kainic acid standard  (Chem Impex International)

Journal: mBio

Article Title: Domoic acid biosynthesis and genome expansion in Nitzschia navis-varingica

doi: 10.1128/mbio.02079-25

Figure Lengend Snippet: Kainoid production across marine eukaryotes. ( A ) Simplified eukaryotic tree of life based on Burki et al., with DA and kainic acid producers highlighted within their respective supergroups . ( B ) Rooted multi-locus phylogenetic analysis of alignments of 18S (SSU) and 23S (LSU) nuclear RNA genes as well as chloroplast genes psbC and rbcL from the Bacillariaceae family. shows a complete version of this phylogeny. Stars indicate dab clusters identified from this species. Bold indicates strains highlighted in this study. Images of Chondria armata (G. Saunders, University of New Brunswick) and Digenia simplex (T. Teruya, University of Ryukyus) are duplicated from our previous publication , reproduced here for context and comparison.

Article Snippet: Kainic acid standard was purchased from Chem-Impex.

Techniques: Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A UMAP plot illustrating the clustering of distinct cardiac cell populations. B UMAP plot comparing the composition of cardiac cell types between control (CON) and lipopolysaccharide (LPS)-treated groups. C Bar graph representing the relative proportion of each cardiac cell type in the CON and LPS groups. D UMAP plot showing the density of MacroD1 -positive cells across various cardiac cell types. E Dot plot displaying the expression levels of MacroD1 across multiple cell types in the CON and LPS groups. F , G Western blotting (WB) examination of MacroD1 protein in major organs of mice ( n = 4). H Immunofluorescent staining to show the colocalization of MacroD1 (red) and TOM20 (green for mitochondria) in neonatal rat cardiomyocytes (NRCMs). The cell nucleus was counterstained with DAPI (blue). I WB of MacroD1 expression in cell fractions of NRCMs (Cyto: Cytoplasm without mitochondria; Mito: Mitochondria). J , K WB of MacroD1 expression in hearts of mice 18 h post-intraperitoneal injection of vehicle (Veh) or LPS (10 mg/kg) ( n = 4). L – O WB, and quantitative analysis of MacroD1 proteins in NRCMs ( L and M ) or AC16 cells ( N and O ) after LPS stimulation (1 μg/ml) in indicated time points ( n = 4 cell samples from independent experiments). Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Dunnett’s multiple comparisons test ( G , M , O ). Data analysis was conducted using a two-tailed unpaired Student t test ( K ). Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Control, Expressing, Western Blot, Staining, Injection, Two Tailed Test

