AML1 EMSA Probe Set
- Known as:
- AML1 EMSA Probe Set
- Catalog number:
- AY1162P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- AML1 EMSA Probe Set
Related genes to: AML1 EMSA Probe Set
- 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 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: AML1 EMSA Probe Set
- - Source: PubMed
Publication date: 2026/04/29
Chang Yu-HanChang Guang-HuiGao Hai-TaoFu QiangZhao Xiao-SuQin Ya-ZhenJiang QianJiang HaoXu Lan-PingWang YuZhang Xiao-HuiHuang Xiao-JunTang Fei-Fei - Acute myeloid leukemia (AML) is a highly lethal hematologic malignancy, and reliable prognostic biomarkers remain urgently needed. We investigated the expression and clinical relevance of the actin cytoskeleton regulator N-WASP in AML. Analysis of TCGA data revealed significantly reduced N-WASP expression in AML compared with normal tissues, and low expression was associated with adverse clinical features, including FAB-M1/M4 subtypes, DNMT3A mutations, and cytogenetic abnormalities such as t(8;21)/RUNX1::RUNX1T1 and del(7q). Patients with low N-WASP expression exhibited shorter overall survival, and multivariate Cox regression identified N-WASP reduction as an independent risk factor, alongside advanced age and FLT3, DNMT3A and TP53 mutations. Co-expression and enrichment analysis highlighted FNIP1, CLIP1, RICTOR and BRAF as N-WASP-associated regulators converging on mTOR signaling. Experimental validation via RT-qPCR and western blotting in AML bone marrow samples and cell lines confirmed the downregulation of N-WASP and key co-expressed genes. Collectively, these results demonstrate that N-WASP is suppressed in AML and is closely associated with disease risk and clinical outcome. N-WASP may serve as a novel prognostic biomarker and potential therapeutic target warranting further investigation. - Source: PubMed
Publication date: 2026/04/22
Liu CuiSun JianLuo YanHuang PeiChen Yan - The 2022 European LeukaemiaNet acute myeloid leukemia (AML) classification allocates AML with t(8;21) RUNX1::RUNX1T1 fusion and AML with inv(16) or t(16;16) CBFB::MYH11 fusion (collectively, core-binding factor AML), AML with NPM1 without FLT3-ITD mutation and AML with CEBPA bZIP in-frame mutation into the favorable-risk strata based on initial molecular diagnostics. Generally, these entities have a relatively low risk of relapse (< 30%-40%) and many patients (> 50%-60%) survive long-term with intensive chemotherapy alone. However, there is growing literature that patterns of co-mutation, and more importantly, postremission measurable residual disease (MRD) status, modify these risks dynamically; necessitating an adaptive approach to optimize patient outcomes. In this review, we summarize evidence on how molecular and MRD features could assist clinicians in identifying high-risk patients within these favorable-risk subgroups, and where escalation of therapy, including with allogeneic transplantation in first remission, may be beneficial. - Source: PubMed
Publication date: 2026/03/20
Tedjaseputra AdityaRussell NigelDillon Richard - - Source: PubMed
Publication date: 2026/04/10
Jagadish GayathriKulkarni Jayashree DKumari PrasannaKorlimarla Aruna - Relapsed/refractory RUNX1::RUNX1T1-positive acute myeloid leukemia remains a therapeutic challenge due to high relapse rates post-allogeneic hematopoietic stem cell transplantation. Preclinical evidence suggests that RUNX1::RUNX1T1 fusion proteins sensitize cells to poly ADP-ribose polymerase inhibitors by suppressing homologous recombination repair. This study explores the safety and efficacy of a novel conditioning regimen incorporating olaparib (a PARPi) for relapsed/refractory RUNX1::RUNX1T1+ AML patients undergoing allo-HSCT. - Source: PubMed
Publication date: 2026/03/25
Xue SongMa WeiChen ManSun Hui-PengCao Xing-Yu