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101 gpx4  (Proteintech)


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    Proteintech 101 gpx4
    101 Gpx4, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/101+gpx4/FITC+Anti-mouse+CD44/pm41856196-47-5-14
    Average 93 stars, based on 4 article reviews
    101 gpx4 - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    other:

    Article Title: Arenobufagin Induces Ferroptosis in Gastric Cancer Stem Cells via the HCAR1-GPX4/SLC7A11 Antioxidant Axis.
    Article Snippet: 30 Arenobufagin (ARBU), a steroid compound extracted from the venom of Bufo 31 gargarizans, exhibits multi-target pharmacological activities, yet its role in regulating 32 ferroptosis in gastric cancer stem cells (GCSCs) remains unclear.. This study 33 systematically evaluated the antitumor effects and mechanisms of ARBU using in 34 vitro sphere culture, organoid models, and xenografts.. ARBU inhibited GCSC 35 proliferation and sphere formation in a concentration-dependent manner, reduced EdU 36 incorporation and SOX2 expression in organoids, and markedly suppressed tumor 37 growth in vivo while downregulating SOX2 and Nanog, with favorable biosafety.



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    Primer sequences used in the present study.

    Journal: International Journal of Molecular Medicine

    Article Title: p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke

    doi: 10.3892/ijmm.2025.5505

    Figure Lengend Snippet: Primer sequences used in the present study.

    Article Snippet: The GPX4 agonist PKUMDL-LC-101-D04 (200 µ M; CAS no. 2143896-83-5; MedChemExpress) was used to treat the cells for 1 h at 37°C after OGD/R and p23 siRNA transfection, whereas the GPX4 inhibitor RAS-selective lethal 3 (RSL3; 200 nM; CAS no. 1219810-16-8; MedChemExpress) was used to treat the cells for 16 h at 37°C after OGD/R and p23 oe.

    Techniques: Sequencing

    Ferroptosis is involved in OGD/R-induced BMEC injury. (A) Expression levels of ZO-1 protein in the rat brain tissue of a middle cerebral artery occlusion after 2 h of Fer-1 pretreatment were determined by western blotting. (B) Viability of BMECs induced by OGD/R following pretreatment with Fer-1 was determined using the Cell Counting Kit-8 assay (n=3). (C) Representative transmission electron microscopy images displaying the morphology of mitochondria in BMECs following OGD/R. The mitochondria presented increased membrane density and a shrunken form (indicated by red arrows) (magnification, ×20,000). Intracellular (D) GSH (n=3), (E) MDA (n=3) and (F) ROS (n=3) levels in BMECs following OGD/R. (G) Representative images of intracellular ROS levels in BMECs following OGD/R (magnification, ×100). (H) Protein expression levels and (I) statistical analysis (n=3), and (J) mRNA levels (n=3) of GPX4 in BMECs following OGD/R. (K) Protein expression levels and (L) statistical analysis (n=3), and (M) mRNA levels (n=3) of COX-2 in BMECs following OGD/R. Data are presented as the mean ± SD. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. OGD/R, oxygen-glucose deprivation/reoxygenation; BMECs, brain microvascular endothelial cells; ZO-1, zonula occludens-1; Fer-1, Ferrostatin-1; GSH, glutathione; GPX4, glutathione peroxidase 4; MDA, malondialdehyde; ROS, reactive oxygen species; COX-2, cyclooxygenase-2.

    Journal: International Journal of Molecular Medicine

    Article Title: p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke

    doi: 10.3892/ijmm.2025.5505

    Figure Lengend Snippet: Ferroptosis is involved in OGD/R-induced BMEC injury. (A) Expression levels of ZO-1 protein in the rat brain tissue of a middle cerebral artery occlusion after 2 h of Fer-1 pretreatment were determined by western blotting. (B) Viability of BMECs induced by OGD/R following pretreatment with Fer-1 was determined using the Cell Counting Kit-8 assay (n=3). (C) Representative transmission electron microscopy images displaying the morphology of mitochondria in BMECs following OGD/R. The mitochondria presented increased membrane density and a shrunken form (indicated by red arrows) (magnification, ×20,000). Intracellular (D) GSH (n=3), (E) MDA (n=3) and (F) ROS (n=3) levels in BMECs following OGD/R. (G) Representative images of intracellular ROS levels in BMECs following OGD/R (magnification, ×100). (H) Protein expression levels and (I) statistical analysis (n=3), and (J) mRNA levels (n=3) of GPX4 in BMECs following OGD/R. (K) Protein expression levels and (L) statistical analysis (n=3), and (M) mRNA levels (n=3) of COX-2 in BMECs following OGD/R. Data are presented as the mean ± SD. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. OGD/R, oxygen-glucose deprivation/reoxygenation; BMECs, brain microvascular endothelial cells; ZO-1, zonula occludens-1; Fer-1, Ferrostatin-1; GSH, glutathione; GPX4, glutathione peroxidase 4; MDA, malondialdehyde; ROS, reactive oxygen species; COX-2, cyclooxygenase-2.

