beclin1 (Proteintech)
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beclin1
Beclin1, supplied by Proteintech, used in various techniques. Bioz Stars score: 98/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/beclin1/Beclin+1+Fusion+Protein/pm41917198-295-92-102
Average 98 stars, based on 68 article reviews
Beclin1, supplied by Proteintech, used in various techniques. Bioz Stars score: 98/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/beclin1/Beclin+1+Fusion+Protein/pm41917198-295-92-102
Average 98 stars, based on 68 article reviews
beclin1 - by Bioz Stars,
2026-10
98/100 stars
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Blocking Assay:Article Title: Atractylenolide I ameliorates acute-on-chronic liver failure (ACLF) by promoting autophagy and preserving mitochondrial function through mTOR inhibition. Article Snippet: Acute-on-chronic liver failure (ACLF) is a severe liver syndrome marked by systemic inflammation and high mortality, often complicated by autophagy impairment and mitochondrial dysfunction.. This study investigates atractylenolide I (AT-1), a compound from Atractylodes macrocephala, for its potential to mitigate ACLF through modulation of mammalian target of rapamycin (mTOR) signaling, autophagy, and mitochondrial integrity.. We hypothesized that AT-1 could attenuate ACLF-induced liver damage by enhancing autophagy and mitochondrial function. Incubation:Article Title: Atractylenolide I ameliorates acute-on-chronic liver failure (ACLF) by promoting autophagy and preserving mitochondrial function through mTOR inhibition. Article Snippet: Acute-on-chronic liver failure (ACLF) is a severe liver syndrome marked by systemic inflammation and high mortality, often complicated by autophagy impairment and mitochondrial dysfunction.. This study investigates atractylenolide I (AT-1), a compound from Atractylodes macrocephala, for its potential to mitigate ACLF through modulation of mammalian target of rapamycin (mTOR) signaling, autophagy, and mitochondrial integrity.. We hypothesized that AT-1 could attenuate ACLF-induced liver damage by enhancing autophagy and mitochondrial function. Article Title: Angiotensin-(1-7) Alleviates Isoproterenol-Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor. Article Snippet: Proteins were separated by 12.5% SDS- polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β- MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066, USA), AT2R (ABclonal, A3654, China), Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor Article Snippet: Proteins were separated by 12.5% SDS‐polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β‐MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066 , USA), AT 2 R (ABclonal, A3654, China), Control:Article Title: Atractylenolide I ameliorates acute-on-chronic liver failure (ACLF) by promoting autophagy and preserving mitochondrial function through mTOR inhibition. Article Snippet: Acute-on-chronic liver failure (ACLF) is a severe liver syndrome marked by systemic inflammation and high mortality, often complicated by autophagy impairment and mitochondrial dysfunction.. This study investigates atractylenolide I (AT-1), a compound from Atractylodes macrocephala, for its potential to mitigate ACLF through modulation of mammalian target of rapamycin (mTOR) signaling, autophagy, and mitochondrial integrity.. We hypothesized that AT-1 could attenuate ACLF-induced liver damage by enhancing autophagy and mitochondrial function. Membrane:Article Title: Angiotensin-(1-7) Alleviates Isoproterenol-Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor. Article Snippet: Proteins were separated by 12.5% SDS- polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β- MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066, USA), AT2R (ABclonal, A3654, China), Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor Article Snippet: Proteins were separated by 12.5% SDS‐polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β‐MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066 , USA), AT 2 R (ABclonal, A3654, China), Aqueous Normal-phase Chromatography:Article Title: Angiotensin-(1-7) Alleviates Isoproterenol-Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor. Article Snippet: Proteins were separated by 12.5% SDS- polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β- MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066, USA), AT2R (ABclonal, A3654, China), Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor Article Snippet: Proteins were separated by 12.5% SDS‐polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β‐MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066 , USA), AT 2 R (ABclonal, A3654, China), Immunopeptidomics:Article Title: Angiotensin-(1-7) Alleviates Isoproterenol-Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor. Article Snippet: Proteins were separated by 12.5% SDS- polyacrylamide gel electrophoresis and transferred onto a 0.2 μm NC membrane (Cytiva, A3085788, USA). .. The membrane was blocked with 5% skim milk powder (Coolaber, CN7861, China) dissolved in TBST buffer at room temperature for 1 h. Subsequently, the membrane was incubated overnight at 4°C with the following primary antibodies: ANP (Affinity, DF6497, China), BNP (Affinity, DF6902, China), β- MHC (ABclonal, A22140, China), MasR (ThermoFisher scientific, MA557066, USA), AT2R (ABclonal, A3654, China), other:Article Title: Aspirin-induced mesenchymal stem cell-derived extracellular vesicles promote osteochondral regeneration by reprogramming macrophages. Article Snippet: Persistent inflammatory responses in osteochondral defects produce a hostile microenvironment that severely compromises endogenous tissue repair mechanisms.. The local immune microenvironment needs to be modulated to facilitate tissue regeneration.. In this study, an innovative bioactive platform was engineered that combined aspirin-induced bone marrow mesenchymal stem cells (BMSCs)-derived extracellular vesicles (Asp-EVs) and a thermoresponsive hydrogel (mPEP) composed of monofunctional polyhedral oligomeric silsesquioxane (mPOSS), polyethylene glycol (PEG), and polypropylene glycol (PPG). |
