YEATS4 antibody - C-terminal region (ARP30117_T100)
- Known as:
- YEATS4 (anti-) - C-terminal region (ARP30117_T100)
- Catalog number:
- arp30117_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- YEATS4 antibody - C-terminal region (ARP30117_T100)
Related genes to: YEATS4 antibody - C-terminal region (ARP30117_T100)
- Gene:
- YEATS4 NIH gene
- Name:
- YEATS domain containing 4
- Previous symbol:
- -
- Synonyms:
- NuBI-1, GAS41, YAF9
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-18
- Date modifiied:
- 2015-07-22
Related products to: YEATS4 antibody - C-terminal region (ARP30117_T100)
Related articles to: YEATS4 antibody - C-terminal region (ARP30117_T100)
- Fetal growth restriction (FGR) is a major contributor to perinatal morbidity and mortality, most commonly arising from placental dysfunction, with increasing evidence implicating aberrant DNA methylation in its pathogenesis. To identify robust epigenetic alterations associated with FGR, we analyzed placental chorionic villi from an in-house early-onset FGR cohort and compared them with a publicly available dataset (GSE100197). DNA methylation profiling was performed using Illumina EPIC (in-house) and 450K (public) arrays, processed with identical normalization and quality-control pipelines, including adjustment for gestational age and estimation of placental cell-type composition. Differentially methylated positions (DMPs) were identified using linear regression models, revealing 10,427 DMPs in the in-house cohort and 7467 in the public dataset, with 108 shared DMPs showing consistent direction of change across both cohorts. Promoter-associated DMPs were mapped to genes involved in angiogenesis, morphogenesis, immune regulation, and transcriptional control, including , , , , and , while additional novel candidates such as , , and family members were also identified. Functional annotation suggests that these methylation changes may influence pathways essential for placental vascular development and structural organization. Overall, this cross-cohort comparison highlights reproducible epigenetic signatures of FGR and underscores the need for standardized approaches to clarify the molecular mechanisms underlying placental insufficiency. - Source: PubMed
Publication date: 2026/01/31
Bednarek-Jędrzejek MagdalenaTaryma-Leśniak OlgaPoniatowska MałgorzataCejko MateuszMaksym KatarzynaDzidek SylwiaBlatkiewicz MałgorzataKwiatkowska EwaTorbé AndrzejKwiatkowski Sebastian - Chromosomal aberrations in tumors are key indicators of genomic instability and important drivers of neoplasia. While chromosomal changes in uterine leiomyomas have been studied for decades, comprehensive evaluation of chromosomal aberrations in uterine leiomyomas on the scale of modern tumor research has been lacking. - Source: PubMed
Publication date: 2026/01/16
Ilves SiniJokinen ViljaKatainen RikuSiili EmmaBützow RalfHeikinheimo OskariPasanen AnnukkaKarhu AuliVälimäki NikoAaltonen Lauri A - Drug resistance is a major challenge for the target therapy of KRAS-mutant non-small cell lung cancer (NSCLC). Here, we observe that ANP32A is tightly associated with KRAS-mutant NSCLC and serves as an unfavorable prognosis factor. ANP32A deficiency impaired cell proliferation, migration, invasion, and cell cycle progression and induced sotorasib (Sot) resistance in KRAS-mutant NSCLC cells, which were reversed by ANP32A reoverexpression in ANP32A-deficient cells. Mechanistically, ANP32A deficiency impaired histone 3 acetylation at lysine 27 (H3K27Ac). Particularly, ANP32A deficiency reduced H3K27Ac of the YEATS4 gene promoter and downregulated YEATS4 expression. ANP32A also interacted with YEATS4 and promoted its binding to H3K27Ac. Furthermore, YEATS4 overexpression partially restored ANP32A deficiency-impaired cell proliferation, H3K27Ac, and Sot sensitivity. Most importantly, trichostatin A mimicked the effect of ANP32A, which restored YEATS4 expression, antagonized Sot resistance, and resensitized ANP32A-deficient cells to Sot in vitro and in vivo, possibly by reactivating the p53 pathway. Our study identifies a new epigenetic mechanism involving the ANP32A that promotes KRAS-mutant lung cancer growth and affects Sot activity. The combination of Sot and histone deacetyltransferase inhibitors could be an effective treatment for KRAS-mutant lung cancer. ANP32A may serve as a biomarker for Sot treatment. - Source: PubMed
Publication date: 2025/12/29
Pan KailingDang MingjingXu BoHuang ZanChen Xianguo - Despite sustained exposure to Mycobacterium tuberculosis (Mtb), some individuals-so-called resisters-have persistently negative results for the tuberculin skin test (TST) and interferon-gamma release assays (IGRAs). "Resistance to immune conversion" is the best-known clinical correlate for absence of Mtb transmission and protection from tuberculosis (TB). We investigated the human genetic basis of this phenotype by hypothesizing that resisters living with HIV, a major risk factor for TB, would be enriched in genotypes conferring resistance. - Source: PubMed
Publication date: 2025/10/15
Conil ClémentBohlen JonathanKroon Elouise EJean-Juste Marc AManry JérémyChaldebas MatthieuBean James MWalsh Kathleen FDallmann-Sauer MonicaRotival MaximeSeeleuthner YoannMarchal AstridMourelatos HaralambosFava Vinicius MZhang PengKerner GaspardSkhoun HanaaAbid AhmedEl Ouazzani HananeRafik AnissBousfiha Ahmed AzizEl Baghdadi JamilaWilkinson Robert JBoisson-Dupuis StéphanieFitzgerald Daniel WPape Jean WMöller MarloHoal Eileen GCasanova Jean-LaurentAbel LaurentSchurr ErwinCobat Aurélie - How histone lysine crotonylation (Kcr) is read and interpreted remains to be elucidated. We report here that YEATS4, a potential breast cancer driver identified recently by two independent genome-wide association studies, is a reader of H3K14cr. Integrative metabolomic, epigenomic, and transcriptomic analyses reveal that H3K14cr reading by YEATS4 is associated with a shift of cellular metabolic profile and transcription activation of a cohort of genes, including CD36, CPT1A, and ACOX1, that are critically involved in the uptake and metabolism of fatty acids. High expression of YEATS4 fortifies fatty acid metabolism, enhances self-renewal and growth of ALDH breast cancer stem cells, and is correlated with poor prognosis of breast cancer patients, especially the ER subtype. Our work uncovers YEATS4 as an "amplifier" in the feedforward circuit of histone crotonylation and lipid metabolism underlying the stemness and cell proliferation, supporting the pursuit of YEATS4 as a potential target for breast cancer intervention. - Source: PubMed
Publication date: 2025/10/07
Peng ZijunYu HuajingWang YizhouZhao DanFa HangweiQin LeyiMa YileiGeng MengyangWu YuqingWu GeWu XinZhang ChengyingWang YueLiu JianyingLi HaitaoLu ZhiminShang YongfengLiang Jing