AKT1 & SRC Protein Protein Interaction Antibody Pair
- Known as:
- AKT1 & SRC Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0453
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AKT1 & SRC Protein Interaction Antibody Pair
Related genes to: AKT1 & SRC Protein Protein Interaction Antibody Pair
- 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 & SRC Protein Protein Interaction Antibody Pair
Related articles to: AKT1 & SRC Protein Protein Interaction Antibody Pair
- Agri-food waste is an underutilized source of valuable bioactive compounds. In this study, olive leaf pruning residues ( L. Soury) were used for the green synthesis of zinc oxide nanoparticles (OL-ZnONPs) as a natural reducing and stabilizing agent. Physicochemical characterization showed that the OL-ZnONPs had a hexagonal wurtzite structure, a crystallite size of approximately 15.5 nm, 82.8% crystallinity, and a zeta potential of -23.7 mV. TEM and SEM-EDX analyses revealed aggregated spherical particles with sizes of 4.15 ± 1.23 nm and 0.192 ± 0.067 µm, respectively, with zinc and oxygen accounting for 75.29% and 24.71%, respectively. LC-ESI-MS/MS-MRM analysis identified and quantified 11 phenolic compounds, with rutin (354.15 µg g), 3,4-dihydroxybenzoic acid (78.21 µg g), and quercetin (45.75 µg g) being the most abundant. OL-ZnONPs showed cytotoxic activity against HepG-2, MDA-MB-231, and HCT-116 cells, with the greatest selectivity toward HepG-2 cells (IC = 0.344 µg mL; SI = 5.279), compared with crude extract and 5-FU. OL-ZnONPs treatment increased intracellular levels of total caspase-3 and caspase-9, reduced TNF-α and IL-6 levels, induced nuclear changes consistent with apoptosis, and reduced HepG-2 cell migration. Network pharmacology was performed using the selected phenolic compounds together with ZnO to explore potential molecular mechanisms associated with the anti-hepatocellular carcinoma (HCC). A total of 801 anti-HCC-HepG-2 targets were predicted including AKT1, TP53, TNF, and IL6, CASP3 as hub genes in protein-protein interaction. The compound-target-pathway network identified quercetin, 3,4-dihydroxybenzoic acid, and ferulic acid as hub compounds. KEGG and GO enrichment analyses highlighted pathways in cancer, apoptosis, PI3K-Akt signaling, and chemical carcinogenesis-reactive oxygen species, providing exploratory mechanistic context for the experimental findings. Molecular docking predicted favorable binding of rutin and quercetin to AKT1. Collectively, these findings highlight the potential of OL-ZnONPs as an anticancer nanomaterial, particularly against HepG-2 cells, while supporting the valorization of olive leaf pruning residues aligns with the 2030 UN Sustainable Development Goal 3 (Good Health), SDG-9 (Industry/Innovation), SDG-12 (Responsible Consumption/Production), and SDG-13 (Climate Action). Further studies are required to clarify the contribution of the ZnO core and associated phytochemicals using size-matched bare ZnONPs, alongside evaluation of efficacy, biosafety, and pharmacokinetics. - Source: PubMed
Publication date: 2026/10/06
Mohamaden Yasmin MounirEl-Hawary Seham SEl-Fakharany Esmail MEl-Maradny Yousra AEl Raey MohamedEl Senousy Amira SafwatRabeh Mohamed AAl-Zaid Mohammad DBassam Samar M - Acetaminophen (APAP) overdose induces systemic oxidative and inflammatory responses, yet its effects on splenic homeostasis remain poorly characterized. We investigated whether prophylactic Viburnum opulus L. protects against APAP-induced splenic injury and the molecular pathways potentially underlying this protection. Forty female Wistar rats were allocated to control, APAP, N-acetylcysteine (NAC), V. opulus 100 (VO-100), and 300 mg/kg (VO-300) groups. NAC or V. opulus was administered orally for seven days, followed by a single oral APAP dose of 3 g/kg. Splenic histomorphology and immunohistochemical expression of cleaved Caspase-3, Ki-67, NF-κB, iNOS, SOD1, NRF2, and GPX4 were evaluated; network pharmacology and independent splenic transcriptomic analyses contextualized the experimental findings. APAP disrupted white- and red-pulp organization, induced lymphoid depletion, follicular disorganization, congestion, and sinusoidal dilatation, and significantly altered all seven markers, increasing cleaved Caspase-3, NF-κB, and iNOS immunoreactivity while reducing Ki-67, SOD1, and NRF2. GPX4 also decreased, but the control-APAP comparison lost significance after multiple-testing correction. VO-300 markedly attenuated the histomorphological alterations, reduced inflammatory and apoptosis-associated marker expression, and increased proliferative and antioxidant markers toward control levels. Network pharmacology identified 44 shared targets between major V. opulus constituents and APAP-toxicity-associated genes, with AKT1, NFKB1, PTGS2, and STAT3 as key hub proteins linked to oxidative-stress, apoptotic, and NF-κB-related pathways; 28 of these targets were confirmed in independent spleen transcriptomic data. Prophylactic V. opulus, particularly at 300 mg/kg, therefore, limits APAP-induced splenic injury by preserving tissue architecture, proliferative activity, and antioxidant defenses while attenuating inflammatory and apoptosis-associated responses. - Source: PubMed
Publication date: 2026/10/07
