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endoplasmic reticulum chaperone bip (Proteintech)

Name: endoplasmic reticulum chaperone bip
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Proteintech endoplasmic reticulum chaperone bip

Experiment design. (A) In Experiment 1, the effect of rtPA on the ICH mouse model was investigated. (B) In Experiment 2, the effect and the possible mechanisms of rtPA in the ICH model using primary cortical neurons in vitro were investigated. (C) In Experiment 3, the mechanism of rtPA’s effect on the ICH model in neurons in vitro was examined using the PI3K pathway inhibitor. (D) In Experiment 4, the protein domain that mediates rtPA’s neuroprotective effect in the ICH model in neurons in vitro was investigated. DMSO: Dimethyl sulfoxide; ER: <t>endoplasmic</t> reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Endoplasmic Reticulum Chaperone Bip, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 931 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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endoplasmic reticulum chaperone bip - by Bioz Stars, 2026-02

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1) Product Images from "Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway"

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

Journal: Neural Regeneration Research

doi: 10.4103/NRR.NRR-D-23-01953

Figure Legend Snippet: Experiment design. (A) In Experiment 1, the effect of rtPA on the ICH mouse model was investigated. (B) In Experiment 2, the effect and the possible mechanisms of rtPA in the ICH model using primary cortical neurons in vitro were investigated. (C) In Experiment 3, the mechanism of rtPA’s effect on the ICH model in neurons in vitro was examined using the PI3K pathway inhibitor. (D) In Experiment 4, the protein domain that mediates rtPA’s neuroprotective effect in the ICH model in neurons in vitro was investigated. DMSO: Dimethyl sulfoxide; ER: endoplasmic reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Techniques Used: In Vitro, Staining, Recombinant, TUNEL Assay

rtPA attenuates neurological behavior impairment and apoptosis after ICH. (A–C) Left forelimb placement experiment, corner turn experiment, and modified Garcia score testing were conducted at 1 hour before surgery and 6, 24, and 72 hours after surgery ( n = 14 per group). (D) H&E staining (top) and Nissl staining (bottom) of peri-hematoma tissue at 72 hours after ICH and rtPA treatments ( n = 3 per group). Scale bars: 100 µm. (E) Representative picture of TUNEL staining of peri-hematoma tissue conducted at 72 hours after ICH and rtPA treatments ( n = 3–6 per group). Scale bars: 100 µm. (F) The proportion of TUNEL-positive cells to all nucleated cells surrounding the hematoma ( n = 3–6 per group). (G–J) Analysis of apoptosis-associated proteins at 24 and 72 hours after treatment ( n = 3). Data are represented as mean ± SEM. * P < 0.05, **** P < 0.0001, vs. sham group; &P < 0.05, && P < 0.01, &&&& P < 0.0001, vs . ICH group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . ICH + vehicle group (two-way analysis of variance followed by Bonferroni post hoc test (A–C) or one-way analysis of variance followed by Tukey’s post hoc test (F, I, J). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; DAPI: 4′,6-diamidino-2-phenylindole; ER: endoplasmic reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Figure Legend Snippet: rtPA attenuates neurological behavior impairment and apoptosis after ICH. (A–C) Left forelimb placement experiment, corner turn experiment, and modified Garcia score testing were conducted at 1 hour before surgery and 6, 24, and 72 hours after surgery ( n = 14 per group). (D) H&E staining (top) and Nissl staining (bottom) of peri-hematoma tissue at 72 hours after ICH and rtPA treatments ( n = 3 per group). Scale bars: 100 µm. (E) Representative picture of TUNEL staining of peri-hematoma tissue conducted at 72 hours after ICH and rtPA treatments ( n = 3–6 per group). Scale bars: 100 µm. (F) The proportion of TUNEL-positive cells to all nucleated cells surrounding the hematoma ( n = 3–6 per group). (G–J) Analysis of apoptosis-associated proteins at 24 and 72 hours after treatment ( n = 3). Data are represented as mean ± SEM. * P < 0.05, **** P < 0.0001, vs. sham group; &P < 0.05, && P < 0.01, &&&& P < 0.0001, vs . ICH group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . ICH + vehicle group (two-way analysis of variance followed by Bonferroni post hoc test (A–C) or one-way analysis of variance followed by Tukey’s post hoc test (F, I, J). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; DAPI: 4′,6-diamidino-2-phenylindole; ER: endoplasmic reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Techniques Used: Modification, Staining, TUNEL Assay, Recombinant

