Journal: Molecules

Article Title: Lactic Acid Bacteria Simultaneously Encapsulate Diverse Bioactive Compounds from a Fruit Extract and Enhance Thermal Stability

doi: 10.3390/molecules27185821

Figure Lengend Snippet: Characterization of MG juice matrix and the encapsulation efficiency of the polyphenolics from the juice using L. casei cell carrier. For this characterization, the antioxidant activity of the juice before and after encapsulation was quantified.

Article Snippet: Lactobacillus casei (ATCC 393) were selected as a model for human probiotic bacteria.

Techniques: Encapsulation, Antioxidant Activity Assay, FRAP Assay

Journal: Molecules

Article Title: Lactic Acid Bacteria Simultaneously Encapsulate Diverse Bioactive Compounds from a Fruit Extract and Enhance Thermal Stability

doi: 10.3390/molecules27185821

Figure Lengend Snippet: Confocal fluorescence microscopy of juice encapsulated cells with a 405 nm excitation, and 500–550 nm emission; ( a ) L. casei control cells; ( b ) L. casei cells encapsulated with MG juice. Lower left is the zoomed-in view of the same image: zoomed-in views in ( b ) demonstrated the uniform intracellular localization of polyphenolic compounds in the cell carriers.

Article Snippet: Lactobacillus casei (ATCC 393) were selected as a model for human probiotic bacteria.

Techniques: Fluorescence, Microscopy, Control

Journal: Molecules

Article Title: Lactic Acid Bacteria Simultaneously Encapsulate Diverse Bioactive Compounds from a Fruit Extract and Enhance Thermal Stability

doi: 10.3390/molecules27185821

Figure Lengend Snippet: Phenolic profile of MG juice encapsulated compounds in L. casei cell carrier.

Article Snippet: Lactobacillus casei (ATCC 393) were selected as a model for human probiotic bacteria.

Techniques: Molecular Weight, Encapsulation

Journal: Cancer Cell International

Article Title: Marine natural product Methyl mycophenolate inhibits gastric cancer growth through regulating p53 and the downstream pathways

doi: 10.1186/s12935-025-03835-6

Figure Lengend Snippet: Identification of Methyl mycophenolate as a novel anti-cancer compound against GC. a Schematic of the compound screening process. b AGS cells were treated with the compounds from the natural marine chemical library (10 µM) for 48 h, and then cell viability was assayed. The bar graph shows the inhibition of cell viability of the 93 compounds. c The Chemical structure of MMP. d AGS cells were treated with MMP (10µM) for 48 h and cell viability was analyzed using the CCK8 kit and their cell viability inhibition was calculated ( n = 3). e Determination of IC 50 of the four GC cells as well as the GES-1 and 293T cell lines for 48 h ( n = 3)

Article Snippet: The natural marine chemical library was obtained from TargetMol Company (TargetMol, #L6400, USA), MMP (C 18 H 22 O 6 , molecular weight: 334.36, purity: 99.48%) (TargetMol, # T19424 , USA), was dissolved in DMSO with a final concentration of 10mM and diluted by RPMI-1640 medium to prepare proper working concentrations.

Techniques: Inhibition

Journal: bioRxiv

Article Title: Palmitoylation Couples DLK to JNK3 to Facilitate Pro-degenerative Axon-to-Soma Signaling

