AKT2 Antibody
- Known as:
- AKT2 Antibody
- Catalog number:
- abx000688
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- AKT2 Antibody
Related genes to: AKT2 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 Antibody
Related articles to: AKT2 Antibody
- : Uterine dysfunction contributes to infertility in PCOS. Jiawei Qi Gong Wan (JQGW) is used to improve endometrial homeostasis, but its mechanism is unclear. This study investigated whether JQGW improves uterine function via gut microbiota and metabolites. : Letrozole-induced PCOS mice received JQGW (low/high dose), metformin, or vehicle for 35 days. Endometrial morphology, receptivity genes, Akt2/NF-κB signaling, gut microbiota (16S rRNA), and serum metabolites (LC-MS) were assessed. : PCOS mice showed reduced endometrial thickness (126.4 ± 10.8 μm vs. 215.6 ± 12.3 μm in controls, < 0.001) and fewer glands (12.6 ± 1.8 vs. 28.4 ± 2.1, < 0.001). JQGW-H increased endometrial thickness (189.3 ± 11.2 μm, < 0.01 vs. PCOS) and gland number (23.1 ± 1.9, < 0.01 vs. PCOS), restored the receptivity markers (, , , and ) toward normal levels, suppressed Akt2/NF-κB activation, and reduced inflammatory cytokines. JQGW shifted the β-diversity structure of the gut microbiota toward the control pattern, with enrichment (LDA > 4). Four metabolites (PA(20:0/16:1(9Z)), 7-methylguanosine, methoxyacetic acid, 8.11-eicosadiynoic acid) showed nominal elevation in PCOS and negative correlations with endometrial thickness (r = -0.73 to -0.89, unadjusted < 0.01), although none survived FDR correction. : JQGW ameliorates PCOS-associated uterine dysfunction, potentially via gut microbiota and metabolite modulation. Future studies should validate causality using fertility-based outcomes and microbiota transplantation. - Source: PubMed
Publication date: 2026/07/24
Zheng RuqunSong JinlongLi JieShen YingyanLiu QiqiShi MengjiaZhuo YuxuanLuo HaoyuLi JingMa HongxiaHu MinWang Chi ChiuLi Juan - Guizhou cattle are important indigenous bovine genetic resources for regional beef production and germplasm conservation. This study characterized the transcriptome-wide N6-methyladenosine (m6A) enrichment landscape in longissimus dorsi muscle from three representative indigenous Guizhou cattle breeds-, , and -and compared these profiles with those of cattle as a commercial reference. MeRIP-seq was used to detect group-level m6A-enriched regions and regions with differential m6A enrichment, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and database-inferred protein-protein interaction analyses. qRT-PCR was used to examine transcript abundance of selected network-prioritized candidate genes, rather than to validate m6A enrichment. MeRIP-seq detected 17,659, 19,530, 17,501, and 16,271 m6A-enriched regions in GL, WC, WN, and XM cattle, respectively. Compared with XM cattle, 2822, 5914, and 3655 regions with differential m6A enrichment were detected in GL, WC, and WN cattle, respectively. , and were prioritized for follow-up, and qRT-PCR showed breed-associated differences in their transcript abundance. These exploratory findings provide an epitranscriptomic resource and candidate targets for future MeRIP-qPCR, phenotypic, and functional studies. - Source: PubMed
Publication date: 2026/07/29
Wu JundaHuang QingyunWang XinWei XiaopingYu BoYang RongXu LongxinZhu Yongcai - Ceritinib, an anaplastic lymphoma kinase (ALK) inhibitor, is associated with cardiovascular adverse events, yet the mechanisms remain incompletely understood. Here, we show that ceritinib impairs left ventricular systolic function in mice and induces cardiomyocyte apoptosis, and identify AKT (Ser473) suppression as a key initiating event. Loss of AKT activity is paralleled by reduced phosphorylation of mTOR (Ser2448) and ULK1 (Ser757), consistent with enhanced autophagy initiation. Concurrently, loss of inhibitory GSK3β (Ser9) phosphorylation correlates with impaired lysosomal function, reflected by disrupted cathepsin