rtPA attenuates neuron apoptosis and autophagy after experimental ICH in vitro . (A–C) The DEGs between control group and hemin group associated with autophagy animals (KEGG: mmu04140), positive regulation of neuron apoptotic process (GO: 0043525), and positive regulation of response to endoplasmic reticulum stress (GO: 1905898) were screened, and the transcriptional levels of DEGs in each group are presented as heatmaps. (D, E) Analysis of apoptosis-associated proteins. (F) Transmission electron microscopy images of neurons after hemin and rtPA treatment. Red asterisk indicates the autophagosome, black arrows indicate the endoplasmic reticulum, and N means nucleus. Scale bars: 1 µm. (G–J) Analysis of autophagy-associated proteins. Data are shown as mean ± SEM ( n = 3–4). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . control group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hemin group (one-way analysis of variance followed by Tukey’s post hoc test). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; beclin1: coiled-coil myosin-like bcl2-interacting protein; DEGs: differential expression genes; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; LC3: microtubule-associated proteins 1A/1B light chain 3B; p62: sequestosome-1/ubiquitin-binding protein p62; rtPA: recombinant tissue plasminogen activator.

Figure Legend Snippet: rtPA attenuates neuron apoptosis and autophagy after experimental ICH in vitro . (A–C) The DEGs between control group and hemin group associated with autophagy animals (KEGG: mmu04140), positive regulation of neuron apoptotic process (GO: 0043525), and positive regulation of response to endoplasmic reticulum stress (GO: 1905898) were screened, and the transcriptional levels of DEGs in each group are presented as heatmaps. (D, E) Analysis of apoptosis-associated proteins. (F) Transmission electron microscopy images of neurons after hemin and rtPA treatment. Red asterisk indicates the autophagosome, black arrows indicate the endoplasmic reticulum, and N means nucleus. Scale bars: 1 µm. (G–J) Analysis of autophagy-associated proteins. Data are shown as mean ± SEM ( n = 3–4). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . control group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hemin group (one-way analysis of variance followed by Tukey’s post hoc test). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; beclin1: coiled-coil myosin-like bcl2-interacting protein; DEGs: differential expression genes; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; LC3: microtubule-associated proteins 1A/1B light chain 3B; p62: sequestosome-1/ubiquitin-binding protein p62; rtPA: recombinant tissue plasminogen activator.

Techniques Used: In Vitro, Control, Transmission Assay, Electron Microscopy, Quantitative Proteomics, Ubiquitin Proteomics, Binding Assay, Recombinant

rtPA ameliorates endoplasmic reticulum stress in the in vitro ICH cell model. (A) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after hemin and rtPA treatment. Scale bars: 3 µm. (B–F) Quantitative analysis of ER stress–associated proteins of neurons. Data are shown as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, vs. control group; # P < 0.05, ## P < 0.01, vs . hemin group (one-way analysis of variance followed by Tukey’s post hoc test). (G) Immunofluorescence staining images of p-PERK (red, labeled by Cy3) in neurons after hemin and rtPA treatment. Scale bars: 50 µm. 3D: Three-dimensional; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; Grp78: endoplasmic reticulum chaperone BiP; PERK: PRKR-like endoplasmic reticulum kinase; rtPA: recombinant tissue plasminogen activator.

