AFF3
- Known as:
- AFF3
- Catalog number:
- 001267A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AFF3
Ask about this productRelated genes to: AFF3
- Gene:
- AFF3 NIH gene
- Name:
- AF4/FMR2 family member 3
- Previous symbol:
- LAF4
- Synonyms:
- MLLT2-like
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-27
- Date modifiied:
- 2016-10-05
Related products to: AFF3
Related articles to: AFF3
- KMT2A-rearranged (KMT2A-r) acute lymphoblastic leukemia (ALL), particularly in infants, represents one of the most aggressive pediatric hematological malignancies with a historically dismal prognosis. While KMT2A-AFF1 (t(4;11)) is the most prevalent fusion, a diverse array of partner genes exists, each conferring distinct biological and clinical features. This review focuses on the rare but clinically significant KMT2A-AFF3 subtype, which arises from the t(2;11)(q11.2;q23) chromosomal translocation. This review summarizes the molecular pathogenesis driven by the KMT2A-AFF3 fusion oncoprotein, which functions as an aberrant transcriptional complex. This complex hijacks essential epigenetic machinery, including the recruitment of DOT1L and interaction with Menin, leading to pathogenic histone modifications (e.g., H3K79 hypermethylation) and the subsequent upregulation of critical target genes, notably the HOXA cluster and MEIS1, thereby enforcing a B-lymphoid differentiation arrest at the pro-B/pre-B stage. Clinically, KMT2A-AFF3 ALL is characterized by high-risk features, including infant onset, hyperleukocytosis, central nervous system (CNS) involvement, and a distinct CD10-negative immunophenotype. This review highlights the evidence defining its poor prognosis, which is primarily driven by profound chemoresistance to conventional therapies, including glucocorticoids. Finally, we discuss the rapidly evolving therapeutic landscape, detailing the limitations of standard intensive chemotherapy and the immense promise of novel targeted strategies, such as Menin inhibitors (e.g., Revumenib), DOT1L inhibitors, and immunotherapies (e.g., CAR-T cells, Blinatumomab), which hold the potential to revolutionize outcomes for this high-risk leukemia subtype. - Source: PubMed
Publication date: 2025/11/26
Zhang YaweiLiang Juan - A major challenge to global vector control efforts is the increasing resistance of Aedes mosquitoes to conventional insecticides. Since they are the main vectors of dengue, Zika, and chikungunya, sustainable and environmentally friendly approaches are essential for vector control. Attractive toxic sugar baits (ATSBs) take advantage of mosquitoes' propensity for sugar and can offer an alternative strategy. However, further research is needed to investigate the performance of ATSBs, especially in determining and assessing attractant combinations that might increase mosquito attraction and feeding efficiency. - Source: PubMed
Publication date: 2026/01/05
Ayub Noor MuokhniKassim Nur Faeza AbuSabar SumiyyahHashim Nur AidaLalung JaparengSulaiman Shaida FarizaAbuelmaali Sara AWebb Cameron E - Colorectal cancer (CRC) is a globally prevalent malignancy associated with high mortality rates. Despite the existence of various treatment modalities, the prognosis for CRC remains relatively poor. This study aims to explore the role of RNA-binding proteins (RBPs) in CRC progression and their potential as prognostic biomarkers and therapeutic targets. We first identified 166 prognosis-related RBPs, including LIN28B, PPARGC1A, RBM47, and AFF3, by performing univariate Cox regression analysis on bulk transcriptomic and clinical data from The Cancer Genome Atlas (TCGA). Next, single-cell RNA sequencing data from normal, adenoma, and CRC tissues of four patients were analyzed to determine cell type-specific expression patterns of RBPs. Ten upregulated RBPs (HSPB1, RBM47, HMGN2, BRD2, BST2, RBM6, YBX3, CANX, PLEC, and RNASET2) were identified as CRC-associated. Among them, HSPB1, RBM47, HMGN2, BRD2, BST2, and PLEC were predominantly