![a , Tau puncta formation (left) and degradation of preformed tau puncta (right) were quantified in HEK293 cells expressing 0N4R P301S Tau-Venus in the presence or absence of ULK1 activator Rac-(BL)-918. n = a total of 50 randomly selected fields per group from 3 biological replicates. b , c , HEK293 P301S tau-Venus cells were transfected with siRNA-ULK1 ( b ), siRNA-ULK2 ( c ) or siRNA-scramble ( b , c ), and transfected cells were incubated with or without 5-μM Rac-(BL)-918 in the presence of 10-nM tau seeds. Graphs in a – c show normalized fluorescence intensity relative to vehicle control ( a ) or in the absence of Rac-(BL)-918 ( b , c ), as indicated. n = a total of 54 randomly selected fields per group from 3 biological replicates. d , Rac-(BL)-918 inhibited the formation of tau puncta dependent on ULK1, FUNDC1, PINK1, Ambra1 and <t>Beclin1.</t> HEK293 P301S tau-Venus cells were transfected with siRNA-scramble or a siRNA candidate, followed by treatment with 10-nM tau seeds and 5-μM Rac-(BL)-918 simultaneously. n = a total of 36–40 randomly selected fields per group from 3 biological replicates. e , Rac-(BL)-918 increased the degradation of preformed tau puncta dependent on ULK1 and Beclin1. HEK293 P301S tau-Venus cells were transfected with siRNA-scramble or a siRNA candidate, followed by subsequent treatment with 10-nM tau seeds and 5-μM Rac-(BL)-918. n = a total of 36–40 randomly selected fields per group from 3 biological replicates. f , Associative memory tests were administered to adult day-2 transgenic C. elegans expressing hTau[P301L] n -sid-1 OV in the presence of siRNA targeting unc-51/ULK1 or control siRNA in the presence of Rac-(BL)-918, where indicated. Data are shown in the format of % CI, where a lower score corresponds to greater response to odorant and better memory function. n = 3 biological sets. g , Associative memory tests were administered to adult day-2 transgenic C. elegans expressing hTau[P301L] n -sid-1 OV in the absence or presence of siRNA to pink-1 or fndc-1/FUNDC1 . Data are shown in the format of % CI, where a lower score corresponds to greater response to odorant and better memory function. n = 5 biological sets. In the box plots, the center line denotes the median, box range indicates the 25th–75th percentile and whiskers denote minimum and maximum values. Unless specified elsewhere, data are mean ± s.e.m. Results represent pooled data from three to five biological replicates. Violin and box plots are centered around the median with interquartile ranges and all data points shown; the shape of the plot reflects the distribution of data. Statistical significance was determined using the Kruskal–Wallis test (non-normal data distribution) or one-way ANOVA (normal data distribution) ( a – e ) or two-way ANOVA followed by Tukey’s multiple comparisons test ( f , g ).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0337/pmc13190337/pmc13190337__43587_2026_1108_Fig7_HTML.jpg)
![( a ) Effects of ULK1 activators (2, 4 µM of LYN-1604 dihydrochloride; 0.5, 5 µM of (Rac)-BL-918) and inhibitors (5, 10 µM of SBI-0206965; 2.5, 5 µM of XST-14) on Tau seed-induced formation of Tau puncta in HEK293 cells expressing 0N4R P301S Tau-Venus. Data are pooled from 3 biological replicates. (b) Effects of ULK1 activators (2, 4 µM of LYN-1604 dihydrochloride; 0.5, 5 µM of (Rac)-BL-918) and inhibitors (5, 10 µM of SBI-0206965; 2.5, 5 µM of XST-14) on degradation of preformed Tau puncta in the HEK293 cells expression 0N4R P301S Tau-Venus. Data are pooled from 3 biological replicates. ( c ) mt-Keima and YPH-Parkin expressing HeLa cells were used to evaluate the effects on mitophagy induction by treating a positive control CCCP. Representative images are shown. ( d-f ) Quantification of mitophagy events by treating ULK1 activators, Rac-BL-918 (0.5, 5 µM) and LYN-1604 (2, 4 µM), as well as ULK1 inhibitors SBI-0206965 (5, 10 µM) and XST-14 (2.5, 5 µM). One dot represents the average value of one image. Data were pooled from 3 biological replicates. ( g-h ) Representative images ( g ) and quantification ( h ) of mitophagy induction from primary cortical neurons by treating ULK1 activators, Rac-BL-918 (5 µM) and LYN-1604 (4 µM), as well as ULK1 inhibitors SBI-0206965 (5 µM) and XST-14 (5 µM). Mitophagy was detected using a mitophagy detection dye kit. Nuclei were stained with DAPI. Scale bar = 20 μm. ( i ) Representative blots of target proteins (ULK1, ULK2, PINK1, GSK3β, Parkin, Atg5, FUNDC1, AMBRA1, BNIP3, Nix, Beclin1) and loading control (GAPDH or β-tubulin) in HEK293 cells expressing 0N4R P301S Tau-Venus transfected with siRNAs (100 nM, 48 h) or scrambled siRNA. ( j ) Associative memory tests were administered to adult day 2 transgenic C. elegans expressing hTau[P301L]n-sid-1 OV in the presence of ULK1 inhibitors (10, 100 µM of SBI-0206965; 5, 50 µM of XST-14). Attraction to odorant is quantified as Chemotaxis Index (% CI), where lower score corresponds to greater response to odorant/better memory function. Unless specified elsewhere, data are mean ± S.E.M. Statistical analyses performed were one-way ANOVA followed by Dunnett’s multiple comparisons test ( a , b , d-f , h ); two-way ANOVA followed by Tukey’s multiple-comparisons test ( j ).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0337/pmc13190337/pmc13190337__43587_2026_1108_Fig17_ESM.jpg)