Figure Legend Snippet: rtPA ameliorates endoplasmic reticulum stress in the in vitro ICH cell model. (A) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after hemin and rtPA treatment. Scale bars: 3 µm. (B–F) Quantitative analysis of ER stress–associated proteins of neurons. Data are shown as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, vs. control group; # P < 0.05, ## P < 0.01, vs . hemin group (one-way analysis of variance followed by Tukey’s post hoc test). (G) Immunofluorescence staining images of p-PERK (red, labeled by Cy3) in neurons after hemin and rtPA treatment. Scale bars: 50 µm. 3D: Three-dimensional; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; Grp78: endoplasmic reticulum chaperone BiP; PERK: PRKR-like endoplasmic reticulum kinase; rtPA: recombinant tissue plasminogen activator.

Techniques Used: In Vitro, Control, Immunofluorescence, Staining, Labeling, Recombinant

The PI3K inhibitor LY294002 reverses the anti-ER stress effect of rtPA and the EGF domain of rtPA may mediate the PI3K/AKT pathway in the ICH in vitro cell model. (A–C) Analysis of ER stress–associated proteins ( n = 3 per group). (D) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 3 µm. (E) Immunofluorescence images of p-PERK (red, labeled by Cy3) in neurons after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 50 µm. (F–H) Analysis of PI3K p85 and p-AKT. Data are represented as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . hemin group; & P < 0.05, && P < 0.01, vs . hemin + rtPA group; # P < 0.05, vs . hemin + rtPA + DMSO group (one-way analysis of variance followed by Tukey’s post hoc test). (I) Transmission electron microscopy images of cells after rtPA and rtPA domain inhibitor treatment. Scale bar: 100 µm. 3D: Three-dimensional; AKT: RAC-alpha serine/threonine-protein kinase; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; EGF: epidermal growth factor; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; LY294002: PI3K inhibitor; mTOR: mammalian target of rapamycin; PERK: PRKR-like endoplasmic reticulum kinase; PI3K: phosphatidylinositol 3-kinase regulatory subunit alpha; rtPA: recombinant tissue plasminogen activator.

Figure Legend Snippet: The PI3K inhibitor LY294002 reverses the anti-ER stress effect of rtPA and the EGF domain of rtPA may mediate the PI3K/AKT pathway in the ICH in vitro cell model. (A–C) Analysis of ER stress–associated proteins ( n = 3 per group). (D) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 3 µm. (E) Immunofluorescence images of p-PERK (red, labeled by Cy3) in neurons after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 50 µm. (F–H) Analysis of PI3K p85 and p-AKT. Data are represented as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . hemin group; & P < 0.05, && P < 0.01, vs . hemin + rtPA group; # P < 0.05, vs . hemin + rtPA + DMSO group (one-way analysis of variance followed by Tukey’s post hoc test). (I) Transmission electron microscopy images of cells after rtPA and rtPA domain inhibitor treatment. Scale bar: 100 µm. 3D: Three-dimensional; AKT: RAC-alpha serine/threonine-protein kinase; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; EGF: epidermal growth factor; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; LY294002: PI3K inhibitor; mTOR: mammalian target of rapamycin; PERK: PRKR-like endoplasmic reticulum kinase; PI3K: phosphatidylinositol 3-kinase regulatory subunit alpha; rtPA: recombinant tissue plasminogen activator.

Techniques Used: In Vitro, Immunofluorescence, Labeling, Transmission Assay, Electron Microscopy, Recombinant

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Journal: Neural Regeneration Research

