HYPB _ SETD2 (C Terminus)
- Known as:
- HYPB _ SETD2 (C Terminus)
- Catalog number:
- Y213586
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HYPB _ SETD2 ( Terminus)
Related genes to: HYPB _ SETD2 (C Terminus)
- Gene:
- SETD2 NIH gene
- Name:
- SET domain containing 2, histone lysine methyltransferase
- Previous symbol:
- -
- Synonyms:
- HYPB, HIF-1, KIAA1732, FLJ23184, KMT3A
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-15
- Date modifiied:
- 2019-04-23
Related products to: HYPB _ SETD2 (C Terminus)
Related articles to: HYPB _ SETD2 (C Terminus)
- - Source: PubMed
Publication date: 2026/04/16
Kumari SubhadraM Kirthik RoshanPal RituparnaJaiswal SushilaJaiswal AwadheshKumar SantoshMuthuswamy Srinivasan - - Source: PubMed
Publication date: 2026/04/15
- Neoadjuvant therapy (NAT) has emerged as a standard treatment strategy for locally advanced breast cancer (BC), yet robust biomarkers for response prediction remain elusive. Here, we established a real-world NAT cohort of 1,161 Chinese BC patients, including 1,145 cases with matched clinicopathological data and targeted sequencing, to systematically evaluate genomic features associated with NAT outcomes. We identified both cross-subtype and subtype-specific genomic associations with treatment response. PI3K-pathway alterations emerged as a consistent feature of resistance across subtypes, whereas mutations such as ERBB2 in HER2+ disease and MAP3K1 in triple-negative breast cancer were associated with subtype-specific response patterns. Regimen-level analyses further showed that some genomic associations were treatment-context dependent across chemotherapy-, endocrine-, anti-HER2-, and immunotherapy-containing regimens. Among patients with non-pathological complete response (non-pCR), genomic profiling further refined risk stratification for distant recurrence by revealing subtype-specific prognostic alterations, including TOP3B and SETD2. Furthermore, a machine-learning model integrating genomic and clinicopathological features showed favorable performance for NAT response prediction. Overall, our study provides a comprehensive genomic framework for response prediction and recurrence risk assessment, supporting more precise stratification and biomarker-guided treatment optimization in Asian breast cancer patients. - Source: PubMed
Publication date: 2026/04/11
Ying Xiao-HanZhang Kun-YuJiang Shu-HaoChen LiLi Jun-JieLiu Guang-YuYu Ke-DaWu JiongDi Gen-HongWang Yun-YiFan LeiHou Yi-FengShao Zhi-MingZhu Xiu-ZhiHu XinChen ChaoWang Zhong-Hua - The euchromatic histone methyltransferase G9a/KMT1C/EHMT-II functions as a corepressor and a coactivator of transcription, depending upon its association with distinct protein complexes. While the mechanisms of G9a-mediated repression are well understood, the molecular mechanism of G9a-mediated activation remains elusive. In the present study, we report that the coactivator function of G9a involves its association with H3K36 histone methyltransferases, including NSD3/KMT3F/WHSC1L1 and SETD2/KMT3A. Functionally, we demonstrate that the association of G9a with NSD3 and SETD2 is necessary for activating G9a target adult and genes in differentiating adult erythroid cells. Mechanistically, G9a recruits NSD3 to the gene, and NSD3 activates its expression by stabilizing Mediator complex binding to the promoter and facilitating SETD2-mediated H3K36 trimethylation in the gene body. Knocking down either NSD3 or G9a in differentiating erythroid cells significantly downregulates mediator complex binding at the promoter and the localization of SETD2 and SETD2-mediated H3K36me3 on the coding region of the G9a target highlighting the necessity of NSD3 in mediating the activation of this gene. Our study reveals a novel crosstalk mechanism in which the histone methyltransferase G9a coordinates with the H3K36 histone methyltransferases NSD3 and SETD2 to mediate gene activation. - Source: PubMed
Publication date: 2026/03/26
Shah ArunimChaturvedi Chandra PrakashSingh KulwantKatiyar ShobhitaSharma Akhilesh - Chromatin modifications are essential for mammalian development, and their aberrant deposition is associated with human disease. While the mechanisms that deposit and remove histone modifications have been largely elucidated, their roles in regulating gene activity during cellular differentiation are yet to be fully understood. Here, we performed a deletion screen to identify stage-specific requirements of chromatin regulators during neuronal differentiation of mouse embryonic stem cells. We show that the H3K36me3 methyltransferase SETD2 is required for the establishment of neuronal gene expression during late stages of differentiation but is dispensable in mature neurons. Notably, this function is independent of its histone methyltransferase activity. Instead, SETD2 promotes interactions between the PAF1 complex and elongating RNA Pol II, suggesting a role in supporting efficient transcription of neuronal genes. - Source: PubMed
Publication date: 2026/04/10
Ambrosi ChristinaPfaendler RamonEleftheriou KristeliButz StefanRecchia DavideBao XueCardoso da Silva RichardKupfer NiklasLagerwaard Ilse MVlaming HannekeSchmolka NinaBhardwaj VivekBaubec Tuncay