AKT2 Antibody (C_term) Blocking Peptide
- Known as:
- AKT2 Antibody (C_term) Blocking Peptide
- Catalog number:
- BP7029b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AKT2 Antibody (C_term) Blocking Peptide
Related genes to: AKT2 Antibody (C_term) Blocking Peptide
- 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 Antibody (C_term) Blocking Peptide
Related articles to: AKT2 Antibody (C_term) Blocking Peptide
- Collagen is a major extracellular matrix component, and soy protein has been reported to influence cellular and immune-related processes. Nanofiber scaffolds incorporating collagen and soy protein isolate (SPI) may provide a platform for modulating cell-material interactions in neural systems. In this study, we fabricated electrospun nanofibers composed of collagen (CO), SPI, and polycaprolactone (PCL) and investigated the cellular and transcriptional responses of human astrocytes to these scaffolds in vitro. The nanofibers were characterized by scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, and contact angle analysis. Human fetal astrocytes exhibited high viability on all nanofiber scaffolds. Flow cytometry analysis indicated that incorporation of SPI into CO/PCL nanofibers did not alter cell cycle distribution. Aligned nanofibers provided directional guidance for astrocyte migration. RNA-sequencing analysis revealed enrichment of the "neurodegeneration" and "antigen processing and presentation" pathways among the down-regulated genes in cells on CO/SPI/PCL fibers compared with CO/PCL fibers. Down-regulated genes in these pathways include IL1B, IL6, HLA-B, HLA-DMB, HLA-DPA1, and HLA-DRA. The "focal adhesion" pathway is enriched among up-regulated genes, which include COL4A1, COL4A2, FN1, LAMB1, LAMB2, AKT2, RAC1, RAC2, ROCK2, and PIP5K1A. These results demonstrate that incorporation of SPI into collagen-based nanofibers modulates astrocyte migration and gene expression profiles associated with focal adhesion and immune-related pathways, providing a foundation for further investigation of SPI-containing biomaterials in neural tissue engineering applications. - Source: PubMed
Publication date: 2026/08/14
Yao LiBustamante-Fuchs KarenCantu KaylaShippy Teresa - Fish oogonial stem cells (OSCs) are vital for fish reproduction research and germplasm conservation, yet stable long-term in vitro culture of fish OSCs remains a major technical bottleneck. Herein, we established an efficient in vitro culture system (termed L15SP) for OSCs derived from Paralichthys olivaceus, consisting of L-15 medium supplemented with15% fetal bovine serum (FBS), 2 μg/L basic fibroblast growth factor (bFGF), 2 μg/L leukemia inhibitory factor (LIF), 50 μmol/L β-mercaptoethanol (β-ME), 1% fish serum, and 18 g/L embryo extract protein, cultured at 23 °C. This system enabled stable long-term passage of P. olivaceus OSCs. Further investigations revealed that interferon-induced transmembrane protein 3 (Ifitm3) was highly expressed on the membrane of P. olivaceus OSCs. Functional assays demonstrated that Ifitm3 significantly enhanced proliferation, migration, and stemness maintenance of long-term cultured OSCs. Ifitm3 positively modulated the expression of key PI3K-AKT signaling components, including pik3cb, pik3r1, and akt2, to regulate downstream OSC functional genes. Upon pathway activation, Ifitm3 facilitated PIP3 enrichment at the OSC plasma membrane, thereby amplifying PI3K-AKT signaling. In conclusion, Ifitm3 governed OSC biological functions by potentiating PI3K-AKT signal transduction. This study establishes a reliable long-term culture system for fish OSCs and identifies a novel functional marker for OSC identification, providing valuable support for fish germplasm preservation and genetic breeding. - Source: PubMed
Publication date: 2026/08/13
Ren YuqinYang YucongWang GuixingHan ZengshengHe NuanWang XiyuanZhang YitongHe ZiyangCui XiaodongHe ZhongweiLiu YufengCao WeiZhang XiaoyanWang YufenKang XianjiangHou Jilun - 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