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

doi: 10.4103/NRR.NRR-D-23-01953

Figure Lengend Snippet: Experiment design. (A) In Experiment 1, the effect of rtPA on the ICH mouse model was investigated. (B) In Experiment 2, the effect and the possible mechanisms of rtPA in the ICH model using primary cortical neurons in vitro were investigated. (C) In Experiment 3, the mechanism of rtPA’s effect on the ICH model in neurons in vitro was examined using the PI3K pathway inhibitor. (D) In Experiment 4, the protein domain that mediates rtPA’s neuroprotective effect in the ICH model in neurons in vitro was investigated. DMSO: Dimethyl sulfoxide; ER: endoplasmic reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Article Snippet: The following primary antibodies were used for analysis: bcl2 (rabbit, 1:1000, Proteintech, Cat# 12789-1-AP, RRID: AB_2227948), bax (rabbit, 1:1000, Proteintech, Cat# 50599-2-Ig, RRID: AB_2061561), coiled-coil myosin-like bcl2-interacting protein (beclin1; rabbit, 1:1000, Proteintech, Cat# 11306-1-AP, RRID: AB_2259061), sequestosome-1/ubiquitin-binding protein p62 (SQSTM1/p62; rabbit, 1:1000, Abclonal, Cat# A11250, RRID: AB_2758477), microtubule-associated proteins 1A/1B light chain 3B (LC3; rabbit, 1:1000, Abcam, Cat# ab48394, RRID: AB_881433), endoplasmic reticulum chaperone BiP (Grp78/BIP; mouse, 1:1000, Proteintech, Cat# 66574-1-Ig, RRID: AB_2881934), cyclic AMP-dependent transcription factor ATF-6 alpha (ATF6; rabbit, 1:1000, Proteintech, Cat# 24169-1-AP, RRID: AB_2876891), PRKR-like endoplasmic reticulum kinase (PERK; rabbit, 1:1000, Cell Signaling Technology, Cat# 3192S, RRID: AB_2095847), phospho-PERK (rabbit, 1:1000, Cell Signaling Technology, Cat# 3179S, RRID: AB_2095853), eukaryotic translation initiation factor 2 subunit alpha (eIF2α; rabbit, 1:1000, Cell Signaling Technology, Cat# 9722S, RRID: AB_2230924), phospho-eIF2α (rabbit, 1:1000, Cell Signaling Technology, 9721S, RRID: AB_330951), phosphatidylinositol 3-kinase regulatory subunit alpha (PI3 kinase p85; rabbit, 1:1000, Cell Signaling Technology, Cat# 4257S, RRID: AB_659889), RAC-alpha serine/threonine-protein kinase (AKT; rabbit, 1:1000, Cell Signaling Technology, Cat# 4691S, RRID: AB_915783), phospho-AKT (rabbit, 1:1000, Cell Signaling Technology, Cat# 4060S, RRID: AB_2315049), mammalian target of rapamycin (mTOR; rabbit, 1:1000, Cell Signaling Technology, Cat# 2983S, RRID: AB_2105622), phospho-mTOR (rabbit, 1:1000, Cell Signaling Technology, Cat# 2971S, RRID: AB_330970), and β-actin (mouse, 1:1000, Proteintech, Cat# 66009-1-Ig, RRID: AB_2687938).

Techniques: In Vitro, Staining, Recombinant, TUNEL Assay

Journal: Neural Regeneration Research

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

doi: 10.4103/NRR.NRR-D-23-01953

Figure Lengend Snippet: rtPA attenuates neurological behavior impairment and apoptosis after ICH. (A–C) Left forelimb placement experiment, corner turn experiment, and modified Garcia score testing were conducted at 1 hour before surgery and 6, 24, and 72 hours after surgery ( n = 14 per group). (D) H&E staining (top) and Nissl staining (bottom) of peri-hematoma tissue at 72 hours after ICH and rtPA treatments ( n = 3 per group). Scale bars: 100 µm. (E) Representative picture of TUNEL staining of peri-hematoma tissue conducted at 72 hours after ICH and rtPA treatments ( n = 3–6 per group). Scale bars: 100 µm. (F) The proportion of TUNEL-positive cells to all nucleated cells surrounding the hematoma ( n = 3–6 per group). (G–J) Analysis of apoptosis-associated proteins at 24 and 72 hours after treatment ( n = 3). Data are represented as mean ± SEM. * P < 0.05, **** P < 0.0001, vs. sham group; &P < 0.05, && P < 0.01, &&&& P < 0.0001, vs . ICH group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . ICH + vehicle group (two-way analysis of variance followed by Bonferroni post hoc test (A–C) or one-way analysis of variance followed by Tukey’s post hoc test (F, I, J). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; DAPI: 4′,6-diamidino-2-phenylindole; ER: endoplasmic reticulum; H&E staining: hematoxylin & eosin staining; ICH: intracerebral hemorrhage; rtPA: recombinant tissue plasminogen activator; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling.

