AKT2 Antibody (N_term)
- Known as:
- AKT2 Antibody (N_term)
- Catalog number:
- AP7029a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AKT2 Antibody (N_term)
Related genes to: AKT2 Antibody (N_term)
- 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 (N_term)
Related articles to: AKT2 Antibody (N_term)
- SET domain-containing 2 (SETD2) mediated H3K36me3 plays a pivotal role in maternal epigenetic regulation; however, its function during in vitro fertilization (IVF) remains largely unexplored. This study investigated the impact of SETD2 inhibition on yak oocyte fertilization competence. Pharmacological inhibition of SETD2 using EZM0414 significantly increased ROS levels and reduced GSH levels in yak oocytes. In parallel, it decreased the second polar body extrusion rate, increased zona pellucida thickness, and downregulated essential genes associated with sperm-oocyte interaction and oocyte activation (Zp2, Zp3, Zp4, Tle6, Wee2, Patl2). Further transcriptomic analysis of mature oocytes and fertilized zygotes using Smart-seq2 revealed that the differentially expressed genes between mature oocytes and zygotes were significantly enriched in the PI3K/AKT signaling pathway. Key survival-related genes (Pik3r1, Pik3c2b, Akt1, Akt2, Creb5, Mcl1) were markedly upregulated in zygotes, indicating activation of PI3K/AKT during fertilization. SETD2 inhibition also suppressed PI3K/AKT pathway activity at both mRNA and protein levels. Furthermore, SETD2 inhibition shifted the apoptotic balance by decreasing BCL2, increasing BAX and Caspase-3, and elevating TUNEL-positive signals in both oocytes and zygotes. Inhibition of SETD2 suppressed H3K36me3 expression in yak oocytes and zygotes. Finally, we found that inhibition of SETD2 significantly increased the rate of early embryonic arrest while reducing the blastocyst formation rate. Collectively, these findings demonstrate that SETD2 is essential for maintaining PI3K/AKT signaling, preventing apoptosis, and preserving fertilization competence in yak oocytes. This work provides new mechanistic insight into the epigenetic regulation of fertilization and offers a potential strategy for improving assisted reproductive efficiency in livestock. - Source: PubMed
Publication date: 2026/05/05
Zuo QiyongZhang HuiZhong DonglanLi TianhaoLiao YuejiaoPan YangyangYu SijiuCui Yan - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - To investigate the effect of Licochalcone A (Lico A) on the function of CD8 T cells in the tumor microenvironment and its underlying mechanism, and to evaluate its role in enhancing the anti-tumor activity of CD8 T cells. - Source: PubMed
Publication date: 2026/05/12
Han PingpingWang HuaiyuCai YunSun YeZhou Dongzhi - High protein diets (HPD), rich in branched-chain amino acids (BCAAs), are proposed to enhance glycemic control. The metabolic implications of elevated BCAAs in insulin resistance (IR) are unclear, but overactivation of ribosomal protein S6 kinase B1 (S6K1)-related signaling pathway may contribute to IR. - Source: PubMed
Publication date: 2026/01/28
Ancu OanaHauge-Evans Astrid CDraicchio FulviaNeculescu Diana-ElenaRogers RalphBurd Nicholas APfeiffer Andreas F HWeickert Martin OHurren Nicholas MMackenzie Richard W A - Triple-negative breast cancer (TNBC) is characterized by hypoxia and impaired fidelity to DNA repair and the activation of survival pathways. However, the role of specific AKT isoforms, particularly AKT2, in regulating residual homologous recombination (HR) activity and PARP inhibitor sensitivity under hypoxic stress remains unclear. This study aimed to establish the effect of AKT2 on hypoxia-induced defects in HR repair, DNA damage accretion, and therapeutic outcomes of PARP inhibition in TNBC. TNBC cells were cultured under chronic hypoxia (1% O) or normoxia. Western blotting was used to measure protein expression and activation of HR- and hypoxia-related markers, including, pAKT (Ser473), RAD51, BRCA1, γH2AX, HIF-1α, and CHK1/CHK2. Immunofluorescence was used to assess the presence of RAD51 foci following 4 Gy of irradiation as a functional measure of HR activity. A cell viability assay was used to determine the sensitivity to olaparib. In vitro findings were confirmed in orthotopic xenograft models with stable AKT2 knockdown. Hypoxia in tumors was measured through pimonidazole staining and HIF-1α expression. Hypoxia increases HIF-1α expression and activates AKT signaling. In our model, chronic hypoxia suppressed RAD51, p-BRCA1, and checkpoint signaling, whereas total BRCA1 did not change and RAD51 foci decreased, indicating impaired and context-dependent disruption of HR. Only AKT2 silencing reduced RAD51 and p-BRCA1 under hypoxia, indicating an isoform-specific role for AKT2 in HR maintenance. In AKT2-deficient hypoxic cells, there was accumulation of persistent γH2AX and a corresponding repair defect. Functionally, AKT2 loss significantly enhanced olaparib sensitivity, resulting in marked RAD51 loss, robust γH2AX accumulation, and decreased viability. Knockdown of AKT2 in vivo increased the efficacy of olaparib, decreasing tumor weight and hypoxia and increasing the extent of DNA damage and suppression of HR markers, demonstrating a synergistic disruption of hypoxia-driven survival pathways. AKT2 plays a vital role in the regulation of the HR repair and hypoxia-driven survival in TNBC. Although hypoxia impaired HR through suppression of RAD51, p-BRCA1, and checkpoint signaling, AKT2 preserved residual HR activity required for tumor cell survival under hypoxic stress. Its loss disrupts HR components, enhances sustained DNA damage, inhibits tumor hypoxia and sensitizes hypoxic tumors dramatically to PARP inhibition. These findings support a mechanistic model in which AKT2 enables hypoxic TNBC cells to tolerate HR dysfunction and survive genotoxic stress, thereby contributing to therapeutic resistance. These results establish AKT2 as a therapeutic target to counteract resistance in hypoxia and increase the efficacy of PARP inhibitors in TNBC. Although AKT2-selective inhibitors have been reported, they remain largely preclinical. Accordingly, our findings support AKT2 as a promising therapeutic target and warrant further validation using AKT2-selective pharmacologic inhibition. - Source: PubMed
Liang YingKong DeyuZhang YiZhao ZhijingLv LiYin ZheAhmad AjazJiang Zongye