doi: 10.1101/2020.11.17.387191

Figure Lengend Snippet: A: Lysates from HEK293T cells transfected to express the indicated cDNA constructs were blotted to detect the phosphorylated active form of JNK (p-JNK, top), myc (middle) or GFP (bottom). GFP-tagged wild type DLK (wtDLK-GFP), but not palmitoyl mutant DLK (DLK-CS-GFP), greatly increases JNK3 phosphorylation, which correlates with a slowing of DLK-GFP mobility on SDS-PAGE. The slowing of DLK mobility is due to phosphorylation (Compare pDLK and DLK. See also Fig S3). B: HEK293T cells were transfected with wtDLK-GFP with or without myc-tagged JNK3 (myc-JNK3) and then treated with 2BrP or vehicle. Lysates were blotted as in A . Wild type DLK markedly increases JNK3 phosphorylation, which correlates with a marked slowing of wtDLK-GFP mobility on SDS-PAGE (pDLK versus DLK, bottom panel). 2BrP prevents both JNK3 phosphorylation and the change in DLK-GFP mobility. Blots in A and B are representative of at least three separate experiments. C : Schematic of set-up to determine functional effect of DLK palmitoylation and feedback phosphorylation by JNK3. Left hand scheme: Wild type DLK should increase phosphorylation of wild type JNK3, which should in turn phosphorylate DLK. Middle scheme: Wild type DLK should be capable of phosphorylating kinase-dead JNK3 (JNK3 kd) but JNK3 kd should be incapable of feedback phosphorylation. Right hand scheme: DLK-CS is incapable of driving phosphorylation of JNK3, which in turn cannot phosphorylate DLK. D: Enabling positive feedback phosphorylation leads to greatly increased phosphorylation of JNK3 by DLK. HEK293T cells were transfected with vector alone, wtDLK-GFP or wtMLK3-GFP (DLK paralog that is not palmitoylated; ) plus either myc-tagged wild type or kinase dead JNK3 (Myc-JNK3wt, Myc-JNK3kd). Lysates were immunoblotted to detect phosphoJNK (p-JNK, top ), myc-JNK3 (middle) or GFP-tagged MAP3Ks (bottom) . JNK3 phosphorylation is markedly higher when feedback loop is engaged (compare top blot, lanes 3, 4). Reduced JNK3 kd phosphorylation is not due to impaired phosphorylatability of the kinase dead JNK3 because phosphorylation of myc-JNK3kd is even more strongly phosphorylated than myc-JNK3wt when MLK3 (MAP3K11) is co-expressed (compare top blot, lanes 5, 6). E: Quantified data from D confirm that phosphorylation of JNK3kd induced by DLK is far lower than that of JNK3wt (*; p=0.0211, n=4, Mann-Whitney test). In contrast, phosphorylation of JNK3kd by MAP3K11 tends toward being greater than that of of JNK3wt (ns; p=0.0636, n=3, Mann-Whitney test). F: Lack of evidence for positive feedback phosphorylation of DLK by p38 MAPK. HEK293T cells were transfected with myc-tagged wild type or kinase dead p38 MAPK (Myc-p38wt, Myc-p38kd), DLK-GFP and HA-tagged MAPKAPK2 (HA-MAPKAPK2, a downstream p38 MAPK substrate ) as indicated. Lysates were blotted to detect phospho–p38 ( top ), myc-p38 ( second row ), DLK-GFP ( third row ), MAPKAPK2 phosphorylated at T334 (p38MAPK phosphorylation site, T334(P), fourth row ) and HA-tagged MAPKAPK2 ( bottom row ). P38 wildtype does not alter DLK-GFP mobility, compared to p38kd. Cotransfected DLK triggers similar phosphorylation of both p38wt and p38kd. The lower molecular weight band at approximately 38 kDa detected by the p-p38 antibody likely represents endogenous phosphop38 (p-p38 Endo, top panel). MAPKAPK2 T334 signal confirms that myc-p38kd is indeed kinase-dead. G: Quantified data from F confirm that p38 kinase dead mutation does not affect DLK-induced p38 phosphorylation (ns; p= 0.2817, Mann-Whitney test, n=4). All data are shown as mean ± SEM.

Article Snippet: Primary antibodies used were as follows: Rabbit anti-phospho c-Jun S63 (#91952, and rabbit anti-phospho c-Jun S63 II (Cell Signaling Technology, #9261, both used for DRG neuron experiments), Rabbit anti-phospho c-Jun Ser-73 (Cell Signaling Technology, #3270, used for RGC experiments); rabbit anti-DLK/MAP3K12 (Sigma/ Prestige, #HPA039936); mouse anti-GFP (Life Technologies, #A11120, clone 3E6 IgG2a), rabbit anti-GFP (Life Technologies, #A11122), mouse anti-Tubulin β3 (BioLegend, TUJ1, Ig2a, Covance catalog# MMS-435P), Myc 9E10 (University of Pennsylvania Cell Center, Catalog #3207), mouse anti-Myc (Enzo, myc9E10), mouse anti-HA11 (BioLegend, 901502, IgG1), rabbit anti HA (Cell Signaling Technology, #3724), mouse anti-tubulin (Millipore Sigma, Catalog #T7451), sheep anti-NGF (CedarLane, catalog #CLMCNET-031), Rabbit anti-phosphoMKK4 (Cell Signaling Technology, #4514, Rabbit anti-MKK4 (Cell Signaling Technology, #9152), Rabbit anti-phosphoAkt T308 (Cell Signaling Technology, #9275, Rabbit anti-Akt (Cell Signaling Technology, #4691), Rabbit anti-phosphoERK (Cell Signaling Technology, #9106), mouse anti-panERK1/2 (Cell Signaling Technology, #9106), mouse anti-phosphoJNK (Cell Signaling Technology, #9255), rabbit anti pan-JNK (Santa Cruz Biotechnology, #SC-571), rabbit anti-phospho-MAPKAPK2 T334 (Cell Signaling Technology, #3041), rabbit anti-phospho-p38 MAPK Cell Signaling Technology, #4511).

Techniques: Transfection, Construct, Mutagenesis, Phospho-proteomics, SDS Page, Functional Assay, Plasmid Preparation, MANN-WHITNEY, Molecular Weight