STAG2
- Known as:
- STAG2
- Catalog number:
- Y213678
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- STAG2
Related genes to: STAG2
- Gene:
- STAG2 NIH gene
- Name:
- stromal antigen 2
- Previous symbol:
- -
- Synonyms:
- SA-2, SCC3B, SA2
- Chromosome:
- Xq25
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-29
- Date modifiied:
- 2019-04-23
Related products to: STAG2
anti-STAG2 (3C6)anti-STAG2 (3C6)anti-STAG2 (3C6)anti-STAG2 (3C6) type: Primary antibodies host: MouseAnti-STAG2 (3C6), Mouse Monoclonal to STAG2, Isotype IgG1, Host Mouseanti-STAG2 (aa1100-1150)Antibodies: STAG2 HOST: Goat Clonality: pAbAntibodies: Stromal antigen 2 _ STAG2 HOST: Goat Clonality: pAbBovine Cohesin subunit SA-2(STAG2) ELISA kitCanine Cohesin subunit SA-2(STAG2) ELISA kitCanine Cohesin subunit SA-2(STAG2) ELISA kitChicken Cohesin subunit SA-2(STAG2) ELISA kitCohesin subunit SA-2,Homo sapiens,Human,SA2,SCC3 homolog 2,STAG2,Stromal antigen 2Cohesin subunit SA-2,Mouse,Mus musculus,Sa2,Sap2,SCC3 homolog 2,Stag2,Stromal antigen 2ELISA Kit FOR Cohesin subunit SA-2; organism: Human; gene name: STAG2 Related articles to: STAG2
- Translocation-associated sarcomas (TAS) represent a heterogeneous group of pathologic entities characterized by specific gene fusions and a low tumor mutational burden (TMB). Although RNA sequencing remains the hallmark molecular platform to establish the fusion type, targeted panel DNA next-generation sequencing (NGS) has been increasingly used in TAS to identify actionable alterations as well as potential mechanisms of resistance to therapy. - Source: PubMed
Publication date: 2026/04/23
Yakoub Mohamed ASaoud CarlaReed Damon RWexler LeonardSlotkin EmilyTap William DHameed MeeraAntonescu Cristina R - While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are a cornerstone of therapy for advanced -mutant non-small cell lung cancer (NSCLC), resistance remains a major clinical challenge. The genomic landscape of early-stage (ES) -mutant NSCLC and its evolution to advanced-stage (AS) disease is not fully understood. This study aimed to characterize the molecular disparities between ES and AS -mutant NSCLC and to identify genomic alterations associated with EGFR-TKI treatment outcomes. - Source: PubMed
Publication date: 2026/02/26
Yoon DayoungLee Ji WonCho Byoung ChulKang Eun JooKim Jung SunLim TaekyuYi Seong YoonKim Yu JungAhn Mi SunKim Young SaingPark Ji HyunLim SeungtaekPark Hyung SoonCho Jang HoJang ByunghyunLee Ji YoonKim JiwonHong JisooKoo HarimChung SeokShin Sang WonKim Yeul HongSa Jason KChoi Yoon Ji - Coffin-Siris syndrome (CSS) is predominantly attributed to variants in ARID1B gene, however, the molecular pathways connecting ARID1B to myelination and neural development are not well elucidated. - Source: PubMed
Publication date: 2026/04/10
Yang XingkunGan ZhongzhiZhou YasiZhang MingmingWu ShuijuanHe FeiShen ZongruiMa ShunfeiSu XiXiong Fu - Ewing sarcoma is driven by chromosomal translocations that fuse a FET RNA-binding protein to an ETS transcription factor, most commonly generating the EWS-FLI1 fusion oncoprotein. EWS-FLI1 engages GGAA microsatellite repeats to form de novo enhancers that activate oncogenic transcriptional programs essential for tumorigenesis. In addition to this truncal driver, recurrent loss-of-function alterations in the cohesin subunit STAG2 occur in approximately 10 to 15% of Ewing sarcomas and are associated with adverse clinical outcomes. However, how STAG2 loss reshapes EWS-FLI1 chromatin engagement and transcriptional output remains poorly understood. Here, using genetic STAG2 loss-of-function