Techniques: Modification, Staining, TUNEL Assay, Recombinant

Journal: Neural Regeneration Research

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

doi: 10.4103/NRR.NRR-D-23-01953

Figure Lengend Snippet: rtPA attenuates neuron apoptosis and autophagy after experimental ICH in vitro . (A–C) The DEGs between control group and hemin group associated with autophagy animals (KEGG: mmu04140), positive regulation of neuron apoptotic process (GO: 0043525), and positive regulation of response to endoplasmic reticulum stress (GO: 1905898) were screened, and the transcriptional levels of DEGs in each group are presented as heatmaps. (D, E) Analysis of apoptosis-associated proteins. (F) Transmission electron microscopy images of neurons after hemin and rtPA treatment. Red asterisk indicates the autophagosome, black arrows indicate the endoplasmic reticulum, and N means nucleus. Scale bars: 1 µm. (G–J) Analysis of autophagy-associated proteins. Data are shown as mean ± SEM ( n = 3–4). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . control group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hemin group (one-way analysis of variance followed by Tukey’s post hoc test). bax: Apoptosis regulator bax; bcl2: apoptosis regulator bcl2; beclin1: coiled-coil myosin-like bcl2-interacting protein; DEGs: differential expression genes; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; LC3: microtubule-associated proteins 1A/1B light chain 3B; p62: sequestosome-1/ubiquitin-binding protein p62; rtPA: recombinant tissue plasminogen activator.

Techniques: In Vitro, Control, Transmission Assay, Electron Microscopy, Quantitative Proteomics, Ubiquitin Proteomics, Binding Assay, Recombinant

Journal: Neural Regeneration Research

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

doi: 10.4103/NRR.NRR-D-23-01953

Figure Lengend Snippet: rtPA ameliorates endoplasmic reticulum stress in the in vitro ICH cell model. (A) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after hemin and rtPA treatment. Scale bars: 3 µm. (B–F) Quantitative analysis of ER stress–associated proteins of neurons. Data are shown as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, vs. control group; # P < 0.05, ## P < 0.01, vs . hemin group (one-way analysis of variance followed by Tukey’s post hoc test). (G) Immunofluorescence staining images of p-PERK (red, labeled by Cy3) in neurons after hemin and rtPA treatment. Scale bars: 50 µm. 3D: Three-dimensional; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; Grp78: endoplasmic reticulum chaperone BiP; PERK: PRKR-like endoplasmic reticulum kinase; rtPA: recombinant tissue plasminogen activator.

Techniques: In Vitro, Control, Immunofluorescence, Staining, Labeling, Recombinant

Journal: Neural Regeneration Research

Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway

doi: 10.4103/NRR.NRR-D-23-01953

Figure Lengend Snippet: The PI3K inhibitor LY294002 reverses the anti-ER stress effect of rtPA and the EGF domain of rtPA may mediate the PI3K/AKT pathway in the ICH in vitro cell model. (A–C) Analysis of ER stress–associated proteins ( n = 3 per group). (D) Confocal images and three-dimensional reconstruction of endoplasmic reticulum continuity of neurons by ER tracker after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 3 µm. (E) Immunofluorescence images of p-PERK (red, labeled by Cy3) in neurons after rtPA and PI3K inhibitor LY294002 treatment. Scale bars: 50 µm. (F–H) Analysis of PI3K p85 and p-AKT. Data are represented as mean ± SEM ( n = 3 per group). * P < 0.05, ** P < 0.01, *** P < 0.001, vs . hemin group; & P < 0.05, && P < 0.01, vs . hemin + rtPA group; # P < 0.05, vs . hemin + rtPA + DMSO group (one-way analysis of variance followed by Tukey’s post hoc test). (I) Transmission electron microscopy images of cells after rtPA and rtPA domain inhibitor treatment. Scale bar: 100 µm. 3D: Three-dimensional; AKT: RAC-alpha serine/threonine-protein kinase; ATF6: cyclic AMP-dependent transcription factor ATF-6 alpha; DAPI: 4′,6-diamidino-2-phenylindole; EGF: epidermal growth factor; eIF2α: eukaryotic translation initiation factor 2 subunit alpha; ER: endoplasmic reticulum; LY294002: PI3K inhibitor; mTOR: mammalian target of rapamycin; PERK: PRKR-like endoplasmic reticulum kinase; PI3K: phosphatidylinositol 3-kinase regulatory subunit alpha; rtPA: recombinant tissue plasminogen activator.

