AML1 (Phospho-Ser435) Antibody
- Known as:
- AML1 (Phospho-Ser435) Antibody
- Catalog number:
- 11783
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- AML1 (Phospho-Ser435) Antibody
Related genes to: AML1 (Phospho-Ser435) Antibody
- Gene:
- RUNX1 NIH gene
- Name:
- RUNX family transcription factor 1
- Previous symbol:
- AML1, CBFA2
- Synonyms:
- PEBP2A2, AMLCR1
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-20
- Date modifiied:
- 2019-04-23
- Gene:
- RUNX1T1 NIH gene
- Name:
- RUNX1 translocation partner 1
- Previous symbol:
- AML1T1, CBFA2T1
- Synonyms:
- CDR, ETO, MTG8, ZMYND2
- Chromosome:
- 8q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-16
- Date modifiied:
- 2016-10-05
Related products to: AML1 (Phospho-Ser435) Antibody
Related articles to: AML1 (Phospho-Ser435) Antibody
- Neuroendocrine prostate cancer (NEPC) or small-cell neuroendocrine prostate cancer (SCNPC) is increasingly recognized as a treatment-resistant disease arising among prostate adenocarcinoma (PRAD) patients. It has no effective therapy due to incomplete understanding of the mechanisms underlying treatment-induced cancer cell identity switching. Here, we identified RUNX1 Partner Transcriptional Co-Repressor 1 (RUNX1T1) as a frequently amplified gene in prostate cancer patients, associated with a poorer prognosis. RUNX1T1 is highly expressed and progression-correlated in NEPC and SCNPC. We found that RUNX1T1 is essential for SCNPC survival, as its knockdown induced apoptotic cell death and the acquisition of PRAD-like identity, including alterations in genes involved in cell-cell adhesion and epithelial cell polarity. Functional assays in prostate cancer cell lines revealed that RUNX1T1 regulates genes associated with stemness and the maintenance of neuroendocrine identity in SCNPC. Using our human cell reprogramming assay, which mimics the development of PRAD or SCNPC , we further demonstrated that RUNX1T1 is required to initiate neuroendocrine differentiation (NED), histological feature changes, and stemness. Its knockout abolished expression of NED and stemness markers and induced loss of SCNPC histological features during SCNPC development. Collectively, these findings establish RUNX1T1 as a critical driver of the cell identity of stem-like SCNPC. Understanding the mechanisms by which RUNX1T1 exerts its versatile regulation of proliferation, stemness, and SCNPC differentiation will in turn pave the way for the discovery of new, specific therapeutic targets to prevent SCNPC progression. - Source: PubMed
Publication date: 2026/08/26
Wang ZiqinJung HyeryeonHong ChanghyeonChen NancyJo YunsolJung IssacKim TaeeunLee GinaChien KeatonChen MingHuang JiaotiPark Jung Wook - Genomic profiling plays a central role in risk stratification and therapeutic decision-making in acute myeloid leukemia (AML), yet the clinical implications of population-specific genomic architectures remain incompletely defined. We conducted a prospective, multicenter study of 603 adults with newly diagnosed AML in Korea, integrating targeted sequencing of 83 recurrently mutated genes with comprehensive clinical annotation across treatment intensities, including allogeneic hematopoietic stem cell transplantation (allo-HSCT). For contextual comparison, genomic profiles were evaluated against the Beat AML cohort. The overall genomic landscape was broadly conserved, supporting shared core disease biology across populations. However, RUNX1::RUNX1T1, CEBPA, GATA2, KIT, and DDX41 mutations were more frequent in the Korean cohort, whereas FLT3 and NPM1 mutations were less common. These differences translated into a distinct distribution of European LeukemiaNet (ELN) 2022 risk categories, with implications for therapeutic stratification. Notably, most DDX41 alterations were germline (3.2%), highlighting the need for systematic germline evaluation with implications for genetic counseling and donor selection. Although unadjusted overall survival appeared longer in the Korean cohort, this difference was not significant after adjustment for key clinical variables. These findings indicate that population-specific genomic distributions reshape the clinical application of risk stratification and support population-aware precision medicine strategies in AML. - Source: PubMed
