Akt2 (PKBb) monocl (clone 8B7)
- Known as:
- Akt2 (PKBb) monocl (clonality 8B7)
- Catalog number:
- ASA905-660
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Akt2 (PKBb) monocl (clone 8B7)
Related genes to: Akt2 (PKBb) monocl (clone 8B7)
- 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
- Gene:
- L3MBTL1 NIH gene
- Name:
- L3MBTL histone methyl-lysine binding protein 1
- Previous symbol:
- L3MBTL
- Synonyms:
- ZC2HC3, dJ138B7.3, DKFZp586P1522, KIAA0681
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2019-04-23
Related products to: Akt2 (PKBb) monocl (clone 8B7)
Related articles to: Akt2 (PKBb) monocl (clone 8B7)
- Vitiligo, an autoimmune skin disorder, is characterized by the loss of melanocytes, resulting in significant skin depigmentation. Ruxolitinib (RUX), which could target the JAK-STAT signaling pathway, plays a crucial role in vitiligo treatment but faces great challenges in transdermal delivery. Here, we developed RUX-laden silk fibroin nanoparticles to achieve transdermal delivery with the assistance of a CO ablative laser. In vitro assays demonstrated that the RUX-laden silk nanoparticles significantly inhibited the secretion of CXCL9 and CXCL10, and the phosphorylation of AKT2 and STAT3, indicating effective modulation of the JAK-STAT pathway. The RUX-laden silk nanoparticles exhibited excellent transdermal delivery capacity comparable to the Opzelura cream, which was further improved through a laser-assisted strategy. In vivo studies revealed that the transdermally delivered RUX-laden nanoparticles exhibited better skin toleration and significantly reduced the expression of multiple inflammatory cytokines such as CXCL9, CXCL10, IFN-γ and TNF-α, bringing substantial melanocyte recovery. The findings underscore the potential of silk-based delivery systems in enhancing therapeutic efficacy against vitiligo, which would improve pigmentation restoration and inflammation modulation in skin disorders. - Source: PubMed
Publication date: 2026/04/24
Wang XueWang QiruiYang YanSong DaweiXiao LiyingZhang ZhenLu Qiang - Gastrointestinal stromal tumors (GIST) can become malignant upon recurrence and metastasis, yet no drugs specifically target these processes. This study explores the effectiveness and mechanism of paeoniflorin in treating GIST. Initially, the impact of paeoniflorin on the viability, proliferation, and migration of GIST cell lines (GIST-T1 and GIST-882) was assessed using CCK-8, transwell, and wound healing assays at low (5 μM) and high (20 μM) concentrations. Subsequently, datasets GSE136755 and GSE21315 were analyzed to identify potential therapeutic targets for inhibiting GIST transfer. Key genes and pathways related to Paeoniflorin's anti-GIST effects were identified through molecular docking and Western blotting. Paeoniflorin influenced cell viability, proliferation, and migration in GIST-T1 and GIST-882 cell lines at low (5 μM) and high (20 μM) concentrations. We identified 761 differentially expressed genes (DEGs) and selected 50 hub genes using a PPI network. By screening paeoniflorin's potential targets, we identified eight key genes (CYP1A2, CYP2C9, CYP3A4, F2, ICAM1, NR1H4, PLG, and SERPINE1) that were significantly elevated in metastatic GIST samples. CYP3A4 was confirmed as a target of Paeoniflorin in GIST treatment through molecular docking and Western blotting. Pan-cancer analysis showed CYP3A4's enrichment in the tight junction pathway and a significant negative correlation with AKT2 protein. Paeoniflorin treatment led to high AKT2 expression in the tight junction pathway in GIST cell lines. Paeoniflorin acts on the CYP3A4 protein to affect the tight junction pathway, inhibiting the malignant metastasis of GIST. - Source: PubMed
Publication date: 2026/04/23
