BORDETELLA HOLMESII F061, titered
- Known as:
- BORDETELLA HOLMESII F061, titered
- Catalog number:
- GEN0801464
- Category:
- -
- Supplier:
- Bio-gentaur
- Gene target:
- BORDETELLA HOLMESII F061 titered
Related genes to: BORDETELLA HOLMESII F061, titered
- Gene:
- ZNF600 NIH gene
- Name:
- zinc finger protein 600
- Previous symbol:
- -
- Synonyms:
- KR-ZNF1, DKFZp686F06123
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-05
- Date modifiied:
- 2014-11-18
Related products to: BORDETELLA HOLMESII F061, titered
Related articles to: BORDETELLA HOLMESII F061, titered
- Cerebral small vessel disease (SVD), manifesting as white matter hyperintensities (WMH), lacunar infarctions, and cerebral microbleeds on magnetic resonance imaging (MRI), has been linked to developmental epigenetic alterations. This study aimed to identify and validate gene-specific promoter methylation changes as epigenetic markers associated with SVD, using MRI-defined imaging features and blood inflammatory cells. - Source: PubMed
Publication date: 2026/03/12
Kim JeeyeonPark JihyeKang KeunsooLee Young HoShin Byoung-SooKim Dae-HyunShin Dong-IckAhn Seong HwanKim Jae GukKang Hyun GooJeong HyeseonYum Kyu SunChae Hee-YunKim Do-HyungKim Jei - This study aims to investigate the role of body mass index (BMI) in modulating the causal relationship between nonalcoholic fatty liver disease (NAFLD) and osteoarthritis (OA), focusing on the impact of BMI on metabolic pathways. Two-sample Mendelian randomization analysis was conducted using genome-wide association study data to assess how BMI affects the relationship between NAFLD and OA. The study was divided into 3 BMI groups: BMI < 25, BMI 25 to 30, and BMI > 30. Additionally, gene expression differences between damaged and undamaged cartilage samples from individuals in these BMI categories were validated through qPCR. Mendelian randomization analysis revealed a negative association between NAFLD and OA in individuals with BMI < 25 (OR: 0.7215, 95% CI [0.5214-0.9984], P = .048), while a positive association was found in individuals with BMI > 30 (OR: 1.0956, 95% CI [1.0294-1.1661], P = .0029). Gene expression analysis showed significant downregulation of ULK3 in damaged cartilage in the BMI < 25 group, while ACER3, RAB14, ZNF600, and ADARB1 exhibited significant upregulation in the BMI > 30 group. Our findings highlight the critical role of BMI in the relationship between NAFLD and OA. In the low BMI group, enhanced autophagy and lower systemic inflammation may protect joint health, while obesity-related metabolic dysfunction and chronic low-grade inflammation contribute to OA progression in the high BMI group. The differential expression of ULK3, ACER3, RAB14, ZNF600, and ADARB1 genes across BMI categories provides potential clinical therapeutic targets for BMI-specific interventions in NAFLD and OA. - Source: PubMed
Yu ShengyuanLiu YishuXue BingZhang XiGao MingLu Daifeng - Boys' pubertal overweight associates with future offspring's asthma and low lung function. To identify how paternal overweight is associated with offspring's DNA methylation (DNAm), we conducted an epigenome-wide association study of father's body silhouette (FBS) at three timepoints (age 8, voice break and 30) and change in FBS between these times, with offspring DNAm, in the RHINESSA cohort (N = 339). We identified 2005 differentially methylated cytosine-phosphate-guanine (dmCpG) sites (FDR < 0.05), including dmCpGs associated with offspring asthma (119), lung function (178) and BMI (291). Voice break FBS associated with dmCpGs in loci including KCNJ10, FERMT1, NCK2 and WWP1. Change in FBS across sexual maturation associated with DNAm at loci including NOP10, TRRAP, EFHD1, MRPL17 and NORD59A;ATP5B and showed strong correlation in reduced gene expression in loci NAP1L5, ATP5B, ZNF695, ZNF600, VTRNA2-1, SOAT2 and AGPAT2. We identified 24 imprinted genes including: VTRNA2-1, BLCAP, WT1, NAP1L5 and PTPRN2. Identified pathways relate to lipid and glucose metabolism and adipogenesis. Father's overweight at puberty and during reproductive maturation was strongly associated with offspring DNA, suggesting a key role for epigenetic mechanisms in intergenerational transfer from father to offspring in humans. The results support an important vulnerability window in male puberty for future offspring health. - Source: PubMed
