Akt2 (Phospho_Ser474) Antibody
- Known as:
- Akt2 (Phospho_Ser474) Antibody
- Catalog number:
- E011124-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Akt2 (Phospho_Ser474) Antibody
Related genes to: Akt2 (Phospho_Ser474) Antibody
- Gene:
- AKT2 NIH gene
- Name:
- AKT serine/threonine kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-05
- Date modifiied:
- 2016-10-05
Related products to: Akt2 (Phospho_Ser474) Antibody
Related articles to: Akt2 (Phospho_Ser474) Antibody
- Breast cancer remains one of the most prevalent malignancies among women, and taxane-based chemotherapies such as paclitaxel and docetaxel are central to standard treatment regimens. However, drug resistance in breast cancer limits therapeutic efficacy and contributes to recurrence and metastasis. Identifying resistance-associated molecular targets is therefore critical for advancing treatment strategies. To investigate paclitaxel resistance, we designed and synthesized four paclitaxel-derived probes. Among these, PTX-4, constructed via a stable C─C bond linkage, exhibited superior efficiency. Using a chemoproteomic approach, we systematically profiled paclitaxel-binding proteins in parental and resistant breast cancer cells. This strategy successfully identified AKT2, an unrecognized paclitaxel-interacting protein in paclitaxel-resistant breast cancer. Functional validation demonstrated that AKT2 is a direct target of paclitaxel in paclitaxel-resistant cells. Knockdown and pharmacological inhibition of AKT2 restored the sensitivity of paclitaxel-resistant cells to paclitaxel. These findings establish AKT2 as a key mediator of paclitaxel resistance in breast cancer. Targeting AKT2 may offer a promising therapeutic strategy to overcome resistance and improve the clinical efficacy of taxane-based chemotherapy. This study highlights the advantage of C─C bond-linked, pharmacologically active probes for chemoproteomic profiling of drug targets. - Source: PubMed
Publication date: 2026/07/30
Wang KaiYuan YuqingShen WeiYang XiuxiuWu XiaokangZhou HaihuaHu YiZhu Qing - B-cell receptor (BCR) is indispensable for B-cell responses, and its signaling relies on the rearrangement of cytoskeletal proteins. Cytoskeletal protein 4.1R has been previously implicated in the regulation of immune function. However, the specific role of 4.1R in BCR-mediated B-cell activation remains unknown. Here, we performed single-cell RNA (scRNA) sequencing on splenic B cells isolated from wild-type (WT) and 4.1R-knockout (4.1R-KO) mice to systematically characterize the functional contribution of 4.1R to B-cell biology. Transcriptomic analyses suggested a critical role for 4.1R in modulating BCR signaling. Ex vivo stimulation of primary B cells with anti-IgM demonstrated that 4.1R-KO B cells exhibited marked overactivation, hyperproliferation, and enhanced antibody secretion. Furthermore, unbiased phosphoproteomic profiling, identified sustained AKT1 phosphorylation as a key feature in 4.1R-KO B cells. Subsequent functional validation confirmed that 4.1R regulates BCR signaling by constraining AKT1 activation. Mechanistically, 4.1R rapidly colocalized with the coreceptor CD19 at the plasma membrane upon BCR engagement, and co-immunoprecipitation confirmed their physical interaction. Loss of 4.1R disrupted this interaction and resulted in sustained and amplified AKT1 phosphorylation (but not AKT2) in stimulated B cells. Collectively, our findings identify 4.1R as a novel negative regulator of BCR signaling that interacts with CD19 to constrain AKT1 activation. - Source: PubMed
Publication date: 2026/07/13
Guo YuyingFan DandanLiu DenghuiShao QiSang SiyaoNiu YutingChen LixiangLiang Taotao - Wet age-related macular degeneration (wAMD), characterized by choroidal neovascularization (CNV), faces a clinical challenge of diminishing efficacy during long-term anti-VEGF monotherapy. An AI-assisted analytical framework pinpointed impaired retinal pigment epithelium (RPE) autophagy and a pro-inflammatory microenvironment driven by retinal microglia-recruited monocytes as co-conspirators in CNV progression. To tackle these dual culprits, we developed an intravitreal injectable hydrogel (Rab&BCL-M@G) that co-encapsulates ranibizumab (Rab) and a small-sized baicalin-loaded microemulsion (BCL-M), enabling controlled and sustained co-delivery of both agents to the retina for over 14 days. Guided by the AI-identified targets, we demonstrated that baicalin promoted dysfunctional mitochondria clearance via the AKT2-PGC-1α-mediated autophagic flux and suppressed monocyte recruitment by disrupting microglial CCL4 signaling. This two-pronged action ameliorated inflammation and angiogenesis, synergizing with Rab. In a laser-induced wAMD mouse model, a single intravitreal injection of Rab&BCL-M@G sustainably reduced CNV area, promoted repair, restored autophagy, and diminished microglial infiltration. Crucially, subsequent wet-lab validation confirmed a positive pathological correlation among defective autophagy, inflammation, and angiogenesis, thereby closing the loop from computational prediction to experimental verification and explaining suboptimal long-term performance after Rab monotherapy. This study proposes a promising synergistic strategy, advancing wAMD therapy through precision delivery and AI-informed mechanism discovery. - Source: PubMed
Publication date: 2026/07/27
Jiang XiYang FengqiGong HuilingMou YanfeiAn JunyiWang LeiWang XiaonaZhang ZhenzhenWei XiaoSun LiWang WenliCao FengleiZhao YangQu Ding - Orchestrating tissue regeneration in complex pathologies like post-ischemic stroke requires materials that can precisely regulate multiple signaling pathways. A central challenge is engineering a single platform integrating mechanical, electrical, and biochemical cues to redirect these pathological networks. Here, we present a computation-driven, multimodal hydrogel engineered to function as a programmable regulatory node. The system integrates a computationally screened de novo vasculogenic peptide scaffold and surface-engineered, inflammation-responsive conductive MXene nanosheets. This rational surface engineering solves the critical bottleneck of MXene instability, preserving colloidal stability for over 2 months and maintaining high conductivity (1.2 mS/cm) within the injectable system. In a mouse model of ischemic stroke, this targeted modulation reconstructed the neurovascular unit integrity, suppressed glial scarring, and promoted remyelination and synaptic repair. Crucially, the platform re-established neural electrical signal transmission, leading to the recovery of neural function. Mechanistically, machine learning-driven transcriptomics highlighted Akt2 as a candidate regulatory hub, while untargeted metabolomics, prompted by a striking hair yellowing phenotype, suggested metabolic remodeling involving the phospholipase D signaling pathway. Our findings demonstrate a promising data-driven, bottom-up rational design paradigm for advanced bioelectronic tissue repair materials. - Source: PubMed
Publication date: 2026/07/25
Wang YueGuo WenChen ZeqiMa JianwenTian FaTian ErkangLuo QiuhaoBai LongWu YuWu DongdongYang LiHu ChengWang Yunbing - Nowadays probiotics have been widely used in the fields of food, medicine and agriculture. In this study, we investigated the anti-aging effects of the probiotic strain of A21041 using . - Source: PubMed
Publication date: 2026/07/10
Meng LiliHuang LianfeiLu EnqiuChai ZhihuiLu ZhilongPang ShifuWei XinliChen ManpingXiao GuilongLin YanjinLuo Weifei