AKT2 Antibody
- Known as:
- AKT2 Antibody
- Catalog number:
- 48-432
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- 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
- Although Angiotensin-(1-7) [Ang-(1-7)], a non-classical peptide of the renin-angiotensin system (RAS), is widely recognized for alleviating cardiovascular stress through activation of the Mas receptor. we identified a largely Mas receptor-independent pathway that expands its therapeutic potential in cardiac diseases. Our study demonstrated that Ang-(1-7) stimulated cardiomyocytes to release small extracellular vesicles (sEV), which exhibit enhanced cardioprotective effects compared with Ang-(1-7) administration alone. In both wild-type C57BL/6J mice and cardiac-specific Mas receptor knockout (cMas-KO) mice subjected to myocardial ischemia/reperfusion injury (MIRI), we found that enriched sEV preserved cardiac function by attenuating cardiomyocyte apoptosis and oxidative stress following MIRI. These protective effects remained evident even when Mas receptor signaling was pharmacologically inhibited or genetically ablated. Moreover, in wild-type mice with MIRI, enriched sEV provided significantly greater therapeutic efficacy in improving cardiac function than direct administration of Ang-(1-7). In AC16 human cardiomyocytes subjected to hypoxia/reoxygenation (H/R), enriched sEV enhanced Akt2 phosphorylation, increased sarco/endoplasmic reticulum Ca-ATPase (SERCA) activity, maintained calcium homeostasis, suppressed endoplasmic reticulum stress signaling (CHOP and p-JNK), and protected AC16 cells against H/R-induced apoptosis. sEV also attenuated oxidative stress under these conditions. Importantly, the protective effects of sEV remained after Mas receptor knockdown. Separately, Akt2 knockdown (Akt2KD) substantially weakened these benefits. These findings identify sEV as an promising therapeutic candidate, offering an effective, largely Mas-independent mechanism to combat MIRI with cardiomyocyte protection. - Source: PubMed
Publication date: 2026/08/28
Wu YalinWang XinZhao JianliYang HuiyuZhang WenjingYao ZhongSun YaoWang YajingLiang BinYang Zhiming - Akt1 and Akt2 isoforms reveal distinct immune-regulatory roles in HSV-1 pathogenesis. Akt3 is a developmentally important protein, and mutations in Akt3 gene are associated with a wide spectrum of developmental disorders, including extreme megalencephaly; however, its role in corneal homeostasis and pathologies remains poorly understood. Here we investigated the role of Akt3 in HSV-1 infection. - Source: PubMed
Publication date: 2026/08/12
Kadam RashmiPatil Chandrashekhar DBorase HemantRahangdale RakeshVolety IpsitaAkinsiku SoromidayoShukla Deepak - : 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