AKT1 (phospho-Thr308) Antibody
- Known as:
- AKT1 (phosphorilated-Thr308) Antibody
- Catalog number:
- abx000352
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- AKT1 (phospho-Thr308) Antibody
Related genes to: AKT1 (phospho-Thr308) Antibody
- Gene:
- AKT1 NIH gene
- Name:
- AKT serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RAC, PKB, PRKBA, AKT
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: AKT1 (phospho-Thr308) Antibody
Related articles to: AKT1 (phospho-Thr308) Antibody
- Biomarker testing is central to precision oncology, enabling effective use of targeted therapies in hormone receptor-positive (HR+), human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (mBC). Recommendations for current and future biomarker testing and diagnostic workflows were developed using a three-step approach: pre-meeting survey, descriptive analysis, and steering committee discussion. A panel of 14 experts from Latin America, Asia Pacific, the Middle East, and Africa developed recommendations using an expert opinion-based approach without a formal consensus methodology. Recommendations with >90% agreement were considered panel recommendations. Some recommendations are expert-driven and not yet standard-of-care. High agreement was observed for biomarker testing at diagnosis for estrogen receptor (ER), progesterone receptor (PR), HER2, and BReast CAncer gene (BRCA)1/2. For endocrine-resistant patients, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) testing is recommended at diagnosis; otherwise, during or after first-line treatment. AKT serine/threonine kinase 1 (AKT1) and phosphatase and tensin homolog (PTEN) testing can occur either during first-line treatment or at progression, while estrogen receptor 1 (ESR1) testing is advised at progression. Tumor tissue (preferably from a re-biopsy) is the preferred sample for PIK3CA, AKT1, and PTEN testing; if unavailable, primary tissue or circulating tumor DNA (ctDNA) may be considered. Blood is recommended for germline BRCA1/2 or PALB2 testing, while ctDNA is preferred for ESR1 detection. Next-generation sequencing (NGS) is the preferred method for most biomarkers, with polymerase chain reaction as an alternative where NGS is unavailable; PTEN may also be assessed using immunohistochemistry. Above 90% of experts proposed future biomarker testing at diagnosis for ER, PR, HER2, germline BRCA1/2, PALB2, PIK3CA, AKT1, PTEN, mismatch repair, microsatellite instability, tumor mutational burden, and neurotrophic tyrosine receptor kinase in all patients with HR+, HER2-negative mBC. This article offers a practical guide for biomarker testing in HR+, HER2-negative mBC. - Source: PubMed
Publication date: 2026/08/16
Reinert TomásAlshehri Ahmed SShafik AmrLin Ching-HungGomez Abuin GonzaloGong GyungyubJung Kyung HaeAmat MoraPathmanathan NirmalaOw Samuel G WRivera-Rivera SamuelAggarwal ShyamLuen Stephen JYong Tay Timothy Kwang - The Xuanshi Choudong Recipe (CDR), a classic traditional Chinese medicine (TCM) formula, has long been clinically prescribed to relieve tic disorder (TD). However, its underlying in-depth mechanism remains largely unknown. - Source: PubMed
Jue HuJingying MaYaqin ChenYulu PanYanhong ChenJiaye XuDanfei ChenJian ChenXiao-Bo Xuan - Cervical cancer represents the second most prevalent malignancy among women in India and is etiologically linked to persistent infection with high-risk human papillomavirus (HPV) strains. Mesua ferrea Linn, a medicinal tree species distributed across the Eastern Himalayan region, Eastern Indian states, and the Western Ghats, has demonstrated anticancer potential in several preclinical investigations; however, its mechanistic basis in cervical cancer remains insufficiently elucidated. In this study, a network pharmacology-based workflow was employed to identify the phytochemicals of Mesua ferrea, predict key targets, analyse protein-protein interactions and construct a compound-target pathway network along with network enrichment analysis. ADMET analysis, molecular docking, and molecular dynamics simulation were used to assess the stability of key compounds relative to potential targets. 16 phytochemicals, based on drug-likeness criteria, were identified, yielding 60 common targets, including AKT1, KDR, PIK3CA, MTOR, and EGFR, which are involved in Ras, PI3K-Akt, Jak-Stat, and HPV-associated pathways. Molecular docking and molecular dynamics simulations verified the stable binding of key phytochemicals to core cervical cancer-associated proteins. Collectively, these findings indicate that Mesua ferrea Linn exerts multi-target, multi-pathway regulatory effects in cervical cancer, supporting its potential as a source of phytotherapeutic agents. The study provides a mechanistic foundation for future in vitro and in vivo validation, contributing to the rational development of plant-derived interventions for cervical cancer management. - Source: PubMed
