atg5 myc (Addgene inc)
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atg5 myc
Atg5 Myc, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcmv+myc+atg5/pCMV-myc-Atg5+(Plasmid+%2324922)/pmc09226670-48-0-8
Average 93 stars, based on 16 article reviews
Atg5 Myc, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcmv+myc+atg5/pCMV-myc-Atg5+(Plasmid+%2324922)/pmc09226670-48-0-8
Average 93 stars, based on 16 article reviews
atg5 myc - by Bioz Stars,
2026-09
93/100 stars
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Expressing:Article Title: Degradation of AF1Q by chaperone-mediated autophagy. Article Snippet: AF1Q, a mixed lineage leukemia gene fusion partner, is identified as a poor prognostic biomarker for pediatric acute myeloid leukemia (AML), adult AML with normal cytogenetic and adult myelodysplastic syndrome.. AF1Q is highly regulated during hematopoietic progenitor differentiation and development but its regulatory mechanism has not been defined clearly.. In the present study, we used pharmacological and genetic approaches to influence chaperonemediated autophagy (CMA) and explored the degradation mechanism of AF1Q. Article Title: Mitophagy Enhances Oncolytic Measles Virus Replication by Mitigating DDX58/RIG-I-Like Receptor Signaling Article Snippet: Cells were maintained in Dulbecco's modified Eagle medium (DMEM) supplemented with 0.1 mM nonessential amino acids, 5% fetal bovine serum, and penicillin-streptomycin (all from Invitrogen). .. Expression plasmids were as follows: pBABEpuro- EGFP-LC3 (Addgene; 22405) was provided by Jayanta Debnath (University of California, San Francisco, CA), Plasmid Preparation:Article Title: Degradation of AF1Q by chaperone-mediated autophagy. Article Snippet: AF1Q, a mixed lineage leukemia gene fusion partner, is identified as a poor prognostic biomarker for pediatric acute myeloid leukemia (AML), adult AML with normal cytogenetic and adult myelodysplastic syndrome.. AF1Q is highly regulated during hematopoietic progenitor differentiation and development but its regulatory mechanism has not been defined clearly.. In the present study, we used pharmacological and genetic approaches to influence chaperonemediated autophagy (CMA) and explored the degradation mechanism of AF1Q. Article Title: Elaiophylin, a novel autophagy inhibitor, exerts antitumor activity as a single agent in ovarian cancer cells Article Snippet: LysoTracker Red (L-7528), DQ Red BSA assay ( {"type":"entrez-nucleotide","attrs":{"text":"D12051","term_id":"2148853","term_text":"D12051"}} D12051 ), Earle balanced salt solution (EBSS; 14155063) and Texas Red dextran (D1863) were purchased from Invitrogen. .. LAMP1-RFP (plasmid 1817), pcDNA3-BECN1 (plasmid 21150) and shRNA:Article Title: Degradation of AF1Q by chaperone-mediated autophagy. Article Snippet: AF1Q, a mixed lineage leukemia gene fusion partner, is identified as a poor prognostic biomarker for pediatric acute myeloid leukemia (AML), adult AML with normal cytogenetic and adult myelodysplastic syndrome.. AF1Q is highly regulated during hematopoietic progenitor differentiation and development but its regulatory mechanism has not been defined clearly.. In the present study, we used pharmacological and genetic approaches to influence chaperonemediated autophagy (CMA) and explored the degradation mechanism of AF1Q. other:Article Title: Suppression of autophagy by mycophenolic acid contributes to inhibition of HCV replication in human hepatoma cells Article Snippet: Plasmids pCMV-myc-Atg3, pCMV-myc-Atg5, |
