ZNF234 antibody - middle region (ARP35806_P050)
- Known as:
- ZNF234 (anti-) - middle region (ARP35806_P050)
- Catalog number:
- arp35806_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF234 antibody - middle region (ARP35806_P050)
Related genes to: ZNF234 antibody - middle region (ARP35806_P050)
- Gene:
- ZNF234 NIH gene
- Name:
- zinc finger protein 234
- Previous symbol:
- ZNF269
- Synonyms:
- HZF4
- Chromosome:
- 19q13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-29
- Date modifiied:
- 2015-08-27
Related products to: ZNF234 antibody - middle region (ARP35806_P050)
Related articles to: ZNF234 antibody - middle region (ARP35806_P050)
- 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 - Human aging is marked by the emergence of a tapestry of clonal expansions in dividing tissues, particularly evident in blood as clonal hematopoiesis (CH). CH, linked to cancer risk and aging-related phenotypes, often stems from somatic mutations in a set of established genes. However, the majority of clones lack known drivers. Here we infer gene-level positive selection in whole blood exomes from 200,618 individuals in UK Biobank. We identify 17 additional genes, ZBTB33, ZNF318, ZNF234, SPRED2, SH2B3, SRCAP, SIK3, SRSF1, CHEK2, CCDC115, CCL22, BAX, YLPM1, MYD88, MTA2, MAGEC3 and IGLL5, under positive selection at a population level, and validate this selection pattern in 10,837 whole genomes from single-cell-derived hematopoietic colonies. Clones with mutations in these genes grow in frequency and size with age, comparable to classical CH drivers. They correlate with heightened risk of infection, death and hematological malignancy, highlighting the significance of these additional genes in the aging process. - Source: PubMed
Publication date: 2024/05/14
Bernstein NicholasSpencer Chapman MichaelNyamondo KudzaiChen ZhenghaoWilliams NicholasMitchell EmilyCampbell Peter JCohen Robert LNangalia Jyoti - Migraine is a complex neurological disorder and a major cause of disability. A wide range of different drug classes such as triptans, antidepressants, anticonvulsants, analgesics, and beta-blockers are used in acute and preventive migraine therapy. Despite a considerable progress in the development of novel and targeted therapeutic interventions during recent years, e.g., drugs that inhibit the calcitonin gene-related peptide (CGRP) pathway, therapy success rates are still unsatisfactory. The diversity of drug classes used in migraine therapy partly reflects the limited perception of migraine pathophysiology. Genetics seems to explain only to a minor extent the susceptibility and pathophysiological aspects of migraine. While the role of genetics in migraine has been extensively studied in the past, the interest in studying the role of gene regulatory mechanisms in migraine pathophysiology is recently evolving. A better understanding of the causes and consequences of migraine-associated epigenetic changes could help to better understand migraine risk, pathogenesis, development, course, diagnosis, and prognosis. Additionally, it could be a promising avenue to discover new therapeutic targets for migraine treatment and monitoring. In this review, we summarize the state of the art regarding epigenetic findings in relation to migraine pathogenesis and potential therapeutic targets, with a focus on DNA methylation, histone acetylation, and microRNA-dependent regulation. Several genes and their methylation patterns such as (migraine symptoms and age of migraine onset), , , and (migraine chronification) and microRNA molecules such as miR-34a-5p and miR-382-5p (treatment response) seem especially worthy of further study regarding their role in migraine pathogenesis, course, and therapy. Additionally, changes in genes including , , , and have been linked to migraine progression to medication overuse headache (MOH), and several microRNA molecules such as let-7a-5p, let-7b-5p, let-7f-5p, miR-155, miR-126, let-7g, hsa-miR-34a-5p, hsa-miR-375, miR-181a, let-7b, miR-22, and miR-155-5p have been implicated with migraine pathophysiology. Epigenetic changes could be a potential tool for a better understanding of migraine pathophysiology and the identification of new therapeutic possibilities. However, further studies with larger sample sizes are needed to verify these early findings and to be able to establish epigenetic targets as disease predictors or therapeutic targets. - Source: PubMed
Publication date: 2023/05/23
Zobdeh FarzinEremenko Ivan IAkan Mikail ATarasov Vadim VChubarev Vladimir NSchiöth Helgi BMwinyi Jessica - A study was conducted to understand the differentially expressed genes in Pectoralis (P) major under woody breast (WB) myopathy condition in a high yielding broiler strain using RNA-sequencing at the growing (d 21) and finishing (d 42 and d 56) grow-out ages. Follow-up study was conducted to understand the in vivo triglyceride (TG) synthesis (d 49) occurring in adipogenic tissues using deuterium oxide (HO) as a metabolic tracer. Results indicated the top physiological systems affected in myopathy broiler were related to the musculo-skeletal system (d 21, 42, and 56) and cardiovascular system (d 42 and 56). Ubiquitin-specific proteases are expressed higher in myopathy broiler at d 21 (OTUD1) and d 42 (SACS) that potentially indicated higher degradation of muscle protein occurring at those ages. While genes related to transcription factors and muscle cell differentiation (ZNF234, BTG2) and muscle growth (IGF1) were upregulated with myopathy broiler suggesting concurrent muscle fiber regeneration. The downregulation of PYGB and MGAM genes related to carbohydrate transport and metabolism at d 42 potentially indicated nutrient-deficient state of myopathy affected fibers; whereas the nutrient-deficient physiological state of cells seemed to be counteracted by up-regulation of genes related to carbohydrate (ALDOB, GPD1L2) at d 56. There was a reduced (P < 0.05) in vivo TG synthesis in liver of the myopathy broiler (0.123 %/hr) compared to non-myopathy broiler (0.197 %/hr). The majority of TG synthesized in liver with myopathy broiler could conceivably be delivered to P. major (rather than to abdominal fat pad storage) to fulfil the increased energy need of muscle cells (via TG lipolysis and fatty acid [FA] oxidation). The increased utilization of FAs in the WB affected muscle could result in reduced secretion of FAs into blood circulation leading to sub-optimal availability of FAs for re-esterification for TG synthesis in liver. Results indicated that myopathy broiler at later age (d 56) of grow-out period were synchronously going through adaptive physiological processes of feedback responses to adverse cellular states. - Source: PubMed
Publication date: 2021/03/12
Maharjan PramirBeitia AntonioWeil JordanSuesuttajit NawinHilton KatieCaldas JustinaUmberson ColeMartinez DiegoKong ByungwhiOwens Casey MCoon Craig