Publication date: 2026/08/14
Gaidhane Aryan ShyamMalvika A MVasava MaheshKevlani VijayPrajapati ApurvaPatel HiteshParmar ShivaliPrakash IlakkyaBhadra K SKhandelwal RiyaParmar ChintanRani ShreyaSreelakshmi O SMore Gayathri - Tumor drug resistance and metastasis are leading causes of cancer‑related mortality, both of which are tightly governed by multiple signaling pathways. The AKT‑GSK‑3β axis is a critical regulator of tumor progression, mediating drug resistance and epithelial‑mesenchymal transition (EMT) through its downstream targets. Aberrantly activated AKT‑GSK‑3β signaling modulates the expression and degradation of the drug efflux pump P-gp, which expels chemotherapeutic agents, including paclitaxel (PTX), from cancer cells, resulting in chemotherapy failure and drug resistance. Moreover, hyperactivated AKT‑GSK‑3β signaling drives EMT, a key process closely linked to tumor metastasis and malignant progression. Dioscin (Dio), a natural steroidal saponin, exhibits significant anti‑tumor activity in multiple cancers. However, whether Dio reverses chemoresistance and inhibits tumor growth by targeting the AKT‑GSK‑3β pathway to promote P-gp degradation and suppress EMT remains elusive, which is the central focus of this study. To explore whether Dio enhances the sensitivity of drug-resistant cancer cells to PTX and inhibits cancer metastasis and the EMT process, as well as its potential mechanism(s). Paclitaxel-resistant TE-1/PTX and HeLa/PTX cells were subjected to SRB, colony formation, Rh123 accumulation, wound-healing, and Transwell assays to evaluate Dio's chemosensitizing, anti-EMT, and anti-metastatic effects. Network pharmacology, molecular docking, CETSA, and proteolysis assays verified a direct Dio-AKT1 interaction. Western blotting, Co-IP, and MG132 and MK2206 rescue experiments clarified AKT/GSK3β-dependent P-gp ubiquitin-proteasomal degradation and EMT suppression. HeLa/PTX xenograft models were generated; H&E staining and immunoblotting were used to assess tumor growth, biosafety, and intratumoral protein profiles for in vivo validation. Dio sensitized PTX-resistant cells to paclitaxel, increased intracellular Rh123 accumulation, and inhibited cell migration and invasion. Mechanistically, Dio directly bound AKT1 to suppress AKT/GSK3β signaling, promoted ubiquitin-proteasomal degradation of P-gp, and reversed EMT by upregulating epithelial markers and repressing mesenchymal markers and EMT transcription factors. In vivo, Dio restrained xenograft tumor growth with negligible systemic toxicity, and intratumoral expression patterns of AKT/GSK3β, P-gp, and EMT-related proteins mirrored in vitro findings. Dio has the potential to be a safe and effective agent for drug-resistant cancer therapy. - Source: PubMed
Zhang KeqiZhao JinzhuLi LinlinWang ZixinMao XinyiYan JieHan ShuhuaHe MingjingBi BingjieXu QiangWang Cong - Hepatic glycogen accumulation is a hallmark of glucose intolerance in carnivorous fish, yet the molecular mechanisms governing the partitioning of surplus carbohydrates remain poorly understood. This study integrated physiology and functional assays to elucidate how insulin-dependent mTOR/SREBP1 signaling governs hepatic glucose partitioning and glycogen accumulation. In the present study, we used largemouth bass (poor glucose utilization) and Nile tilapia (efficient glucose utilization) fed diets containing graded carbohydrate levels for 8 weeks. The results revealed that high-carbohydrate (HC) diets suppressed the PI3K/AKT1/mTOR axis in largemouth bass, reducing nuclear SREBP1 and causing massive hepatic glycogen accumulation. Conversely, tilapia efficiently activated this axis to promote lipid synthesis in response to excessive carbohydrates. Meanwhile, srebp1 knockdown in primary hepatocytes of largemouth bass decreased lipogenic gene expression and triglyceride content while increasing glycogen level. Mechanistic validations in largemouth bass demonstrated that insulin treatment restored AKT1/mTOR pathway activity and SREBP1 nuclear translocation, alleviating glycogen overload while promoting lipogenesis. Knockdown of akt1 or s6k1 prevented SREBP1 activation, whereas tsc2 knockdown rescued mTOR phosphorylation. Furthermore, mTOR inhibition by rapamycin abolished insulin-induced SREBP1 transactivation of lipogenic targets, mimicking the HC-induced glycogen-overload phenotype. In summary, this study identifies the insulin-responsive mTOR/SREBP1 signaling axis as the critical pathway governing lipogenesis in largemouth bass. Functional impairment of the insulin-responsive mTOR/SREBP1 signaling axis is associated with a metabolic shift favoring glycogen storage over lipogenesis, providing mechanistic insights relevant to glucose intolerance across vertebrates. - Source: PubMed
Tao JiajieChen ShiwenLiu NingGong YeZhang SenHe JiaxiongHuang XuxiongChen NaisongLi Songlin