Birinci BuseAlis NevruzOnguncan OnurSeyidoglu NilayGuler Sabire - This study investigated the immunotoxic effects of chronic waterborne chlorpyrifos (CPO) exposure in Nile tilapia (Oreochromis niloticus) and evaluated the protective efficacy of dietary cinnamaldehyde (CA). Fish were exposed to 15 μg/L CPO for 60 days, while CIN was incorporated into the diet at 0.42 g/kg feed. Immune function was comprehensively assessed through hematological profiling, serum innate immune responses, splenic oxidative stress and apoptotic biomarkers, expression of immune- and cell survival-related genes, and histopathological examination of the spleen. Chronic CPO exposure caused marked hematological disturbances, characterized by significant reductions in erythrocyte count, hematocrit, hemoglobin concentration, and platelet count, together with pronounced leukocytosis and alterations in differential leukocyte populations. Moreover, CPO significantly suppressed innate immune responses, as proved by decreased serum lysozyme activity and nitric oxide production. Splenic oxidative injury was confirmed by elevated malondialdehyde, accompanied by marked depletion of reduced glutathione, catalase, and superoxide dismutase. At the molecular level, CPO markedly dysregulated the expression of akt-1, mtor, becn-1, jnk, bcl-2, and caspase-3. Histopathological examination further revealed severe splenic lesions, including lymphoid depletion, melanomacrophage center activation, vascular congestion, and disruption of normal splenic architecture. In contrast, dietary CA markedly alleviated CPO-induced immunotoxicity by restoring hematological indices, enhancing innate immune responses, reinforcing antioxidant defenses, and normalizing the expression of akt-1, mtor, becn-1, jnk, caspase-3, and bcl-2 toward physiological levels. Histological observations corroborated these biochemical and molecular findings, demonstrating substantial preservation of splenic architecture in CA-treated fish. Collectively, these findings indicate that dietary CA effectively protects Nile tilapia against CPO-induced immunotoxicity through enhancement of antioxidant capacity, restoration of innate immune competence, inhibition of apoptosis, modulation of autophagy, and regulation of the AKT/mTOR signaling pathway. - Source: PubMed
Publication date: 2026/10/06
Abd-Elhakim Yasmina MIbrahim Rowida EKhamis TarekAlsubaie NawalAlotaibi Badriyah SAbdel-Rahman Mohamed Amany - Calmodulin-binding transcription activators (CAMTAs) are key components of calcium-mediated regulation of diverse developmental and stress-responsive processes in plants. Although the functions of several Arabidopsis CAMTA family members have been investigated, the role of CAMTA4 remained largely unexplored. In the present study, we demonstrate that CAMTA4 acts as a negative regulator of salinity tolerance. Integrated physiological, transcriptomic, metabolomic and small RNA analyses revealed that camta4 mutants exhibit reduced membrane damage, lower Na and reactive oxygen species (ROS) accumulation, and extensive transcriptional reprogramming under salt stress. Reduced Na accumulation appears to result primarily from enhanced SOS1-mediated Na exclusion and attenuated induction of HKT1;1. While stable levels of AKT1 accompanied with elevated levels of TPK1 suggests complementary mechanisms to maintain cellular Na/K homeostasis by preferential mobilization of vacuolar K reserves. Lower ROS levels were associated with differential expression of CAT2 and CAT3, together with increased accumulation of proline, glutamine and lysine, indicating coordinated regulation of antioxidant defence and osmo-protective metabolism. In addition, CAMTA4 substantially reshaped the sRNA landscape by regulating conserved salinity-responsive miRNA modules, including miR156-SPL9, miR169-NF-YA and miR408-LAC thereby extending its regulatory influence into post-transcriptional gene regulation. Although CAMTA3/4/6 have all been implicated in salinity responses, their mechanisms appear to be distinct. Unlike the pleiotropic camta3, camta4 mutants exhibited no obvious developmental abnormalities under normal growth conditions, suggesting that CAMTA4 has evolved a specialized regulatory niche. The apparent absence of major developmental defects also identifies CAMTA4 as a promising target for engineering salinity tolerance with minimal pleiotropic effects. - Source: PubMed
Publication date: 2026/10/02
Chithung Tonu AngailaKansal ShivaniRaghuvanshi UtkarshDabral SwetaXavier AleenaGhosh DebasishMathur SaloniRaghuvanshi Saurabh - Black Sesame Seeds (BSS) are consumed as an edible herbal food with medicinal food homology and possess potent antioxidant properties; however, their metabolic compositions and corresponding antioxidant efficacies substantially vary across different geographical origins. This study investigates the underlying multi-component and multi-target antioxidant mechanisms of BSS from various geographical origins. An integrated computational and experimental approach combining UHPLC-Q-Exactive Orbitrap MS/MS-based metabolomics, network pharmacology, and molecular docking was employed. Metabolomic profiling identified a diverse array of active phytochemicals enriched in BSS, including lipophilic lignans (e.g., (+)-eudesmin), vitamin E derivatives (e.g., γ-tocotrienol), and hydrophilic flavonoids (e.g., quercetin). Subsequent network and structural biology analyses revealed that these diverse compounds exert complementary multi-target effects to mitigate oxidative stress by targeting core hub proteins, particularly AKT1 and TP53. Specifically, molecular docking demonstrated that lipophilic components exhibit strong binding affinities to the hydrophobic cavities of AKT1, whereas hydrophilic polyphenols establish robust hydrogen-bonding networks with TP53. Pathway enrichment analyses further suggested that BSS exerts its profound cytoprotective effects primarily by modulating the PI3K-Akt and apoptosis signaling cascades, thereby restoring intracellular redox homeostasis. In conclusion, this study systematically predicts the complex structural and pharmacological basis of BSS against oxidative damage, laying a solid theoretical hypothesis for the future development of BSS-derived natural antioxidants and functional therapeutics. - Source: PubMed
Publication date: 2026/09/25
Wang LeiGong HuihuiSun ChenxiZhao JunshengZhao ShancangDong Yanjie