Publication date: 2026/09/08
Kim MiheeSong Ik-ChanPark JooheonLee ChangseonKim Mi YeonSohn Sang KyunYhim Ho-YoungPark YongKim InhoShin Ho-JinPark Seong KyuKim Sung-HyunCheong June-WonLee Ho SupLee HyewonBae Sung HwaChoi YunsukLee Hong-GhiDo Young RokHan Jae JoonKim Min KyoungPark SilviaCho Byung-SikKim Hee-JeKim Hyeoung-JoonAhn Jae-Sook - The RUNX1::RUNX1T1 translocation, also termed AML1-ETO, is one of the most frequent cytogenetic abnormalities in acute myeloid leukemia (AML) and is associated with variable clinical outcomes. The R222G hotspot mutation, located in the RNA helicase gene DHX15, is enriched and predominantly found in AML with this translocation, but its diagnostic significance and underlying mechanism remain largely unclear. In this study, we show that pediatric AML patients carrying DHX15 mutations exhibit an inferior prognosis. Functional analysis demonstrates that DHX15 cooperates with AML1-ETO fusion protein to enhance AML leukemia stem cell (LSC) activity and promote resistance to standard chemotherapy. Mechanistically, AML1-ETO transcriptionally upregulates mitochondrial transcription factor A (TFAM), while DHX15 promotes TFAM protein stabilization and nuclear translocation, resulting in robust activation of oxidative phosphorylation (OXPHOS) gene expression and mitochondrial respiration. Inhibition of oxidative phosphorylation by the Complex V inhibitor S-Gboxin exerts strong anti-leukemic effects and efficiently circumvents chemotherapy resistance in AML1-ETO DHX15 leukemia. These findings underscore the pivotal role of oncogenic DHX15 mutations in regulating AML LSC activity and identify DHX15 as a potential genetic biomarker for AML risk stratification. Moreover, this mutation may predict therapeutic vulnerability to OXPHOS inhibition. - Source: PubMed
Publication date: 2026/08/21
Li QilongXing PeiqiXu JinLi JifeiChen LiangjieLi XinluBai YinpengLi GangXie TingWang LuzhenWang YuanQing GuoliangWang HuafengShao LiangWu WeiLiu ZhaoqiLiu Hudan - Acute myeloid leukemia (AML) with RUNX1::RUNX1T1 usually has a favorable outcome. However, it sometimes relapses and is refractory; in these cases, allogeneic hematopoietic stem cell transplantation (HSCT) is indicated. When HLA-matched sibling donors (MSDs) are unavailable, alternative donor sources, such as unrelated umbilical cord blood cells (UCB), are considered. However, the outcomes of UCB for AML with RUNX1::RUNX1T1 have not yet been fully examined. We retrospectively analyzed the outcomes of HSCT with UCB. - Source: PubMed
Publication date: 2026/08/19
Sakurai KazukiYokoyama HisayukiKomatsu HirokaTakenaka KentaNarumi YoshihiroHatta ShunsukeOnodera KoichiFukuhara NorikoOnishi YasushiKatsuoka YunaSaito YoKamata MayumiHarazaki YorikoTomiya YasuoIzumi ToruSasaki OsamuHarigae Hideo - Although measurable residual disease (MRD) is an established prognostic marker in pediatric acute myeloid leukemia (AML), its dynamic prognostic value during treatment and its integration with the variant status in core-binding factor (CBF)-AML remain incompletely defined. We evaluated the prognostic impact of sequential MRD and variants in pediatric CBF-AML. - Source: PubMed
Publication date: 2026/08/19
Yeh Ting-ChiJaing Tang-HerLiu Hsi-CheChen Shih-HsiangWang Shih-ChungHsiao Chih-ChengChiou Shyh-ShinHou Jen-YinLin Pei-ChinHuang Fang-LiangYang Shang-HsienHuang Ting-YuYang Chao-PingShih Lee-Yung