Techniques: In Vitro, Immunofluorescence, Labeling, Transmission Assay, Electron Microscopy, Recombinant

SPH regulates NLRP3 inflammasome, ER stress, oxidative stress, and apoptosis/survival pathways in the hearts of hypertensive mice. (A, B) Representative Western blots and densitometric analysis for ER stress (GRP78), NLRP3 inflammasome components (NLRP3, ASC, C-Caspase-1, C-IL-1β, C-GSDMD), and oxidative stress (SOD1). (C–H) Relative mRNA expression of Nlrp3, Asc, Casp1, Gsdmd, IL1b, and IL18 by qRT-PCR. (I, J) Representative Western blots and densitometric analysis for apoptosis markers (BAX, BCL2, C-Caspase-3) and PI3K/AKT pathway proteins (p-PI3K, PI3K, p-AKT, AKT). GAPDH or total proteins were used for normalization. Data are mean ± SEM (n = 3 per group). Statistical analysis was by one-way ANOVA with Tukey's post-hoc test.

Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention

Article Title: The sphingolipid metabolite sphingosine protects against hypertension by targeting metabolic-inflammatory crosstalk via the NLRP3 inflammasome

doi: 10.1016/j.ijcrp.2025.200562

Figure Lengend Snippet: SPH regulates NLRP3 inflammasome, ER stress, oxidative stress, and apoptosis/survival pathways in the hearts of hypertensive mice. (A, B) Representative Western blots and densitometric analysis for ER stress (GRP78), NLRP3 inflammasome components (NLRP3, ASC, C-Caspase-1, C-IL-1β, C-GSDMD), and oxidative stress (SOD1). (C–H) Relative mRNA expression of Nlrp3, Asc, Casp1, Gsdmd, IL1b, and IL18 by qRT-PCR. (I, J) Representative Western blots and densitometric analysis for apoptosis markers (BAX, BCL2, C-Caspase-3) and PI3K/AKT pathway proteins (p-PI3K, PI3K, p-AKT, AKT). GAPDH or total proteins were used for normalization. Data are mean ± SEM (n = 3 per group). Statistical analysis was by one-way ANOVA with Tukey's post-hoc test.

Article Snippet: The following primary antibodies were used: NLRP3 (Abcam, Cat# ab270449), ASC (Abcam, Cat#ab307560), Caspase-1 (Proteintech, Cat# 31020-1-AP), Cleaved Caspase-1 (CST, Cat# 89332), IL-1β(Abcam, Cat# ab254360), Cleaved IL-1β (CST, Cat#63124), IL- 18 (Proteintech, Cat# 33710-1-AP), SOD1 (Proteintech, Cat# 10269-1-AP), BCL2 (Proteintech, Cat# 26593-1-AP), BAX(Proteintech, Cat# 50599-2-Ig), and GRP78 (Proteintech, Cat# 11587-1-AP),GAPDH (Proteintech, Cat#60004-1-Ig), Phospho-PI3 Kinase p85 (CST, Cat#4228T), Phospho-AKT(Proteintech, Cat#66444-1-Ig), AKT(Proteintech, Cat#60203-2-Ig), GSDMD (N-Terminal) (Affinity,Cat# DF13758),GSDMD (Proteintech,Cat# 20770-1-AP).