![Figure 3. BMMs from Lacc1–/– mice show reduced bacterial uptake and intracellular bacterial clearance, and reduced PRR- induced ROS, RNS, and autophagy pathways. BMMs were harvested from Lacc1þ/þ, Lacc1þ/–, or Lacc1–/– mice. (A, B) Cells were treated with 0.1 mg/mL lipid A for 48 hours. (A) Western blot LACC1. (B) S Typhimurium–GFP uptake (4 replicates; representative of 3 independent experiments). (C) Cells were treated with 0.1 mg/mL lipid A for 15 minutes. Fold p-PDK1 induction (3 replicates, representative of 2 independent experiments). (D) Cells were treated with 0.1 mg/mL lipid A for 48 hours. Cells were additionally treated with a PDK1 inhibitor (GSK2334470) or a PDK1 activator (PS48), and uptake of S Typhimurium– GFP was assessed (3 replicates, representative of 2 independent experiments). (E–G, I–K, M–O, Q–R) Cells were treated with 0.1 mg/mL lipid A for 48 hours. (E) Intracellular clearance of S Typhimurium or C rodentium (colony-forming units) (6 replicates, representative of 4 independent experiments). (F) ROS (4 replicates, representative of 4 independent experiments) and mtROS (4 replicates, representative of 3 independent experiments). (G, K, O) Expression of the indicated proteins by flow cytometry (3 replicates). (I, M, Q) Cells were transfected with an empty vector (EV) or (I) p47phox-expressing, (M) Nos2-expressing, or (Q) <t>Atg5-expressing</t> vectors. Intracellular S Typhimurium clearance (6 replicates, representative of 3 independent experiments). (J) Nitrite (5 replicates, representative of 4 independent experiments). (N) LC3II by Western blot. (H, L, P) Lacc1þ/þ BMMs (8 replicates) were treated with 0.1 mg/mL lipid A for 48 hours in the absence (control vehicle) or presence of inhibitors for (H) ROS (N-acetylcysteine [NAC]), (L) RNS (L-NAME), or (P) autophagy (3-MA) and then intracellular S Typhimurium clearance was assessed. (R) Cells were transfected with p47phox-, Nos2-, and Atg5-expressing vectors in combination (comb). Intracellular S Typhimurium clearance (6 replicates, representative of 2 independent experiments). Significance is to Lacc1+/+ BMMs in each respective treatment group or as indicated for (B-C, E-G, J-K, O). Mean þ standard error of the mean. *P < .05; **P < .01; ***P < .001; †P < 1 10–4; ††P < 1 10–5.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_3188/pm32693188/pm32693188__page8_image1.jpg)
![MDMs from high TNFSF15-expressing rs6478108 TT IBD risk carriers show increased NOD2-initiated antimicrobial pathways. MDMs from rs6478108 TT, TC, or CC carriers were left untreated or treated with 100 μg/mL MDP. ( A ) TNFSF15 surface expression by flow cytometry at 24 hours (n = 10 donors/genotype). ( B ) TNFSF15 secretion at 24 hours (n = 10/genotype). ( C ) Fold PDK1 activation at 20 minutes (n = 10/genotype). ( D ) Bacterial uptake at 20 minutes (n = 10/genotype). ( E ) p47phox expression and ROS production at 48 hours (n = 10/genotype). ( F ) NOS2 expression at 48 hours (n = 10/genotype). ( G ) ATG5 and LC3II expression at 48 hours (n = 10/genotype). ( H ) After 48 hours intracellular bacterial clearance was assessed (colony-forming units [CFU]) (n = 10/genotype). Means + SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; † P < 1 × 10 -4 ; †† P < 1 × 10 -5 . MFI, mean fluorescence intensity; Tx, treatment.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9184/pmc07689184/pmc07689184__gr14.jpg)
![MDMs from high TNFSF15-expressing rs6478108 TT IBD risk carriers show increased DR3-initiated antimicrobial pathways. MDMs from rs6478108 TT, TC, or CC carriers were left untreated or treated with 10 ng/mL TNFSF15. ( A ) Fold PDK1 activation at 20 minutes (n = 10 donors/genotype). ( B ) Bacterial uptake at 20 minutes (n = 10/genotype). ( C ) p47 expression and ROS production at 48 hours (n = 10/genotype). ( D ) NOS2 expression at 48 hours (n = 10/genotype). ( E ) ATG5 and LC3II expression at 48 hours (n = 10/genotype). ( F ) After 48 hours intracellular bacterial clearance was assessed (colony-forming units [CFU]) (n = 10/genotype). Means + SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; † P < 1 × 10 -4 ; †† P < 1 × 10 -5 . Tx, treatment.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9184/pmc07689184/pmc07689184__gr15.jpg)