    Article Snippet: The GPX4 agonist PKUMDL-LC-101-D04 (200 µ M; CAS no. 2143896-83-5; MedChemExpress) was used to treat the cells for 1 h at 37°C after OGD/R and p23 siRNA transfection, whereas the GPX4 inhibitor RAS-selective lethal 3 (RSL3; 200 nM; CAS no. 1219810-16-8; MedChemExpress) was used to treat the cells for 16 h at 37°C after OGD/R and p23 oe.

    Techniques: Expressing, Western Blot, Cell Counting, Transmission Assay, Electron Microscopy, Membrane

    p23 protects against OGD/R-induced ferroptosis of BMECs. (A) Cell viability induced by OGD/R following transfection with p23 siRNA in BMECs was detected using the CCK-8 assay (n=3). (B) Cell viability induced by OGD/R following transfection with p23 OE vector in BMECs was detected using the CCK-8 assay (n=3). Intracellular (C) GSH (n=3), (D) MDA (n=3) and (E) ROS (n=3) levels following the transfection of BMECs with p23 siRNA. (F) mRNA expression levels of ACSL4 in BMECs following p23 siRNA transfection (n=3). (G) Western blot analysis of GPX4 in BMECs following p23 siRNA transfection and (H) statistical analysis (n=3). (I) mRNA expression levels of SLC7A11 in BMECs following p23 siRNA transfection (n=3). Intracellular (J) GSH (n=3), (K) MDA (n=3) and (L) ROS (n=3) levels in BMECs with p23 OE. (M) Western blot analysis of GPX4 and (N) statistical analysis in BMECs with p23 OE (n=3). mRNA expression levels of (O) SLC7A11 (n=3) and (P) ACSL4 (n=3) in BMECs with p23 OE. Data are presented as the mean ± SD. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. CCK, Cell Counting Kit; OGD/R, oxygen-glucose deprivation/reoxygenation; BMECs, brain microvascular endothelial cells; GSH, glutathione; MDA, malondialdehyde; ROS, reactive oxygen species; ACSL4, acyl-CoA synthetase long-chain family member 4; GPX4, glutathione peroxidase 4; SLC7A11, subunit solute carrier family 7 member 11; COX-2, cyclooxygenase-2; OE, overexpression; siRNA, small interfering RNA; NC, negative control; RSL3, RAS-selective lethal 3; ns, not significant.

    Journal: International Journal of Molecular Medicine

    Article Title: p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke

    doi: 10.3892/ijmm.2025.5505

    Figure Lengend Snippet: p23 protects against OGD/R-induced ferroptosis of BMECs. (A) Cell viability induced by OGD/R following transfection with p23 siRNA in BMECs was detected using the CCK-8 assay (n=3). (B) Cell viability induced by OGD/R following transfection with p23 OE vector in BMECs was detected using the CCK-8 assay (n=3). Intracellular (C) GSH (n=3), (D) MDA (n=3) and (E) ROS (n=3) levels following the transfection of BMECs with p23 siRNA. (F) mRNA expression levels of ACSL4 in BMECs following p23 siRNA transfection (n=3). (G) Western blot analysis of GPX4 in BMECs following p23 siRNA transfection and (H) statistical analysis (n=3). (I) mRNA expression levels of SLC7A11 in BMECs following p23 siRNA transfection (n=3). Intracellular (J) GSH (n=3), (K) MDA (n=3) and (L) ROS (n=3) levels in BMECs with p23 OE. (M) Western blot analysis of GPX4 and (N) statistical analysis in BMECs with p23 OE (n=3). mRNA expression levels of (O) SLC7A11 (n=3) and (P) ACSL4 (n=3) in BMECs with p23 OE. Data are presented as the mean ± SD. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. CCK, Cell Counting Kit; OGD/R, oxygen-glucose deprivation/reoxygenation; BMECs, brain microvascular endothelial cells; GSH, glutathione; MDA, malondialdehyde; ROS, reactive oxygen species; ACSL4, acyl-CoA synthetase long-chain family member 4; GPX4, glutathione peroxidase 4; SLC7A11, subunit solute carrier family 7 member 11; COX-2, cyclooxygenase-2; OE, overexpression; siRNA, small interfering RNA; NC, negative control; RSL3, RAS-selective lethal 3; ns, not significant.

