. - Source: PubMed
Publication date: 2024/10/24
Li XiaoCui MengnaXu LongGuo Qie - Bone mineral density (BMD) is an independent risk factor of osteoporosis-related fractures. We performed gene-based burden tests to assess the association between rare variants and BMD, and identified several BMD candidate genes. - Source: PubMed
Publication date: 2023/02/28
He DPan CZhao YWei WQin XCai QShi SChu XZhang NJia YWen YCheng BLiu HFeng RZhang FXu P - Vulvar lichen sclerosus (LS) is known to occur in families, suggesting a genetic link. Genomic profiling of patients with vulvar LS was investigated to find underlying pathogenetic mechanisms, with the hope that targeted therapies and future clinical research will arise. - Source: PubMed
Haefner Hope KWelch Kathryn CRolston Aimee MKoeppe Erika SStoffel Elena MKiel Mark JBerger Mitchell B - Dl is a widely used pulmonary function test in clinical practice and a particularly useful measure for assessing patients with chronic obstructive pulmonary disease (COPD). We hypothesized that elucidating genetic determinants of Dl could lead to better understanding of the genetic architecture of COPD. We estimated the heritability of Dl using common genetic variants and performed genome-wide association analyses in four cohorts enriched for subjects with COPD (COPDGene [Genetic Epidemiology of COPD], NETT [National Emphysema Treatment Trial], GenKOLS [Genetics of Chronic Obstructive Lung Disease study], and TESRA [Treatment of Emphysema With a Gamma-Selective Retinoid Agonist study]) using a combined European ancestry white dataset and a COPDGene African American dataset. We assessed our genome-wide significant and suggestive associations for Dl in previously reported genome-wide association studies of COPD and related traits. We also characterized associations of known COPD-associated variants and Dl. We estimated the SNP-based heritability of Dl in the European ancestry white population to be 22% ( = 0.0004). We identified three genome-wide significant associations with Dl: variants near , , and loci ( < 5 × 10). In addition, 12 loci were suggestively associated with Dl in European ancestry white ( < 1 × 10 in the combined analysis and < 0.05 in both COPDGene and GenKOLS), including variants near , , , , , , , , , , , and . Some Dl-associated variants were also associated with COPD, emphysema, and/or spirometric values. Among 25 previously reported COPD loci, , , , and were associated with Dl ( < 0.001). We identified several genetic loci that were significantly associated with Dl and characterized effects of known COPD-associated loci on Dl. These results could lead to better understanding of the heterogeneous nature of COPD. - Source: PubMed
Sakornsakolpat PhuwanatMcCormack MeredithBakke PerGulsvik AmundMake Barry JCrapo James DCho Michael HSilverman Edwin K - Lung cancer is one of the most common causes of cancer-related mortality worldwide. Effective early diagnosis and targeted therapies for lung cancer to reduce incidence and mortality would benefit from a better understanding of the key molecular changes that occur from normal to malignant tumor cells during lung cancer initiation and development, but these are largely unknown. Previous studies have shown that DNA methylation, an important mechanism for the regulation of gene expression, plays a key role in lung carcinogenesis. In this study, we screened a novel methylation gene, ANKRD18A, encoding ankyrin repeat domain 18A, to determine whether it is regulated by DNA methylation in lung cancer. Methylation-specific PCR and bisulfite sequencing PCR were used to analyze gene methylation status, and real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) examined mRNA levels. Promoter hypermethylation of ANKRD18A was detected in 68.4% (26/38) of lung cancer tissues but not (0/20) in normal lung tissues (P<0.01), whereas ANKRD18A mRNA expression was significantly decreased in lung cancer tissues compared with adjacent normal tissues. In addition, we found that ANKRD18A expression was significantly decreased in 9 of 10 lung cancer cell lines. This was associated with hypermethylation of the ANKRD18A promoter region. Moreover, weak expression of ANKRD18A in methylated lung cancer cell lines increased markedly after treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine. These results suggest that ANKRD18A hypermethylation and consequent mRNA alterations might be a vital molecular mechanism in lung cancer. - Source: PubMed
Publication date: 2012/11/03
Liu Wen-BinHan FeiJiang XiaoYang Lu-JunLi Yong-HongLiu YongChen Hong-QiangAo LinCui Zhi-HongCao JiaLiu Jin-Yi