Techniques: Western Blot, Expressing, Quantitative RT-PCR

SPH protects human umbilical vein endothelial cells (HUVECs) from Angiotensin IIinduced injury, pyroptosis, and oxidative stress by inhibiting the NLRP3 inflammasome pathway. (A) Cell viability of HUVECs treated with AngII (1 μM) for 12 h followed by various concentrations of SPH (0.5–6 μM) for 24 h. (B) Cell viability of HUVECs treated with SPH alone for 24 h. (C, D) Representative Western blots and densitometric analysis for NLRP3 inflammasome components (NLRP3, ASC, c-Caspase-1, c-IL-1β), the pyroptosis effector N-GSDMD, ER stress marker GRP78, and oxidative stress marker SOD1. (E–J) Relative mRNA expression of NLRP3, ASC, CASP1, IL1B, IL18, and GSDMD by RT-qPCR. Data are the mean ± SEM of three independent experiments. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001 vs. the AngII-only group, unless otherwise indicated.

Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention

Article Title: The sphingolipid metabolite sphingosine protects against hypertension by targeting metabolic-inflammatory crosstalk via the NLRP3 inflammasome

doi: 10.1016/j.ijcrp.2025.200562

Figure Lengend Snippet: SPH protects human umbilical vein endothelial cells (HUVECs) from Angiotensin IIinduced injury, pyroptosis, and oxidative stress by inhibiting the NLRP3 inflammasome pathway. (A) Cell viability of HUVECs treated with AngII (1 μM) for 12 h followed by various concentrations of SPH (0.5–6 μM) for 24 h. (B) Cell viability of HUVECs treated with SPH alone for 24 h. (C, D) Representative Western blots and densitometric analysis for NLRP3 inflammasome components (NLRP3, ASC, c-Caspase-1, c-IL-1β), the pyroptosis effector N-GSDMD, ER stress marker GRP78, and oxidative stress marker SOD1. (E–J) Relative mRNA expression of NLRP3, ASC, CASP1, IL1B, IL18, and GSDMD by RT-qPCR. Data are the mean ± SEM of three independent experiments. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001 vs. the AngII-only group, unless otherwise indicated.

Techniques: Western Blot, Marker, Expressing, Quantitative RT-PCR

Bulk RNA-seq identification of early regulatory genes and signals in bone defects. ( A ) Experimental workflow for bulk RNA-seq in early stages of bone defects in rats. ( B ) Construction of interaction networks and molecular dynamics simulations for key regulatory proteins in early-stage femoral and alveolar bone defects. ( C – E ) Immunohistochemical detection and quantitative analysis of Heat Shock Protein Family A (Hsp70) Member 5 (HSPA5) and interleukin-6 (IL-6) expression levels in early healing tissues of the femoral and alveolar regions. Scale bars: 2 mm, 100 μm, and 50 μm. ( F , G ) Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis results for differentially expressed genes (DEGs) in early healing stages of femoral and alveolar bone defects. Statistical significance was determined using a t -test.

Journal: Bioactive Materials

Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

doi: 10.1016/j.bioactmat.2025.09.005

Figure Lengend Snippet: Bulk RNA-seq identification of early regulatory genes and signals in bone defects. ( A ) Experimental workflow for bulk RNA-seq in early stages of bone defects in rats. ( B ) Construction of interaction networks and molecular dynamics simulations for key regulatory proteins in early-stage femoral and alveolar bone defects. ( C – E ) Immunohistochemical detection and quantitative analysis of Heat Shock Protein Family A (Hsp70) Member 5 (HSPA5) and interleukin-6 (IL-6) expression levels in early healing tissues of the femoral and alveolar regions. Scale bars: 2 mm, 100 μm, and 50 μm. ( F , G ) Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis results for differentially expressed genes (DEGs) in early healing stages of femoral and alveolar bone defects. Statistical significance was determined using a t -test.

