ASXL2
- Known as:
- ASXL2
- Catalog number:
- 002103A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ASXL2
Related genes to: ASXL2
- Gene:
- ASXL2 NIH gene
- Name:
- ASXL transcriptional regulator 2
- Previous symbol:
- -
- Synonyms:
- ASXH2, FLJ10898, KIAA1685
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-11
- Date modifiied:
- 2018-05-10
Related products to: ASXL2
Related articles to: ASXL2
- The expansion of cancer immunotherapy has made it increasingly important to identify tumor-specific human leukocyte antigen (HLA) class I epitopes and to define the molecular determinants of peptide-HLA binding and stability. Posttranslationally modified epitopes, particularly phosphorylation, can reflect oncogenic signaling states and offer highly tumor-selective targets. Despite their potential, the structural and biophysical mechanisms by which phosphorylation reshapes the conformational ensemble and interaction network of peptide-HLA complexes remain unclear. Here, we investigate a phosphorylated ASXL transcriptional regulator 2 (ASXL2)-derived epitope supported by confident tandem mass spectrometry-based phosphosite localization and detected across multiple cancer types. We performed all-atom molecular dynamics simulations of peptide-HLA complexes to compare the phosphorylated peptide, its nonphosphorylated counterpart and its protonated-phosphorylated state. Our simulations indicate that phosphorylation reconfigures the noncovalent interaction network within the binding groove by introducing new local contacts. Principal component analysis further revealed that phosphorylation restricts peptide conformational fluctuations, thereby altering the conformational ensemble of the peptide-HLA complex. Furthermore, protonation of the phosphorylated peptide remodels the noncovalent interaction network and conformational ensemble. Together, these findings provide a structural and biophysical basis for how phosphorylation can modulate the conformational ensemble and interaction network of peptide-HLA complexes, which may help prioritize cancer-specific targets for immunotherapeutic development. - Source: PubMed
Publication date: 2026/07/23
Zhang JiahuiLv LinChen BairunYi Xinpei - Age-related skeletal muscle aging can lead to sarcopenia and is closely associated with cellular senescence and mitochondrial dysfunction. Neonatal mammalian muscle exhibits a strong regenerative capacity, and neonatal muscle extracellular vesicles (NMEVs) show therapeutic potential against skeletal muscle aging. In this study, we isolated NMEVs for the first time and found that they significantly alleviated palmitic acid (PA)-induced senescence, mitochondrial dysfunction, and lipid accumulation in C2C12 cells. , we developed a bilayer microneedle (MN) system loaded with NMEVs (NMEVs@PLGA@Fucoidan-HA MN) and applied it to aged mice. The MN effectively enhanced mitochondrial function, reduced muscle aging and fibrosis, and decreased lipid deposition. Mechanistically, miR-542-3p enriched in NMEVs directly targeted and downregulated Asxl2-PPARγ, leading to reduced lipid accumulation. At the same time, it suppressed Eef1a1 to activate the AMPK pathway, thereby improving mitochondrial function and attenuating cellular senescence. Our findings demonstrate the protective role of NMEVs delivered via an innovative MN system against muscle aging, where miR-542-3p plays a central role by concurrently targeting Eef1a1 and Asxl2 to mitigate senescence and lipid dysregulation. This study reveals a novel molecular mechanism underlying the anti-aging potential of NMEVs and offers a promising therapeutic strategy for skeletal muscle aging. - Source: PubMed
Publication date: 2026/06/13
Yuan FeifeiChen YongLi WenjieZhang LinDu RuixueXu ShengHu ZhiyuZhang TaoQin LingLu HongbinLi Chengjun - Diffuse large B-cell lymphoma (DLBCL) exhibits 30-40% rates of relapse or refractory disease after R-CHOP. Identifying patients at risk for treatment failure is essential for planning subsequent therapeutic strategies, including stem cell mobilization or cellular therapy. To identify genomic predictors in Chinese patients, we performed targeted sequencing of tumor and matched oral DNA from 147 cases. Mutations in TP53 (hazard ratio (HR) = 2.78; P = 0.002), SRP72 (HR = 2.79; P = 0.010), MYC (HR = 1.97; P = 0.033), BCL2 (HR = 2.54; P = 0.021), and ASXL2 (HR = 2.20; P = 0.048) were significantly associated with poor PFS. A five-gene mutation risk score combined with baseline lactate dehydrogenase (LDH) and bone marrow tumor cell status improved PFS prediction over the International Prognostic Index (IPI). In addition, TP53 (HR = 4.45; P = 0.003), SRP72 (HR = 4.16; P = 0.014), and MYC (HR = 2.64; P = 0.047) mutations were strongly associated with increased risk of relapse. Integrating the three-gene mutation risk score with baseline LDH showed superior ability to predict relapse compared with the IPI. Combining mutation-derived scores with clinical factors enhanced prognostic discrimination, aiding early identification of patients for stem cell or cellular therapy. - Source: PubMed
Publication date: 2026/06/03
Han ShiZhou LinghuiZheng HaiqiongZhao YiCai ZhenHe JingsongYe XiujinWu WenjunSun JieZheng WeiyanWei GuoqingYu LiWang LixinGao KeYue JuanZhang MingmingHu YongxianHuang He - The human ASXL gene family consists of ASXL1, ASXL2, and ASXL3, first described as the additional sex combs (Asx) in Drosophila. The encoded proteins scaffold BAP1-mediated histone H2A deubiquitination. ASXL genes are implicated in pre-cancerous, cancerous, and neurodevelopmental conditions. Truncating mutations predominate and were originally predicted to result in protein loss of function (LOF); however, mounting evidence from population genetics and in vitro studies supports gain-of-function (GOF) mechanisms. Sequence analysis suggests that such mechanisms require both escape from nonsense-mediated mRNA decay and removal of a putative C-terminal degron signal within ASXL proteins. We propose GOF as a generalized mechanism for ASXL mutations, resulting in increased protein stability and altered histone modifications, with implications for diagnosis and therapy for these medical conditions. - Source: PubMed
Publication date: 2026/03/31
Nakamura YujiNguyen ToanMor NofarTorio Christopher JThulaseedharan HarikrishnaDominissini DanGleeson Joseph G - Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is a leading cause of maternal and perinatal morbidity and mortality. Its early-onset form (EO-PE), requiring delivery before 34 weeks of gestation, is particularly severe and closely linked to defective trophoblast differentiation. Here, we identify BRCA1-associated protein 1 (BAP1) and its cofactors ASXL2 and ASXL3 as upregulated in EO-PE placentas. Enforced BAP1 expression in human trophoblast stem cells reinforced epithelial identity, enhanced adhesion, and impaired both extravillous trophoblast differentiation and syncytiotrophoblast formation. Integrated transcriptomic and proteomic analyses revealed suppression of lineage-specific pathways alongside maintenance of progenitor-like and pro-inflammatory signatures. In trophoblast organoids, an excess of BAP1 disrupted syncytial maturation and induced interferon-driven pathways overlapping with EO-PE transcriptomes. Together, these findings establish BAP1 as a key regulator of human trophoblast differentiation and implicate its dysregulation in the pathogenesis of EO-PE, providing mechanistic insight into the cellular basis of placental dysfunction. - Source: PubMed
Publication date: 2026/03/26
Doria-Borrell PaulaFerrero-Micó AnaNavarro-Serna SergioMellado-López MaravillasGrinat JohannaMurphy Ciara NYoussef LinaCrispi FàtimaJ Kaitu'u-Lino Tu'uhevahaPérez-García Vicente