Cui DapengCui ZeyinLi YansenFan ShuangLi LeiYang ChengYu RuixiaCui JiaxinFu RunjiaFei Jiandong - Tributyl citrate (TBC), a widely used substitute for phthalate plasticizers, has shown increasing environmental accumulation, raising concerns about its potential human health risks. However, its toxicological effects, particularly regarding gastrointestinal disease progression, remain largely unexplored. In this study, animal experiments first demonstrated that TBC aggravates colonic inflammation in a mouse model of microplastic-induced colitis. Computational toxicology analysis further predicted TBC to possess potential carcinogenic properties, suggesting its role in promoting colitis-associated carcinogenesis. Using integrated bioinformatics approaches, we combined network toxicology, molecular docking, and molecular dynamics simulations to identify the putative toxicological targets and molecular pathways involved in TBC-induced inflammation-to-cancer transition. A total of 299 TBC-related targets were identified from multilevel databases, and 13 core targets were highlighted through STRING and Cytoscape analyses, including AKT2, MAPK1, MAPK3, HSP90AA1, PIK3CD, BCL2, PIK3R1, PIK3CB, ESR1, CASP3, KRAS, and ERBB2. GO and KEGG enrichment analyses indicated that TBC may drive carcinogenic progression via pathways associated with oxidative stress and inflammatory responses. Molecular docking and dynamics simulations validated the stable interactions between TBC and key targets. To further confirm TBC's role in colitis-associated tumorigenesis, we employed an AOM/DSS-induced colorectal cancer mouse model and found that TBC significantly exacerbated both intestinal inflammation and tumor formation. Transcriptomic analysis further validated the enrichment of ROS-mediated chemical carcinogenesis pathways and revealed that intestinal barrier disruption may also be a critical contributor to TBC-mediated cancer progression. Collectively, this study provides a theoretical basis for understanding the molecular mechanisms by which TBC aggravates inflammation-associated colorectal cancer, and offers a framework for risk assessment and regulatory strategies addressing plasticizer exposure in digestive health. - Source: PubMed
Publication date: 2025/10/08
Chen HaosongCheng YixianZhou YaoFu RuiJia JianguangZhang ShuyuanChen JunjieCao HaikunZhang PengGeng QilongGu JinghuaChen BoHan WenxiuXiong MaomingLi TingCao Guodong - Herpes simplex virus 1 (HSV-1) infection contributes to immunopathogenic diseases and lacks an effective vaccine. Improving antigen presentation is key to better vaccine strategies and more robust immune responses. Here, we show that optineurin (OPTN), an autophagy receptor traditionally involved in protein recycling, unexpectedly stabilizes RICTOR (mechanistic target of rapamycin complex 2 [mTORC2]), a crucial step in enhancing MHC class II surface expression in dendritic cells. OPTN regulates the AKT/mTOR/signal transducer and activator of transcription 3 (STAT3) pathway, with the AKT2 isoform playing a central role. Using single-cell RNA sequencing (scRNA-seq) and transgenic mouse models, we identify the mechanistic details of this pathway. Dysregulation impairs antigen presentation, weakening immunity and vaccine efficacy. Our findings uncover a previously unknown function of OPTN and highlight its role in coordinating innate and adaptive immune defenses, with implications for vaccine development and immune response modulation in HSV-1 and other viral and bacterial diseases. - Source: PubMed
Publication date: 2026/04/16
Kadam RashmiPatil ChandrashekharFeferman LeonidMaienschein-Cline MarkChlipala GeorgeBorole PiyushBhattacharya IlinaOrameh ChimaNyugen TaraTseng HenryShukla Deepak - Glioma, the most common primary intracranial tumor, exhibits high recurrence and mortality rates. Ginsenoside-Rh2 (GS-Rh2), an active compound from , has shown anti-tumor potential. Gab2, a tyrosine kinase substrate, is implicated in glioma pathogenesis; however, the mechanism by which GS-Rh2 might inhibit glioma cell migration and invasion via the Gab2/Akt2 pathway remains unexplored. - Source: PubMed
Publication date: 2026/04/01
Sun WeiLi RuifangWang LinjuanHan WenjieLi JiakeXu ShuangliSun Xiuning