Article Snippet: First, HSPA5 (bs-1219R, Bioss, CN) was used, followed by IL-6 (MA5-51298, Thermo Fisher Scientific, US), ARG1 (bsm-56207R, Bioss, CN), FHOD3 (bs-13156R, Bioss, CN), RUNX2 (bs-1134R, Bioss, CN), and Osterix (YA3539, MCE, US).

Techniques: RNA Sequencing, Immunohistochemical staining, Expressing

Protein identification for key proteins and signals in early bone defects. ( A ) Workflow for tissue protein identification at early stages of bone defects in rats. ( B , C ) KEGG and GO enrichment analysis of differential proteins in early healing tissues of femoral and alveolar bone defects. ( D , E ) Interaction network analysis of HSPA5 and IL-6 within the enrichment signals of femoral and alveolar bones. ( F ) Protein expression levels of HSPA5 and IL-6 in early healing tissues of femoral and alveolar defects. ( G ) Quantitative analysis of HSPA5 and IL-6 protein expression. Statistical analysis employed a t -test.

Journal: Bioactive Materials

Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

doi: 10.1016/j.bioactmat.2025.09.005

Figure Lengend Snippet: Protein identification for key proteins and signals in early bone defects. ( A ) Workflow for tissue protein identification at early stages of bone defects in rats. ( B , C ) KEGG and GO enrichment analysis of differential proteins in early healing tissues of femoral and alveolar bone defects. ( D , E ) Interaction network analysis of HSPA5 and IL-6 within the enrichment signals of femoral and alveolar bones. ( F ) Protein expression levels of HSPA5 and IL-6 in early healing tissues of femoral and alveolar defects. ( G ) Quantitative analysis of HSPA5 and IL-6 protein expression. Statistical analysis employed a t -test.

Techniques: Expressing

IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.

Journal: Bioactive Materials

Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

doi: 10.1016/j.bioactmat.2025.09.005

Figure Lengend Snippet: IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.

Techniques: Extraction, Gene Expression, Immunohistochemical staining, Expressing

M2 macrophages release IL-6 in alveolar bone defect repair. ( A ) Extraction of Il-6 -expressing cell populations. ( B ) Identification and classification of subpopulations within Il-6 -expressing cells. ( C ) Identification of the Il-6 + M2 cell subpopulation. ( D ) Temporal association between Il-6 + M2 cell subpopulation and samples. ( E – G ) Multiplex immunofluorescence for HSPA5 (GRP78/BiP), M2 macrophages (ARG1), and IL-6, combined with statistical analysis of fluorescence intensity and colocalization analysis. Scale bars: 1 mm, 100 μm and 50 μm. ( H ) KEGG and GO enrichment analysis of DEGs in the Il-6 + M2 cell subpopulation.

Journal: Bioactive Materials

Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

doi: 10.1016/j.bioactmat.2025.09.005

Figure Lengend Snippet: M2 macrophages release IL-6 in alveolar bone defect repair. ( A ) Extraction of Il-6 -expressing cell populations. ( B ) Identification and classification of subpopulations within Il-6 -expressing cells. ( C ) Identification of the Il-6 + M2 cell subpopulation. ( D ) Temporal association between Il-6 + M2 cell subpopulation and samples. ( E – G ) Multiplex immunofluorescence for HSPA5 (GRP78/BiP), M2 macrophages (ARG1), and IL-6, combined with statistical analysis of fluorescence intensity and colocalization analysis. Scale bars: 1 mm, 100 μm and 50 μm. ( H ) KEGG and GO enrichment analysis of DEGs in the Il-6 + M2 cell subpopulation.

Techniques: Extraction, Expressing, Multiplex Assay, Immunofluorescence, Fluorescence

IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.

Journal: Bioactive Materials

Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

doi: 10.1016/j.bioactmat.2025.09.005

Figure Lengend Snippet: IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.

Techniques: Expressing, Western Blot, TUNEL Assay, Staining

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