Ask about this productRelated genes to: ZNF621 Blocking Peptide
- Gene:
- ZNF621 NIH gene
- Name:
- zinc finger protein 621
- Previous symbol:
- -
- Synonyms:
- FLJ45246
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-15
- Date modifiied:
- 2016-10-05
Related products to: ZNF621 Blocking Peptide
Related articles to: ZNF621 Blocking Peptide
- To investigate the whole-genome differential methylation profile of patients with high-altitude polycythemia (HAPC). - Source: PubMed
Ji Jun-HuaYang MinJiang YanYang Ting-XianMa Xiao-JingYin Qi-ChaoYin Hong-WeiJi Lin-Hua - Nasopharyngeal carcinoma (NPC) is one of the most lethal head and neck cancers, threatening the health of people across the globe, especially in East and Southeast Asia, the Arctic, the Middle East and North Africa. Long non-coding RNAs (lncRNA) have been reported to regulate multiple cancers, including NPC. However, the role of LINC01140 in NPC remains to be covered. In this study, we found that LINC01140 is downregulated in NPC cells. It was uncovered from functional assays that LINC01140 inhibits the proliferation and improves the apoptosis and radiosensitivity of NPC cells. The downstream mechanism by which LINC01140 exerted its functions was explored in subsequent. As proven by mechanism experiments, cytoplasmic LINC01140 positively regulated the expression of ZNF621 through competitively binding to miR-452-5p. ZNF621 can also enhance the radiosensitivity of NPC cells. To summarize, LINC01140 regulates the radiosensitivity of NPC cells through the competing endogenous RNA (ceRNA) mode. Our study aims to identify novel biomarkers for regulating the radiosensitivity of NPC. - Source: PubMed
Publication date: 2022/04/30
Li JiaLi YanLiu LiangWu DanYang TaoFan Yuwei - Epigenetic mechanisms may underlie air pollution-health outcome associations. We estimated gaseous air pollutant-DNA methylation (DNAm) associations using twelve subpopulations within Women's Health Initiative (WHI) and Atherosclerosis Risk in Communities (ARIC) cohorts (n = 8397; mean age 61.3 years; 83% female; 46% African-American, 46% European-American, 8% Hispanic/Latino). We used geocoded participant address-specific mean ambient carbon monoxide (CO), nitrogen oxides (NO; NOx), ozone (O), and sulfur dioxide (SO) concentrations estimated over the 2-, 7-, 28-, and 365-day periods before collection of blood samples used to generate Illumina 450 k array leukocyte DNAm measurements. We estimated methylome-wide, subpopulation- and race/ethnicity-stratified pollutant-DNAm associations in multi-level, linear mixed-effects models adjusted for sociodemographic, behavioral, meteorological, and technical covariates. We combined stratum-specific estimates in inverse variance-weighted meta-analyses and characterized significant associations (false discovery rate; FDR<0.05) at Cytosine-phosphate-Guanine (CpG) sites without among-strata heterogeneity (P > 0.05). We attempted replication in the Cooperative Health Research in Region of Augsburg (KORA) study and Normative Aging Study (NAS). We observed a -0.3 (95% CI: -0.4, -0.2) unit decrease in percent DNAm per interquartile range (IQR, 7.3 ppb) increase in 28-day mean NO concentration at cg01885635 (chromosome 3; regulatory region 290 bp upstream from ZNF621; FDR = 0.03). At intragenic sites cg21849932 (chromosome 20; LIME1; intron 3) and cg05353869 (chromosome 11; KLHL35; exon 2), we observed a -0.3 (95% CI: -0.4, -0.2) unit decrease (FDR = 0.04) and a 1.2 (95% CI: 0.7, 1.7) unit increase (FDR = 0.04), respectively, in percent DNAm per IQR (17.6 ppb) increase in 7-day mean ozone concentration. Results were not fully replicated in KORA and NAS. We identified three CpG sites potentially susceptible to gaseous air pollution-induced DNAm changes near genes relevant for cardiovascular and lung disease. Further harmonized investigations with a range of gaseous pollutants and averaging durations are needed to determine the effect of gaseous air pollutants on DNA methylation and ultimately gene expression. - Source: PubMed
Publication date: 2022/04/30
Holliday Katelyn MGondalia RahulBaldassari AntoineJustice Anne EStewart James DLiao DuanpingYanosky Jeff DJordahl Kristina MBhatti ParveenAssimes Themistocles LPankow James SGuan WeihuaFornage MyriamBressler JanNorth Kari EConneely Karen NLi YunHou LifangVokonas Pantel SWard-Caviness Cavin KWilson RoryWolf KathrinWaldenberger MelanieCyrys JosefPeters AnnetteBoezen H MarikeVonk Judith MSayols-Baixeras SergiLee MikyeongBaccarelli Andrea AWhitsel Eric A - Pulmonary function (PF) progressively declines with aging. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) are predictors of morbidity of pulmonary and cardiovascular diseases and all-cause mortality. In addition, reduced PF is associated with elevated chronic low-grade systemic inflammation, glucose metabolism, body fatness, and low muscle strength. It may suggest pleiotropic genetic effects between PF with these age-related factors. - Source: PubMed
Publication date: 2022/02/18
Feitosa Mary FWojczynski Mary KAnema Jason ADaw E WarwickWang LihuaSantanasto Adam JNygaard MarianneProvince Michael A - Benign smooth-muscle tumors, leiomyomas, occur in nearly every organ but are most common in the uterus. Whereas much is known about the genetics of uterine leiomyomas, little genetic information exists about leiomyomas of other organs. Here, we report and discuss the genetic findings in a para-testicular leiomyoma. - Source: PubMed
Panagopoulos IoannisGorunova LudmilaAndersen KristinLobmaier IngvildHeim Sverre