SUV39H1 antibody - N-terminal region (ARP32471_P050)
- Known as:
- SUV39H1 (anti-) - N-terminal region (ARP32471_P050)
- Catalog number:
- arp32471_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SUV39H1 antibody - N-terminal region (ARP32471_P050)
Related genes to: SUV39H1 antibody - N-terminal region (ARP32471_P050)
- Gene:
- SUV39H1 NIH gene
- Name:
- suppressor of variegation 3-9 homolog 1
- Previous symbol:
- SUV39H
- Synonyms:
- KMT1A
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-12
- Date modifiied:
- 2015-12-04
Related products to: SUV39H1 antibody - N-terminal region (ARP32471_P050)
Related articles to: SUV39H1 antibody - N-terminal region (ARP32471_P050)
- Not available. - Source: PubMed
Publication date: 2026/04/16
Alibert LauraOvejero SaraDevin JulieThomas MorganeKassambara AlboukadelAngles MatthieuRequirand GuilhemRobert NicolasVincent LaureCartron GuillaumeMartinez Anne MarieHerbaux CharlesCavalli GiacomoMoreaux JérômeBret Caroline - In livestock, understanding the genetic basis of adaptation to the environment is essential for enhancing resilience to climate change and sustaining productivity in diverse environments. Indigenous Ethiopian cattle represent an ideal model for such studies, as they have evolved across a wide range of environments from the cool, oxygen-limited highlands to the hot, pathogen-rich lowlands. These environmental gradients imposed intense selective pressures, shaping their genomic landscape. In this study, we performed the first comprehensive analysis of X-linked adaptive signatures in Ethiopian indigenous cattle using whole-genome sequencing data. - Source: PubMed
Publication date: 2026/04/10
Ayalew WondossenTarekegn Getinet MXiaoyun WuChu MinNaboulsi RakanTessema Tesfaye SBongcam-Rudloff ErikNegussie EnyewPing YanZhang Zhe - Robust liver regeneration counteracts and facilitates recovery from liver injuries. The underlying epigenetic mechanisms, however, are not fully understood. Here we investigated the role of suppressor of variegation 3-9 homolog 1 (Suv39h1), a histone H3K9 methyltransferase, in liver regeneration. Suv39h1 expression was repressed by DNMT1 during liver regeneration. Systemic or hepatocyte-specific deletion of Suv39h1 in mice enhanced liver regeneration and post-surgery survival following partial hepatectomy. RNA sequencing revealed high-mobility group protein B2 (HMGB2) as a target for Suv39h1. Suv39h1 downregulation in proliferating hepatocytes allowed E2F1 to activate HMGB2 transcription. Consistently, HMGB2 knockdown attenuated proliferation of hepatocytes in response to HGF treatment and suppressed liver regeneration in mice. Integrated transcriptomic analysis indicated that HMGB2 may contribute to proliferation of hepatocytes by regulating a panel of proregenerative genes. Importantly, Suv39h1 inhibition by chaetocin boosted liver regeneration in mice. Finally, a significant correlation between Suv39h1, HMGB2 and proliferative markers was identified in patients with acute liver failure. In conclusion, our data uncover an unrecognized role for Suv39h1 in liver regeneration. Therefore, targeting Suv39h1 may be considered as a viable strategy to boost liver regeneration after injury. - Source: PubMed
Publication date: 2026/04/10
Lu YunjieZhou JiawenMiao XiulianZeng ShengQin LeiXu YongWang ShuaiLi Zilong - Epigenetic regulation of chromatin structure is a key determinant of transcriptional control and nuclear organization in cancer. Among histone lysine methyltransferases, SUV39H1 and SUV39H2 catalyze the trimethylation of histone H3 lysine 9 (H3K9me3), establishing repressive heterochromatin domains that are important for genomic stability. However, their pan-cancer expression dynamics, prognostic value, and structural implications remain poorly defined. In this study, we performed an integrative analysis of SUV39H1 and SUV39H2 across the Cancer Genome Atlas (TCGA) cohort to investigate their expression, prognostic relevance, associations with the immune landscape, and interactions with nuclear lamina genes. Both enzymes were significantly overexpressed in multiple tumor types, with SUV39H2 showing particularly high expression in high-grade serous ovarian cancer (HGSOC), where elevated levels correlated with poor overall survival (HR = 3.27, p < 0.001). Immune infiltration analysis revealed that high SUV39H2 expression was inversely associated with tumor-infiltrating lymphocytes, indicating reduced immune infiltration. Correlation studies demonstrated strong positive associations between SUV39H1/H2 and Lamin B genes (LMNB1, LMNB2), suggesting an association with nuclear lamina-linked heterochromatin. Conversely, Lamin A (LMNA) exhibited weak or negative correlation with SUV39 enzymes. Functional validation in A2780 ovarian cancer cells demonstrated that pharmacological inhibition of SUV39H2 by Chaetocin resulted in the upregulation of Lamin A, suggesting that SUV39H1/H2 inhibition is associated with Lamin A regulation. Collectively, our findings uncover a previously underappreciated association between SUV39H2, chromatin-lamina interactions, and immune evasion in ovarian cancer, highlighting SUV39H2 as a potential chromatin-associated biomarker and regulator of nuclear organization and providing a rationale for targeting SUV39H2 in therapeutic epigenetic interventions. - Source: PubMed
Publication date: 2026/04/09
Kundu SubhadipAkhtar Abdur RahmaanKumar ArunSharma Ashok - Many regions of heterochromatin associate with the nuclear periphery and are known as Lamin-associated domains (LADs). Histone acetyltransferase 1 (Hat1) is a highly conserved enzyme which acetylates newly synthesized histones H4 on lysines 5 and 12 prior to their deposition on chromatin. Hat1 is required to preserve chromatin accessibility within a subset of LADs called Hat1-dependent accessibility domains (HADs). Here we profile a diverse set of histone modifications in Hat1 KO and WT immortalized mouse embryonic fibroblasts (iMEFs) and find that Hat1 regulates diverse aspects of the structure of HADs and non-HAD LADs (nhLADS). In HADs, these changes include the conversion of H3K9me2 to H3K9me3. Analysis of H3K9-specific histone methyltransferases (HMTs) shows that that Suv39h1 and Suv39h2 have distinct localization patterns, where only Suv39h2 localizes to LADs. G9a only localizes to LADs in regions enriched for H3K9me2. We find that Hat1 loss results in a redistribution of these HMTs in both HADs and nh LADs. There is a decrease in the levels of G9a with a concomitant increase in Suv39h2. These results suggest Hat1 functions to restrain the formation of a more strongly heterochromatic state and highlight a role for Hat1 as an essential regulator of heterochromatin inheritance. - Source: PubMed
Publication date: 2026/03/23
Martin Caden JPopova Liudmila VNagarajan PrabakaranOser Elizabeth ALovejoy Callie MSunkel Benjamin DStanton Benjamin ZFreitas Michael AParthun Mark R