Ask about this productRelated genes to: JARID2 antibody
- Gene:
- JARID2 NIH gene
- Name:
- jumonji and AT-rich interaction domain containing 2
- Previous symbol:
- JMJ
- Synonyms:
- -
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: JARID2 antibody
Related articles to: JARID2 antibody
- Computer-assisted sperm analysis was conducted to phenotypically and genetically assess the sperm motility traits of Jinding drakes. The phenotypic evaluation revealed moderate variability across motility parameters, consistent with a polygenic inheritance pattern. Correlation analysis further demonstrated strong associations among velocity-related traits and inverse relationships between linearity and lateral head displacement metrics. Genome-wide association studies identified 15 significant single-nucleotide polymorphisms (SNPs) associated with five key sperm motility traits (straight-line velocity, curvilinear velocity, average path velocity, amplitude of lateral head displacement, and mean angular displacement) at a genome-wide threshold of < 1 × 10. Notably, of these 15 SNPs, nine were concentrated on chromosome 1, indicating the presence of a genomic hotspot for regulation of sperm motility. Pleiotropic effects were evident, as several SNPs were found to influence multiple motility traits. Candidate genes implicated in essential sperm functions included (cytoskeletal dynamics), (flagellar structure), and (epigenetic regulation during spermatogenesis), as well as genes involved in membrane integrity, mitochondrial function, and immune regulation. These findings provide novel insights into the genetic architecture underlying sperm motility of Jinding drakes and establish a basis for molecular breeding strategies to enhance reproductive efficiency of waterfowl. - Source: PubMed
Publication date: 2026/06/01
Zhu ChunhongGu HaotianWang ZhichengSong WeitaoTao ZhiyunZhang ShuangjieChen LiLi HuifangLiu Hongxiang - Loss-of-function mutations in BCOR, a subunit of the non-canonical Polycomb Repressive Complex 1.1 (PRC1.1), are frequently observed in acute myeloid leukemia (AML) and associate with adverse risk. Paradoxically, leukemic stem cell viability in BCOR wild-type AMLs strongly depends on PRC1.1 activity. Here, we use BCOR and KDM2B degron models to study PRC1.1 dependency in leukemic cells and find that BCOR is a bridging factor tethering the catalytic and chromatin-binding moieties of the PRC1.1 complex. BCOR degradation induces a quick localized loss of H2AK119ub at PRC1.1 target genes, whereas PRC2-induced H3K27me3 remains unaffected. Degron-mediated depletion of BCOR or KDM2B induces a rapid but time-dependent transcriptional induction, whereby late-upregulated genes are more heavily decorated with H3K27me3 compared to early-upregulated genes. Combined PRC1.1 inactivation and PRC2 inhibition further amplifies gene induction, suggesting collaborative yet distinct control over target genes. Strikingly, both JARID2/AEBP2 and SUZ12 knockout cells, devoid of PRC2.2 or PRC2.1/PRC2.2 respectively, retain PRC1.1 loss-induced transcriptional activation, underscoring that PRC1.1 can repress target genes independently of a downstream PRC2.2-canonical PRC1 repressive axis. Finally, combined targeting of PRC1.1 and PRC2 induces differentiation of leukemic cells, emphasizing that co-targeting PRC1.1 and PRC2 represents a promising strategy to improve treatment of AML patients. - Source: PubMed
Mojallali FatemehDe Meis AlessandraAlkema Sinne GAtsma Tjerk JanHogeling Shanna MKloosterman RianneIoannou EveWierenga Albertus T JHuls GerwinMartens Joost H ASchuringa Jan Jacobvan den Boom Vincent - Hyperthermic intraperitoneal chemotherapy (HIPEC) for colorectal peritoneal metastases relies primarily on DNA-damaging agents whose efficacy depends on sustained cytotoxic exposure. Whether brief treatment can induce durable transcriptional remodeling remains unclear. Mithramycin A (MA) is a GC-rich DNA-binding agent with transcriptional regulatory activity involving chromatin-associated pathways. Here, we investigated the molecular and functional consequences of a single 90-min HIPEC-mimetic MA exposure in colorectal cancer models. RNA sequencing revealed extensive and coordinated transcriptional remodeling, affecting a substantial fraction of expressed genes and producing a response qualitatively distinct from mitomycin C. MA selectively suppressed key chromatin-associated regulatory factors, including DNMT1, JARID2, and HDAC4, while coordinately activating canonical cyclin-dependent kinase inhibitors CDKN1A, CDKN1C, and CDKN2C. Gene set enrichment analysis demonstrated enrichment of G2/M checkpoint pathways and suppression of oncogenic gene networks. These molecular changes translated into sustained inhibition of clonogenic growth and activation of caspase-dependent apoptosis following drug washout, with hyperthermia potentiating apoptotic signaling. Collectively, these findings indicate that brief MA exposure induces selective modulation of chromatin regulators and durable transcriptional reorganization, supporting modulation of chromatin regulatory networks as a potential therapeutic strategy for HIPEC-based colorectal cancer therapy. - Source: PubMed