Publication date: 2025/05/24
Kitaba Negusse TadesseØstergaard Toril MørkveLønnebotn MarianneAccordini SimoneReal Francisco GómezMalinovschi AndreiOudin AnnaBenediktsdottir BryndisGonzález Francisco Javier CallejasGómez Leopoldo PalaciosHolm MathiasJõgi Nils OskarDharmage Shyamali CSkulstad Svein MagneSchlünssen ViviSvanes CecilieHolloway John W - For this study, we investigated comprehensive expression of conjoined genes (CGs) in non-Hodgkin B-cell lymphoma (B-NHL) cell line KPUM-UH1 by using paired-end RNA sequencing. Furthermore, we analyzed the expression of these transcripts in an additional 21 cell lines, 37 primary samples of various malignancies and peripheral blood mononuclear cells of four normal individuals. Seventeen CGs were detected in KPUM-UH1: CTBS-GNG5, SRP9-EPHX1, RMND5A-ANAPC, OTX1-EHBP1, ATF2-CHN1, PRKAA1-TTC33, LARP1-MRPL22, LOC105379697-BAK1, TIAM2-SCAF8, SPAG1-VPS13B, WBP1L-CNNM2, NARS2-GAB2, CTSC-RAB38, VAMP1-CD27-AS1, LRRC37A2-NSF, UBA2-WTIP and ZNF600-ZNF611. To our knowledge, 10 of these genes have not been previously reported. The various characteristics of the CGs included in- and out-of-frame fusions, chimeras involving non-coding RNA and transcript variants. A finding of note was that LARP1-MRPL2 was characterized as in-frame fusion and was recurrently expressed in B-NHL samples. In this study, variety of CGs was expressed both in malignant and normal cells, some of which might be specific to lymphoma. - Source: PubMed
Publication date: 2021/04/20
Matsumoto YosukeTsukamoto TakuChinen YoshiakiShimura YujiSasaki NanaNagoshi HisaoSato RyuichiAdachi HirokoNakano MasakazuHoriike ShigeoKuroda JunyaTaki TomohikoTashiro KeiTaniwaki Masafumi - Rare or novel gene variants in patients with proliferative diabetic retinopathy may contribute to disease development. We performed whole exome sequencing (WES) on patients at the phenotypic extremes of diabetic retinal complications: 57 patients diagnosed with proliferative diabetic retinopathy (PDR) as cases and 13 patients with no diabetic retinopathy despite at least 10years of type 2 diabetes as controls. Thirty-one out of the 57 cases and all 13 controls were from the African American Proliferative Diabetic Retinopathy Study (AA). The rest of the cases were of mixed ethnicities (ME). WES identified 721 candidate genes with rare or novel non-synonymous variants found in at least one case with PDR and not present in any controls. After filtering for genes with null alleles in greater than two cases, 28 candidate genes were identified in our ME cases and 16 genes were identified in our AA cases. Our analysis showed rare and novel variants within these genes that could contribute to the development of PDR, including rare non-synonymous variants in FAM132A, SLC5A9, ZNF600, and TMEM217. We also found previously unidentified variants in VEGFB and APOB. We found that VEGFB, VPS13B, PHF21A, NAT1, ZNF600, PKHD1L1 expression was reduced in human retinal endothelial cells (HRECs) cultured under high glucose conditions. In an exome sequence analysis of patients with PDR, we identified variants in genes that could contribute to pathogenesis. Six of these genes were further validated and found to have reduced expression in HRECs under high glucose conditions, suggestive of an important role in the development of PDR. - Source: PubMed
Publication date: 2017/05/09
Ung CindySanchez Angie VShen LishuangDavoudi SamanehAhmadi TinaNavarro-Gomez DanielChen Ching JHancock HeatherPenman AlanHoadley SuzanneConsugar MarkRestrepo CarlosShah Vinay AArboleda-Velasquez Joseph FSobrin LuciaGai XiaowuKim Leo A