Ask about this productRelated genes to: JAZF1 antibody
- Gene:
- JAZF1 NIH gene
- Name:
- JAZF zinc finger 1
- Previous symbol:
- -
- Synonyms:
- TIP27, DKFZp761K2222, ZNF802
- Chromosome:
- 7p15.2-p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-10-05
- Date modifiied:
- 2018-02-13
Related products to: JAZF1 antibody
Related articles to: JAZF1 antibody
- Alzheimer's disease (AD) and related dementias are a growing health and economic burden in India. Blood levels of amyloid beta (Ab), tau, and other proteins marking neuronal injury are biomarkers of AD risk and are potentially important for AD prevention. - Source: PubMed
Publication date: 2026/08/19
Abu-Amara HasanZhao WeiLi ZhengLeung Yuk YeeSchellenberg Gerard DWang Li-SanCrimmins Eileen MThyagarajan BharatAnwar MasroorHu PerryDey SharmisthaDey Aparajit BZhou XiangThangaraj KumarasamyLee JinkookKardia Sharon L RSmith Jennifer A - Facial aging reflects genetic, metabolic, and environmental influences. Although obesity has been associated with older perceived facial age, the shared genetic basis and direction of the BMI-facial aging relationship remain uncertain. - Source: PubMed
Publication date: 2026/08/25
Hu YuanLi Ke-HanHe Ming-JieYu Chun-ShuiWang Shao-Bo - : Prostate cancer (PCa) and benign prostatic hyperplasia (BPH) are highly prevalent among African men. While single-nucleotide polymorphisms (SNPs) in , and are established risk markers in Western cohorts, their specific allele frequencies and diagnostic utility remain poorly characterized in African populations. This study evaluated the diagnostic accuracy, sensitivity, and cost-effectiveness of High-Resolution Melting (HRM) PCR for germline SNP genotyping in a cohort of Nigerian men. Peripheral blood buffy coat DNA was extracted from 31 male participants attending the urology clinic at Lagos University Teaching Hospital, classified into PCa ( = 13), BPH ( = 12), and healthy controls ( = 6). Real-time PCR and HRM analysis were optimized to genotype three specific risk variants: rs2735839 , rs4430796 , and rs10486567 . Allelic discrimination was validated using sequence-verified, synthetic positive controls for homozygous wild-type and mutant variants. HRM analysis generated reproducible amplification and melting profiles that enabled clear discrimination of wild-type, heterozygous, and variant genotypes for all three loci. The risk-associated alleles of (G), (C), and (T) occurred more frequently among patients with prostate cancer than among those with benign prostatic hyperplasia. Clinically, prostate cancer patients also presented with markedly higher PSA concentrations, older age at diagnosis, and higher Gleason scores, consistent with more aggressive disease. The optimized HRM workflow required less than two hours from amplification to genotype assignment and eliminated the need for post-PCR processing, making it suitable for routine molecular testing in resource-constrained laboratories. HRM-based genotyping of (rs2735839), (rs4430796), and (rs10486567) provides a highly reproducible, rapid, and low-cost molecular tool for mapping prostate disease risk variants. Because it requires no post-PCR processing, this closed-tube HRM workflow is ideally suited for resource-limited clinical settings to enhance early risk stratification and differentiate malignant PCa from benign BPH. - Source: PubMed
Publication date: 2026/08/10
Sulaimon Lateef AdegboyegaJames Ayorinde BabatundeAkinbami Aishat AbisolaBabalola Oladayo MusaOni Grace FolashayoIdris Ganiu AdigunAgbi MayowaAkintola Akintayo AshrafLawal Modinat OlawunmiJames Adewale Segun - The spectrum of causal variants, mechanisms, and immunologic gene networks that influence pediatric atopic traits is not completely understood. Human genetic variation associated with transcript abundance (expression quantitative trait loci [eQTLs]) can help to advance our understanding, yet prior work has focused on profiling immune cell populations collected from peripheral blood primarily in adult populations, leaving tissue-resident lymphocytes collected from children uncharacterized. - Source: PubMed
Publication date: 2026/08/20
Lorenz KimYoon SamuelLe Coz CaroleZur Karen BWells AndrewRomberg NeilVoight Benjamin F - In the United States, sickle cell disease (SCD) is a rare inherited hemoglobinopathy affecting about 100,000 individuals, mostly with African ancestry. SCD causes damage to multiple organ systems and SCD nephropathy (SCDN) is a common complication associated with early mortality. We previously performed a genome-wide association study (GWAS) for SCDN and identified a modest number of genome-wide significant loci. Here, we leveraged the ancestral composition of participants from two well-characterized adult SCD cohorts to boost statistical power and perform a local ancestry-aware GWAS for estimated glomerular filtration rate (eGFR), resulting in the identification of novel genome-wide significant loci within the African (AFR) and European (EUR) ancestral components of participants. Meta-analysis identified 12 significant genomic regions in the AFR tract, including PPIL6, ARHGAP24, RAB11A, and STEAP3, and 38 regions in the EUR tract, including UBLCP1, ADAMTS6, JAZF1, MYO7B, MYO1C, PDGFA, GPC5, LRP1B, KANK1, and TRPV5. The identified regions encompass genes affecting inflammation, extracellular matrix (ECM) integrity, iron metabolism, magnesium ion homeostasis, B cell apoptosis, tumor necrosis factor (TNF) production, and estrogen signaling. Many of these genes and pathways are important not only for renal function, but also for SCD biology, providing additional support for the hypothesis that SCDN pathophysiology is unique from other forms of kidney disease. This study represents the largest local ancestry-aware analysis of SCDN to date, furthers our understanding of the genetic risk factors underlying SCDN, and proposes new targets that could be useful for the early identification and treatment of kidney dysfunction in SCD patients. - Source: PubMed
Publication date: 2026/08/19
Garrett Melanie ENouraie Seyed MehdiMachado Roberto FGordeuk Victor RGladwin Mark TTelen Marilyn JAshley-Koch Allison ETOPMed Nhlbi Trans-Omics For Precision Medicine