D maturation and reduced lysosomal acidification. This mismatch between enhanced autophagy initiation and impaired lysosomal clearance impairs autophagic flux despite preserved autophagosome-lysosome fusion, and causes mitochondrial damage, evidenced by reduced TOMM20 and HSP60 expression and membrane potential loss. Transcriptomic and functional analyses identify AKT2 as a particularly vulnerable isoform in this network. Metformin co-treatment preserves cardiac function and attenuates apoptosis. Mechanistically, metformin increases AMPK (Thr172) phosphorylation and reduces TFEB (Ser122) phosphorylation, restores CTSD maturation, and decreases LC3-II accumulation. These protective effects occur without reversing the suppressed AKT (Ser473) or GSK3β (Ser9) phosphorylation. Together, these findings establish that AKT suppression drives ceritinib cardiotoxicity through autophagic flux impairment and mitochondrial injury, and position AMPK-driven, TFEB-associated lysosomal restoration as a mechanism-based cardioprotective strategy independent of AKT recovery. - Source: PubMed
Publication date: 2026/08/21
Jiang FengFu Huang-XiWang LanPan Ze-ZhengJiang Yan-QiLiu NingChen Xue-QinGao Zi-ZhengWu Wen-TongYan HaoYang Xiao-ChunYang BoHe Qiao-JunLuo Pei-HuaXu Zhi-Fei - Primary liver cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), arise from the neoplastic transformation of hepatocytes and cholangiocytes, respectively. Loss or downregulation of PTEN, a tumor suppressor negatively regulating the PI3K/AKT pathway, is frequently observed in CCA and HCC. Notably, PTEN mutations are observed at nearly twice the frequency in combined CCA-HCC tumors than either HCC or CCA alone. Using lineage-specific liver-targeted PTEN-deficient mouse models, we demonstrate that PTEN loss drives cellular dedifferentiation and tumorigenesis, a process that is critically dependent on AKT2. Mechanistically, PTEN deficiency induces activation of NOTCH and upregulation of transcriptional factor SOX9, which plays a central role in tumor cell transformation. In parallel, PTEN loss increases SMAD4 expression and sensitizes the tumor cells to TGFβ signaling, with TGFβ treatment repressing SOX9 expression in tumor cells lacking PTEN. Together, our study defined a critical role for PTEN-AKT2 signaling in maintaining liver epithelial lineage fidelity and revealed how its disruption promotes the conversion of mature hepatocytes or cholangiocytes into liver cancer stem-like cells (LCSCs). Furthermore, we identify a PTEN-dependent crosstalk between NOTCH and TGFβ pathways that governs liver tumor development. Together, this work provides mechanistic insight into lineage plasticity in liver cancer with implications for pathway-directed therapy. - Source: PubMed
Publication date: 2026/08/20
Tang QiSlarve IelyzavetaChen JingyuZeng NiGu YiweiHe LinaHu ShunanAlhousari DialaXu ZifeiHua BrittneyZhang GuoNguyen PhillipAlba MarioBharadwaj AjayLee JihyeonKreimer SimionXu JianJi BaoanLu Shelly CVan Eyk JenniferChopra ShefaliKanel GaryYuan LiyunStiles Bangyan L - Metastasis significantly contributes to cancer-related mortality and therapeutic failure. Cancer cells acquire metastatic potential by losing epithelial characteristics and gaining mesenchymal properties through the epithelial-mesenchymal transition (EMT). Differential poly(A) site (PAS) usage, known as alternative polyadenylation (APA), generates mRNA isoforms differing in coding sequence, subcellular localization, stability, or translation efficiency. In cancer, 3'UTR shortening increases expression of proto-oncogenes by escaping miRNA-mediated repression. High expression of CPSF73, which cleaves mRNA precursors at PASs, is associated with unfavorable prognoses in cancer patients. However, the role of APA in regulating EMT remains poorly understood. - Source: PubMed
Publication date: 2026/08/05
Naseri MarziehLiu HuiyunWang LuyangMostafa Salwa MohdRanaei Pirmardan EhsanTian BinMoore Claire L