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MedChemExpress akt inhibitor
E2 and VitD3 improves osteogenesis by <t>PI3K/AKT/mTOR</t> pathway. (A) Q-PCR analysis of mRNA level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (B) The protein level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (C) The WB analysis of protein level of pan and phsopho-PI3K, pan and phospho-Akt, pan and phospho-mTOR, and pan and phospho-FOXO3 in MC3T3-E1 cells treated with PBS, E2, VitD3, E2 plus VitD3. (D) The MC3T3-E1 cells were pretreated with or <t>without</t> <t>Akti1/2</t> (5uM), and were induced to osteoblasts with PBS, E2, VitD3, E2+VitD3. The ALP staining was utilized to evaluate the osteogenic differentiation in each group.
Akt Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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akt1  (Bioss)
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
Akt1, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Proteintech phospho akt ser473 monoclonal antibody
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Bioss rapid blocking solution
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Proteintech p akt
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Proteintech 10176 2 ap
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Proteintech akt proteintech cat 60203 2 ig
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Image Search Results


E2 and VitD3 improves osteogenesis by PI3K/AKT/mTOR pathway. (A) Q-PCR analysis of mRNA level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (B) The protein level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (C) The WB analysis of protein level of pan and phsopho-PI3K, pan and phospho-Akt, pan and phospho-mTOR, and pan and phospho-FOXO3 in MC3T3-E1 cells treated with PBS, E2, VitD3, E2 plus VitD3. (D) The MC3T3-E1 cells were pretreated with or without Akti1/2 (5uM), and were induced to osteoblasts with PBS, E2, VitD3, E2+VitD3. The ALP staining was utilized to evaluate the osteogenic differentiation in each group.

Journal: Materials Today Bio

Article Title: Alendronic acid modified PLGA drug delivery system loaded with 17β-Estradiol and vitamin D3 has anti-osteoporotic effect

doi: 10.1016/j.mtbio.2026.102789

Figure Lengend Snippet: E2 and VitD3 improves osteogenesis by PI3K/AKT/mTOR pathway. (A) Q-PCR analysis of mRNA level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (B) The protein level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (C) The WB analysis of protein level of pan and phsopho-PI3K, pan and phospho-Akt, pan and phospho-mTOR, and pan and phospho-FOXO3 in MC3T3-E1 cells treated with PBS, E2, VitD3, E2 plus VitD3. (D) The MC3T3-E1 cells were pretreated with or without Akti1/2 (5uM), and were induced to osteoblasts with PBS, E2, VitD3, E2+VitD3. The ALP staining was utilized to evaluate the osteogenic differentiation in each group.

Article Snippet: The AKT inhibitor (Akti1/2, MedChemExpress, USA) was dissolved in DMSO and used at a final concentration of 10 μM.

Techniques: Staining

Molecular docking and dynamics simulations of AKT1, eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes

Journal: Chinese Medicine

Article Title: Optimized New Shengmai Powder suppresses ferroptosis in ischemic cardiomyocytes via cGMP-PKG signalling

doi: 10.1186/s13020-026-01364-6

Figure Lengend Snippet: Molecular docking and dynamics simulations of AKT1, eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes

Article Snippet: For IF co-localization, two primary antibodies from different host species were mixed and incubated together: AKT1 (bsm-52010R, BIOSS, Beijing, China) with eNOS (bsm-33176 M, BIOSS, Beijing, China), and STAT3 (bsm-33301 M, BIOSS, Beijing, China) with PKG1 (A01708-3, Boster, Wuhan, Hubei, China).

Techniques:

ONSMP activates the cGMP–PKG signaling pathway to inhibit cardiomyocyte ferroptosis. ONSMP activates AKT1, thereby regulating the cGMP–PKG signaling pathway and promoting GPX4 expression. GPX4 then uses GSH as an electron donor to maintain its antioxidant activity, effectively eliminating lipid peroxides and suppressing ferroptosis in cardiomyocytes

Journal: Chinese Medicine

Article Title: Optimized New Shengmai Powder suppresses ferroptosis in ischemic cardiomyocytes via cGMP-PKG signalling

doi: 10.1186/s13020-026-01364-6

Figure Lengend Snippet: ONSMP activates the cGMP–PKG signaling pathway to inhibit cardiomyocyte ferroptosis. ONSMP activates AKT1, thereby regulating the cGMP–PKG signaling pathway and promoting GPX4 expression. GPX4 then uses GSH as an electron donor to maintain its antioxidant activity, effectively eliminating lipid peroxides and suppressing ferroptosis in cardiomyocytes

Article Snippet: For IF co-localization, two primary antibodies from different host species were mixed and incubated together: AKT1 (bsm-52010R, BIOSS, Beijing, China) with eNOS (bsm-33176 M, BIOSS, Beijing, China), and STAT3 (bsm-33301 M, BIOSS, Beijing, China) with PKG1 (A01708-3, Boster, Wuhan, Hubei, China).

Techniques: Expressing, Antioxidant Activity Assay