    Article Snippet: The GPX4 agonist PKUMDL-LC-101-D04 (200 µ M; CAS no. 2143896-83-5; MedChemExpress) was used to treat the cells for 1 h at 37°C after OGD/R and p23 siRNA transfection, whereas the GPX4 inhibitor RAS-selective lethal 3 (RSL3; 200 nM; CAS no. 1219810-16-8; MedChemExpress) was used to treat the cells for 16 h at 37°C after OGD/R and p23 oe.

    Techniques: Transfection, CCK-8 Assay, Plasmid Preparation, Expressing, Western Blot, Cell Counting, Over Expression, Small Interfering RNA, Negative Control

    GPX4 mediates the protective effect of p23 on ferroptosis in BMECs. (A) Protein docking mimicking the interaction between p23 (green), GPX4 (violet) and HSP90 (cyan). (B) Interaction between p23, GPX4 and HSP90 was detected using co-immunoprecipitation. (C) Structural domain of p23 interacting with GPX4 was detected using co-immunoprecipitation. (D) Co-localization of p23 and GPX4 was detected using immunofluorescence (magnification, ×400). (E) Effect of p23 on the stability of the GPX4 protein. (F) Expression of ZO-1 in GPX4 Fos CreERT2 mice following p23 overexpression was detected using immunofluorescence (magnification, ×100). BMECs, brain microvascular endothelial cells; GPX4, glutathione peroxidase 4; HSP90, heat shock protein 90; ZO-1, zonula occludens-1; CHX, cycloheximide.

    Journal: International Journal of Molecular Medicine

    Article Title: p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke

    doi: 10.3892/ijmm.2025.5505

    Figure Lengend Snippet: GPX4 mediates the protective effect of p23 on ferroptosis in BMECs. (A) Protein docking mimicking the interaction between p23 (green), GPX4 (violet) and HSP90 (cyan). (B) Interaction between p23, GPX4 and HSP90 was detected using co-immunoprecipitation. (C) Structural domain of p23 interacting with GPX4 was detected using co-immunoprecipitation. (D) Co-localization of p23 and GPX4 was detected using immunofluorescence (magnification, ×400). (E) Effect of p23 on the stability of the GPX4 protein. (F) Expression of ZO-1 in GPX4 Fos CreERT2 mice following p23 overexpression was detected using immunofluorescence (magnification, ×100). BMECs, brain microvascular endothelial cells; GPX4, glutathione peroxidase 4; HSP90, heat shock protein 90; ZO-1, zonula occludens-1; CHX, cycloheximide.

    Article Snippet: The GPX4 agonist PKUMDL-LC-101-D04 (200 µ M; CAS no. 2143896-83-5; MedChemExpress) was used to treat the cells for 1 h at 37°C after OGD/R and p23 siRNA transfection, whereas the GPX4 inhibitor RAS-selective lethal 3 (RSL3; 200 nM; CAS no. 1219810-16-8; MedChemExpress) was used to treat the cells for 16 h at 37°C after OGD/R and p23 oe.

    Techniques: Immunoprecipitation, Immunofluorescence, Expressing, Over Expression

    p23 protects against ferroptosis of BMECs in ischemic stroke. p23 was significantly upregulated following stroke-like conditions in in vitro and in vivo models, and formed a complex with HSP90 and GPX4 through its N-terminal structure (1-90aa), which improved their stability, inhibited GPX4 degradation, and ultimately inhibited ferroptosis in BMECs, thereby protecting against ischemia/reperfusion-induced blood-brain barrier injury. BMECs, brain microvascular endothelial cells; GSH, glutathione; GPX4, glutathione peroxidase 4; HSP90, heat shock protein 90.

    Journal: International Journal of Molecular Medicine

    Article Title: p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke

    doi: 10.3892/ijmm.2025.5505

    Figure Lengend Snippet: p23 protects against ferroptosis of BMECs in ischemic stroke. p23 was significantly upregulated following stroke-like conditions in in vitro and in vivo models, and formed a complex with HSP90 and GPX4 through its N-terminal structure (1-90aa), which improved their stability, inhibited GPX4 degradation, and ultimately inhibited ferroptosis in BMECs, thereby protecting against ischemia/reperfusion-induced blood-brain barrier injury. BMECs, brain microvascular endothelial cells; GSH, glutathione; GPX4, glutathione peroxidase 4; HSP90, heat shock protein 90.

    Article Snippet: The GPX4 agonist PKUMDL-LC-101-D04 (200 µ M; CAS no. 2143896-83-5; MedChemExpress) was used to treat the cells for 1 h at 37°C after OGD/R and p23 siRNA transfection, whereas the GPX4 inhibitor RAS-selective lethal 3 (RSL3; 200 nM; CAS no. 1219810-16-8; MedChemExpress) was used to treat the cells for 16 h at 37°C after OGD/R and p23 oe.

    Techniques: In Vitro, In Vivo