AFF3 Antibody
- Known as:
- AFF3 Antibody
- Catalog number:
- GWB-ML800H
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- AFF3 Antibody
Related genes to: AFF3 Antibody
- 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 Antibody
Related articles to: AFF3 Antibody
- Protein-based ageing clocks can be used to help identify individuals at high risk of death or morbidity. There is a lack of evidence in non-European populations on clocks derived from combining different proteomic platforms and their relationship with age-related traits, diseases and genetic architecture. - Source: PubMed
Publication date: 2026/07/29
Bennett Derrick AWang BaihanXiao SihaoWright NeilEdris AhmedWang YunheMillwood Iona YWalters Robin GDu HuaidongYang LingChen YipingAvery DanielSchmidt Dan ValleYu CanqingSun DianjianyiLv JunHill MichaelLi LimingClarke RobertChen Zhengming - Transcriptional condensates anchored by chromatin readers are increasingly recognized as organizing hubs for gene expression, but how their assembly and stability are regulated remains poorly understood. Here, we identify an acetylation-dependent feed-forward circuit that controls the integrity of the Super Elongation Complex (SEC), a key driver of transcriptional elongation. We show that the SAGA histone acetyltransferase catalytic subunits KAT2A/KAT2B license acetylation of both histone H3 lysine 9 (H3K9ac) and SEC components themselves, including ENL, AFF1, and AFF3. Loss of this dual acetylation activity, achieved via a cereblon-recruiting PROTAC (GSK983/GSK699), displaces the chromatin reader ENL from target loci, dissolves ENL-anchored transcriptional condensates, and disrupts SEC-dependent transcriptional output - linking histone and non-histone acetylation to the physical integrity of a core transcriptional machine. Using genome-scale dependency data, we show that the SAGA complex is a selective chromatin dependency in acute myeloid leukemia (AML) AML and hematological malignancies and disrupting this feed-forward transcriptional circuit in AML demonstrates subtype independent antileukemia effects. KAT2A/B degradation drives potent, broad-spectrum antileukemic activity across genetically diverse AML cell lines, primary patient samples, and an isogenic KMT2A-rearranged model bearing cooperating oncogenic mutations, with H3K9ac loss concentrated asymmetrically at core AML oncogene loci such as MYC, MYB, and the HOXA cluster. Together, these findings define an acetylation-dependent circuit governing SEC integrity and establish KAT2A/B degradation as a mechanism-based, pan-AML therapeutic strategy, with implications for transcriptional condensate regulation beyond leukemia. - Source: PubMed
Publication date: 2026/07/14
Deshpande AnaghaChiang Cho-YingPerales MarlenneNiranjan NehaSinha NeelamFinlay DarrenStevens AlexandraZahn EmilyGarcia Benjamin AJeremias IrmelaWunderlich MarkJensen-Pergakes KristenUdyavar AkshataCarr AmyNager Andrew RYang YanlingMurad RabiJones CourtneyO'Connell ShawnPaul ThomasVuori KristiinaDeshpande Aniruddha J - Arthrogryposis Multiplex Congenita (AMC) is a heterogeneous group of disorders characterized by multiple contractures, often associated with central nervous system (CNS) involvement. To date, advances in Next Generation Sequencing (NGS) have enabled the identification of more than 400 genes implicated in AMC. Genetic causes of AMC and CNS involvement are especially challenging due to their heterogeneous clinical presentation, overlapping phenotypes, and often uncertain etiology. Pathogenic variants in AFF3 degron motif were identified as a cause of KINSSHIP syndrome (MIM #619297) which is clinically characterized by horseshoe kidney, Nievergelt/Svarirayan type of mesomelic dysplasia, seizures, generalized hypertrichosis, intellectual disability, and pulmonary involvement. We describe a patient presenting distal contractures at birth and neurodevelopmental delay, in whom Whole Genome Sequencing (WGS) revealed a previously reported missense variant in AFF3. We also conducted a literature review of published cases associated with this gene. This case highlights the importance of recognizing and characterizing the phenotypic presence of multiple congenital contractures and neurodevelopmental impairment as a clinical pattern that may prompt consideration of AFF3-related KINSSHIP syndrome among the differential diagnoses. Our findings underscore the relevance of integrating genomic testing into the evaluation of patients with AMC and CNS involvement to support accurate diagnostic classification. - Source: PubMed
Publication date: 2026/07/24
Ordaz-Robles ThaniaRamírez-García DanielDahan-Oliel NoémiTavukcu SenaGiampietro Philip FRíos-Ruíz José GilbertoCárdenas-Conejo AlanGustafson Anxhela GjyshiBardai GhalibRauch Frank - It is necessary for naive CD8 T cells to be actively maintained in a quiescent metabolic state in order to respond robustly to infection while avoiding inappropriate activation during homeostasis. With age, this quiescent state is lost and the CD8 T cell response to infection decreases. The factors regulating metabolic quiescence of CD8 T cells and how this regulation is lost during aging are not completely understood. Herein, we identify the transcription factor AFF3 as a regulator of metabolic quiescence in naive CD8 T cells. While naive AFF3-deficient CD8 T cells are more metabolically active prior to infection, they have reduced accumulation in response to viral infection, and this is correlated with a poor capacity to engage glycolysis. During aging in both murine and human CD8 T cells, AFF3 expression is decreased. In mice, this is associated with a loss of metabolic quiescence and reduced capacity to accumulate following infection. Our data highlight the role of metabolic regulation in CD8 T cell quiescence and identify a transcription factor that may be a target to reinvigorate CD8 T cell responses during aging. - Source: PubMed
Publication date: 2026/06/23
Lumnitzer Molly EValbon Stefanie FCondotta Stephanie ANorlander Allison ELiu ShengWan JunRicher Martin J - Ossifying fibromyxoid tumor (OFMT) is a rare mesenchymal neoplasm of uncertain lineage of differentiation driven by a broad spectrum of gene fusions. It manifests primarily in soft tissues of the extremities. In this study, we performed a comprehensive clinicopathological, molecular-genetic, and epigenetic analysis of 70 cases of OFMT, with a specific focus on rare fusion subtypes, particularly ZC3H7B::BCOR, PHF1::TFE3, and MEAF6::PHF1. In addition, we included 7 tumors with novel fusions, namely, AFF3::PHF1, PHF1::KLF15, PHF1::PRKAG1, CREBBP::PHF1, EPC1::BMI1, MEAF6::BCOR, and EP300::BCORL1. The clinicopathological characteristics revealed a correlation between specific fusions and aggressive clinical behavior; notably, tumors with ZC3H7B::BCOR fusions were always classified as morphologically atypical or malignant and were associated with significantly higher recurrence and metastatic rates compared with other fusion groups, particularly EP400::PHF1. Immunohistochemical analysis further revealed a distinct immunophenotype in the ZC3H7B::BCOR group. Whereas immunopositivity for cytokeratins and myogenic markers was observed in approximately one-quarter and more than one-third of OFMT cases overall, respectively, ZC3H7B::BCOR-rearranged tumors were negative for both. In contrast, the majority showed immunopositivity for pan-Trk. Additionally, DNA methylation profiling distinguished ZC3H7B::BCOR-rearranged cases from other fusion-positive OFMT cases. The former group clustered closely with a subset of high-grade endometrial stromal sarcomas. This study supports the recognition of ZC3H7B::BCOR-positive tumors as a distinct clinicopathological entity, contributing to the refined molecular taxonomy of this neoplasm. - Source: PubMed
Publication date: 2026/06/16
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