Publication date: 2026/04/17
Coburn-Flynn OliviaButchy M VirginiaGhanem YazidEmery RobertVerchio VincentKnapp KristenCollier JessicaJethi SahilSpitz Francis RZhang PingElbezanti Weam OthmanHong Young Ki - The "loss of control" over drug consumption, known as escalation of intake in opioid use disorder (OUD), is well-established in preclinical rodent models. However, little is known about how antecedent behavioral characteristics, such as valuation of hedonic reinforcers prior to drug use, influence fentanyl intake trajectories. Moreover, it is unclear if distinct escalation phenotypes are driven by transcriptomic markers predictive of OUD susceptibility. Male and female Sprague-Dawley rats (n = 72) were trained in a sucrose reinforcement task using a progressive ratio schedule. Individual differences in responsivity to sucrose were hypothesized to predict escalation of fentanyl intake. Rats underwent daily 1-h acquisition sessions for i.v. fentanyl self-administration (2.5 µg/kg; FR1) for 7 days, followed by 21 6-h escalation sessions, then tissue from prefrontal cortex was collected for RNA sequencing and qPCR. Latent growth curve and group-based trajectory modeling were used, respectively, to evaluate the association between sucrose reinforcement and fentanyl self-administration and to identify whether distinct escalation phenotypes can be linked to gene expression patterns. Sucrose breakpoints did not predict fentanyl acquisition nor change during escalation but did predict fentanyl intake on the first day of extended access. Permutation analyses found no associations between behavior and single gene expression, either overall or within our ascertained phenotypes. However, weighted genome correlation network analysis (WGCNA) and gene set enrichment analysis (GSEA) determined several gene modules linked to escalated fentanyl intake, including genes coding for voltage-gated potassium channels, calcium channels, and excitatory synaptic signaling. Transcription factor analyses identified EZH2 and JARID2 as potential transcriptional regulators associated with escalated fentanyl intake. Further, these modules were enriched for genome-wide association study (GWAS) term categories relating to substance use disorders. Escalation of opioid intake largely differs from motivation for natural rewards like sucrose. Further, the gene networks associated with fentanyl escalation suggest that engagement of select molecular pathways were associated with "addiction prone" behavioral endophenotypes, potentially representing druggable targets for OUD. Our extended in silico analysis found that gene networks associated with the "addiction prone" high escalating rats were enriched for genes with known risk alleles for substance use disorders and identified transcription factors that may regulate these networks, highlighting the importance of integrating findings from translational preclinical models, supporting patient-centered treatment options for OUD. - Source: PubMed
Publication date: 2026/04/22
Keady JackCharnigo RichardShaykin Jakob DPrantzalos Emily RXia MengfanDenehy EmilyBumgardner CodyMiller JustinOrtinski PavelBardo Michael TTurner Jill R - Copy number variants (CNVs) are large-scale genomic alterations that contribute substantially to genetic diversity and may influence phenotypic variation in livestock. This study investigated the genome-wide CNV landscape of three Vietnamese indigenous chicken breeds. Whole-genome sequencing on the Illumina platform (3-5× coverage) was performed on 24 individuals from Dong Tao (DT), Cay Cum (CC), and Ri (RI) breeds. A total of 1743 CNVs were detected, clustering into 315 copy number variation regions (CNVRs). Most CNVRs were rare, with 31.7% present in only one animal among breeds. Across the genome, 122 unique CNVRs were distributed over 28 chromosomes, predominantly the first five. Losses were the most frequent type (45.9%), followed by gains (39.3%), and mixed events (14.8%). Within these CNVRs, 3633 genes were identified. In DT and RI, CNVR-embedded genes included several candidates, potentially related to adaptability, development, and phenotypic diversification. Notably, DT harbored genes such as , , , (adaptation, stress/immune response) and , , , , , , , and (developmental and skeletal traits), whereas in RI they included genes such as , , , and , which may contribute to muscle, bone, and physiological regulation. Functional enrichment analysis revealed numerous genes and Quantitative Trait Loci (QTLs) associated with metabolic, developmental, and immune-related pathways. This study provides the first comprehensive genome-wide CNV profile of Vietnamese indigenous chickens and offers a valuable genomic resource for investigating the genetic basis of breed-specific and adaptive phenotypes. - Source: PubMed
Publication date: 2026/04/01
Nguyen Thuy Thi-DieuTzvetkova AnaBui Mai Thi-DieuDo Vo-Anh-KhoaDinh Thuy Thi-NgocNguyen Phuong ThanhKuss Andreas WalterPenasa MauroCendron Filippo