expressed in epithelial cell subsets, whereas RNASET2, RBM6, YBX3, and G3BP2 showed higher expression in T cell subpopulations. Aberrant expression of these RBPs was significantly associated with clinical features such as age, cancer stage, and overall survival ( < 0.05). To validate the above findings, we performed qRT-PCR experiments on 15 paired CRC tumor and adjacent normal tissue samples. The results showed that the expression levels of CANX, RNASET2, YBX3, and BST2 were significantly higher in tumor tissues compared to adjacent normal tissues. Furthermore, we validated the expression levels and prognostic significance of these genes using the TCGA-COAD and READ cohorts, and found that their high expression was significantly associated with poorer overall survival. We suggest that RBPs may influence the occurrence and progression of CRC by affecting epithelial cells and T-cell subtypes, thus serving as promising prognostic biomarkers and potential targets for cancer immunotherapy in CRC. - Source: PubMed
Publication date: 2025/11/27
Lin MengxinWeng ZongqiLin YuyuanLai JinhongXu MeifangWang KangmeiChen XianqiangChen HongbinPan Jie - : Systemic sclerosis (SSc) is a heterogeneous connective tissue disease characterized by immune dysregulation, vasculopathy, and fibrosis. Objectives: To evaluate the genetic architecture and autoantibody profile in a Kazakh cohort of patients with SSc. : A total of 26 Kazakh patients with diffuse SSc were examined for disease activity and organ impairment using EScSG and the modified Rodnan skin score (mRSS). Eighteen healthy volunteers were enrolled in the control group. Antinuclear factor (ANF) was estimated on HEp-2 cells, while antibodies to Scl-70, CENP-B, U1-snRNP, SS-A/Ro52, SS-A/Ro60, Sm/RNP, Sm, SS-B, Rib-P0, and nucleosomes were determined by immunoblotting. The level of IL-6 cytokine was detected using ELISA. To investigate the genetic basis of SSc in Kazakh patients, a custom AmpliSeq panel including targeting immune/fibrosis pathways and 120 genes was used on the Ion Proton sequencer. The statistical analysis of categorical variables was conducted using Fisher's exact test and Chi-square (χ) test. : The examination of SSc patients (mRSS 16 ± 7.2; EScSG 3.54 ± 2.18) revealed a broad range of antibodies to Scl-70, CENP-B, SS-A/Ro60, SS-A/Ro52, U1-snRNP, and RNP/Sm, which were undetectable in the control group. Genetic analysis identified multiple variants across immune regulatory genes, including likely pathogenic changes in SAMD9L, REL, IL6ST, TNFAIP3, ITGA2, ABCC2, AIRE, IL6R, AFF3, and TREX1. Variants of uncertain clinical significance were detected in LY96, IRAK1, RBPJ, IL6ST, ITGA2, AIRE, IL6R, JAZF1, IKZF3, IL18, IL12B, PRKCQ, PXK, and DNASE1L3. Novel variants at the following genomic coordinates were identified and have not been previously reported in association with SSc: LY96 (chr8:74922341 CT/C), PTPN22 (chr1:114381166 CT/C), IRAK1 (indels at chrX:153278833), and SAMD9L (chr7:92761606 GT/G; chr7:92764981 T/TT). : The first immunogenetic investigation of SSc in Kazakhstan revealed a polygenic architecture involving immune signalling pathways that partially overlap with international cohorts while exhibiting region-specific variation. Although the limited sample size and lack of functional validation constrain the interpretability of the findings, the results provide a framework for larger research to confirm the pathogenic mechanisms and establish clinical relevance. - Source: PubMed
Publication date: 2025/10/28
Zaripova LinaBaigenzhin AbaiBoltanova AlyonaZhabakova ZhannaSolomadin MaximKozina Larissa - Physical and cognitive decline are common in older individuals, and traits related to grip strength and cognitive function are used to assess the common genetic structure between the two and to identify common risk loci and genes as well as the genetic mechanisms involved. - Source: PubMed
Publication date: 2025/08/14
Liu HongWu GangqiangTan JunYuan Chunyun