models combined with integrative multiomic profiling, we demonstrate that STAG2-cohesin deficiency reprograms the EWS-FLI1 chromatin landscape by altering its binding at GGAA-microsatellite enhancers. Despite increased EWS-FLI1 protein abundance, STAG2 loss eliminates over 40% of EWS-FLI1 binding sites, predominantly at enhancers containing short (1-4) GGAA repeats, while concurrently increasing binding at multimeric enhancers with ≥5 GGAA-repeat motifs. These reprogrammed sites show changes in both chromatin accessibility and H3K27ac, leading to selective amplification of EWS-FLI1 activity at multimeric microsatellite enhancers. By integrating Hi-C chromatin interaction maps with altered EWS-FLI1 occupancy, we define distinct monomeric and multimeric GGAA enhancer-driven transcriptional gene signatures and demonstrate that STAG2 loss selectively augments the multimeric transcriptional program. Consistently, the long GGAA microsatellite-activated gene signature is enriched in patient tumors with aggressive clinical features and deleterious STAG2 alterations. Together, these findings reveal that STAG2 loss reprograms, rather than globally attenuates, EWS-FLI1 function, amplifying a high-risk oncogenic transcriptional state in Ewing sarcoma. - Source: PubMed
Publication date: 2026/04/08
Eyunni SanjanaChu Shih-ChunGuan Mary LLouw MichaelaYoung EleanorCarson Sandra EGong JianhuiCieslik MarcinChinnaiyan Arul MParolia Abhijit - Children with Down syndrome (DS) have an elevated risk of developing myeloid leukemia in DS (ML-DS). In addition to mutations in GATA1, which generate the truncated isoform GATA1-short (GATA1s), ML-DS requires additional somatic gene mutations, most frequently in cohesion and polycomb repressive complex 2 (PRC2) genes. Here, we show that PRC2 insufficiency underlies ML-DS pathogenesis. Transplantation of Gata1s fetal liver cells followed by deletion of the cohesion subunit Stag2 and/or the PRC2 component Ezh2 induced megakaryocyte-biased differentiation and expansion of megakaryocytic progenitors, culminating in lethal myelofibrosis. Mechanistically, loss of Stag2 or Ezh2 reinforced Gata1s-driven reduced chromatin accessibility at erythroid transcription factor target loci in pre-megakaryocyte/erythroid progenitors (pre-MegEs), thereby promoting megakaryocytic skewing. Ezh2 loss attenuated the Gata1s-mediated global elevation of H3K27me3 in pre-MegEs, resulting in derepression of a broad set of PRC2 target genes and establishing a functionally PRC2-insufficient state. Similarly, Stag2 loss induced a moderate but significant degree of PRC2-insufficient state in Gata1s progenitors. Furthermore, chromosome 21-encoded miR-125b blocked megakaryocytic differentiation of Gata1s progenitors lacking either Stag2 or Ezh2 alone, but drove full transformation and expansion of CD150+Sca-1+c-Kit+ leukemic stem cell-like populations only upon concurrent loss of both Stag2 and Ezh2, leading to acute megakaryoblastic leukemia in mice. These findings reveal that cohesin and PRC2 insufficiencies converge on PRC2 dysfunction while exerting distinct epigenetic effects, and synergize with trisomy 21 and GATA1s to remodel the epigenetic landscape, driving progression from a preleukemic state to overt leukemia. - Source: PubMed
Publication date: 2026/04/08
Suzuki YutaroNakajima-Takagi YaekoOshima MotohikoOchi YotaroTsuchiya AkihoKoide ShuheiYokomizo-Nakano TakakoKurosawa ShuheiRizq OlaKon AyanaMiyano SatoruRahmutulla BahityarKaneda AtsushiNakayama ManabuKoseki HaruhikoYu EugeneToki TsutomuIto EtsuroOgawa SeishiIwama Atsushi