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Schematic overview of the breeding strategy for creating mice with an inducible, heart-specific MacroD1 knockout. Mice carrying the αMHC- MCM + MacroD1 flox/flox genotype, and upon tamoxifen induction, served as the experimental group (cKO). MacroD1 flox/flox littermate mice (Flox) constituted the control cohort. B Western blotting validation of the knockout of MacroD1 in left ventricular tissues and quadriceps muscle from 10-week-old mice. C Kaplan-Meier survival rates analysis of 10-week-old mice subjected to intraperitoneal injection of LPS (10 mg/kg) within 96 h ( n = 15). D – F Representative echocardiography ( D ) and echocardiographic analysis ( E , F ) in mice 18 h after LPS or saline administration (LVEF: left ventricular ejection fraction; LVFS: left ventricular fractional shortening; n = 7 mice for Flox and cKO; n = 8 mice for Flox + LPS and cKO + LPS). G and H , Serum levels of lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) in Flox and cKO mice injected intraperitoneally with/without LPS for 18 h ( n = 5 mice for Flox and cKO; n = 7 mice for Flox + LPS and cKO + LPS). I – K Immunofluorescent staining and quantitative analysis of Myeloperoxidase (MPO; I and J ) and α-smooth muscle actin (α-SMA; I and J ), and MASSON staining and quantification ( I , K ) in heart sections. MPO staining was performed from mice 18 h after LPS injection, and α-SMA and MASSON stainings were performed from mice 96 hours after LPS injection ( n = 5 for J ; n = 6 for K ). L Kaplan-Meier survival rates analysis of mice subjected to CLP surgery within 96 hours ( n = 15). M – O Representative echocardiography ( M ) and echocardiographic analysis ( N , O ) in mice 24 h after CLP or sham surgery ( n = 6). P , Q Serum levels of LDH and cTnT in mice 24 h after CLP surgery ( n = 5). R , S MPO and α-SMA immunofluorescent staining and quantitative analysis of heart tissues. MPO and α-SMA staining was performed on mice 24 h and 96 h after CLP or sham surgery, respectively ( n = 5). Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. The log-rank test was employed to analyze survival data. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Knock-Out, Control, Western Blot, Biomarker Discovery, Injection, Saline, Staining, Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Heatmap showing the relative expression of genes involved in the indicated metabolism pathway in the hearts of Flox and cKO mice injected intraperitoneally with/without LPS (10 mg/kg) for 18 h. B , C Gene set enrichment analysis (GSEA) of genes involved in indicated metabolism and oxidative phosphorylation pathways in the hearts of Flox and cKO mice 18 hours after LPS injection. D mRNA expression of genes involved in indicated metabolism pathways in the hearts of mice ( n = 4). E , F Representative dihydroethidium (DHE) fluorescent images and quantification of hearts from Flox and cKO mice with and without LPS administration for 18 h ( n = 6). G Myocardial ATP contents from Flox and cKO mice 18 hours after saline or LPS injection ( n = 6). H Representative transmission electron microscopy images of hearts from mice 18 h after LPS administration. I , J Quantification of cristae number/mitochondria ( I ; n = 85, 88, 97, and 84 mitochondria were analyzed in the Flox, cKO, Flox + LPS, and cKO + LPS groups, respectively.) and mitochondrial area ( J ; n = 352, 362, 389, and 384 mitochondria were analyzed in the Flox, cKO, Flox + LPS, and cKO + LPS groups, respectively) from ( H ). Each group consisted of 5 heart samples from different animals, with five randomly selected electron microscopy fields per sample for analysis of mitochondria. n represents the number of mitochondria. The box boundaries represent the 25th (Q1) and 75th percentiles (Q3) with a central line at the median (50th percentile). The box height spans the interquartile range (IQR = Q3–Q1). Whiskers extend to the lowest/highest data points within Q1–1.5 × IQR and Q3 + 1.5 × IQR bounds, respectively. Minima and maxima correspond to actual extreme values within the whisker-defined range. Data are shown as the mean ± SD for ( D – G ). Flox: MacroD1 flox/flox controls; cKO: MacroD1 flox/flox /αMHC MerCreMer mice. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Expressing, Injection, Phospho-proteomics, Saline, Transmission Assay, Electron Microscopy, Whisker Assay, Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: Neonatal rat cardiomyocytes (NRCMs) transfected with MacroD1 SiRNAs (Si-M) or scrambled control (NC) for 36 h and then treated with and without LPS (1 μg/ml) for 18 h to examine mitochondrial function. A , B Representative fluorescence images and quantification of MitoSOX in NRCMs ( n = 8). C Seahorse mitochondrial stress test was carried out in NRCMs ( n = 8) (OCR: Oxygen consumption rate; Oligo: Oligomycin; Rot/AA: Rotenone/Antimycin). D – G Quantification of basal respiration ( D ), maximal respiration ( E ), ATP-linked respiration ( F ), and spare respiration capacity ( G ) from C ( n = 8). H – K Measurements of oxygen consumption rate and corresponding indexes for seahorse fatty acid oxidation in NRCMs in the presence of bovine serum albumin (BSA) ( n = 7) (ETO: Etomoxir, FAO inhibitor). L – O Oxygen consumption rate and corresponding indexes for seahorse fatty acid oxidation in NRCMs in the presence of BSA and palmitate (PAL) ( n = 7). Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Transfection, Control, Fluorescence, Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Blue native gel analysis of the expression of myocardial mitochondrial complexes in mice 18 hafter saline or LPS (10 mg/kg) injection. B – F Mitochondrial complexes activities in the hearts of mice 18 h after saline or LPS injection ( n = 5 mice). G Schematic diagram of the sequence of MacroD1 and the MacroD1 mutant protein without the Macro domain (MacroD1 mut). H – K MitoSOX fluorescent staining ( H , I ; n = 5 cell samples from independent experiments), mitochondrial complex I activity ( J ; n = 4 cell samples from independent experiments), ATP levels ( K ; n = 5 cell samples from independent experiments) analysis in AC16 human cardiomyocytes transfected with plasmids of His- MacroD1 , Flag- Ndufb9 , or His- MacroD1 mut for 36 h and treated with and without LPS (1 μg/ml) for 18 h. L Venn diagram of MacroD1-binding proteins identified by antibody affinity proteomics, complex I-related proteins, and mono-ADP-ribosylated proteins immunocaptured by mono-ADP antibody. M Co-immunoprecipitation (Co-IP) for identifying endogenous interaction of MacroD1 and Ndufb9 in the hearts of mice. N Co-IP of MacroD1 and Ndufb9 in HEK293 cells transfected with His- MacroD1 and/or Flag- Ndufb9 plasmids for 48 hours. O His- MacroD1 or His- MacroD1 mutant with truncation of the Macro domain and Flag- Ndufb9 were co-expressed in HEK293 cells for Co-IP assay. Flox: MacroD1 flox/flox controls; cKO: MacroD1 flox/flox /αMHC MerCreMer mice. Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Expressing, Saline, Injection, Sequencing, Mutagenesis, Staining, Activity Assay, Transfection, Binding Assay, Immunoprecipitation, Co-Immunoprecipitation Assay, Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Co-IP assay for Ndufb9 MARylation in the hearts of mice injected intraperitoneally with and without LPS (10 mg/kg) for 18 h. B Co-IP assay for Ndufb9 MARylation in AC16 cells transfected with MacroD1 siRNA (Si-M) or scrambled control (NC) for 36 h and then treated or untreated with LPS (1 μg/ml) for 18 h. C Co-IP assay for Ndufb9 MARylation in AC16 cells transfected with Si-M, His- MacroD1 , or His- MacroD1 mutant plasmids for 48 h. D Mass spectrum identification of the MARylation site of Ndufb9 based on mitochondrial lysates isolated from mice hearts with anti-MARylation antibody. E Sequence conservation display on the MARylation site of Ndufb9 from Homo sapiens, Mus musculus, and Rattus. The red dotted box indicates the MARylation site of Ndufb9. F MARylation site mutation display of the Ndufb9 sequence. The red dotted box indicates the MARylation site mutation (Ndufb9 R173A ). G Co-IP assay for Ndufb9 MARylation in AC16 cells transfected with Flag- Ndufb9 or Flag- Ndufb9 R173A plasmid for 36 h and then treated with/without LPS (1 μg/ml) for 18 h. H Co-IP assay for Ndufb9 MARylation in AC16 cells transfected with the indicated siRNA or plasmids for 48 h. I – L Mitochondrial complex I activity ( I ; n = 5 cell samples from independent experiments), ATP levels ( J ; n = 5 cell samples from independent experiments), and MitoSOX fluorescent staining analysis ( K , L ; n = 5 cell samples from independent experiments) in AC16 cells transfected with indicated siRNA or plasmids for 36 hours and treated with/without LPS (1 μg/ml) for 18 h. The targeted sequence of the Ndufb9 plasmid corresponding to Si- Ndufb9 was synonymously mutated to avoid the interference of Si- Ndufb9 (Flag-SM- Ndufb9 ). Flox: MacroD1 flox/flox controls; cKO: MacroD1 flox/flox /αMHC MerCreMer mice. Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Co-Immunoprecipitation Assay, Injection, Transfection, Control, Mutagenesis, Isolation, Sequencing, Plasmid Preparation, Activity Assay, Staining, Comparison

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Heatmap showing the expression of NLRP3 inflammasome pathway-related genes in the hearts of mice injected intraperitoneally with/without LPS (10 mg/kg) for 18 h based on bulk RNA sequence analysis. B – D Expression of IL-1β , IL-18 , and TNF-α mRNAs in the hearts of mice with/without LPS administration ( n = 5). E – H Expression of NLRP3 inflammasome pathway-related proteins in the heart of mice 18 h after intraperitoneal LPS (10 mg/kg) injection ( n = 4). I – K Expression of ASC and NLRP3 proteins in the cytoplasm (Cyto; I and J ) and mitochondria (Mito; I and K ) isolated from hearts of mice together with LPS administration ( n = 4). L Co-IP assay for ASC-NLRP3 interaction in the hearts of mice, together with LPS administration. M , N Proximity Ligation Assay fluorescence detecting interaction between ASC and NLRP3 in isolated ventricular cardiomyocytes from adult mice treated or untreated with LPS (1 μg/ml) for 18 h ( n = 60). Red dots show ASC-NLRP3 interaction. Dotted lines outline cardiomyocytes. O – R Expression of NLRP3 pathway-related proteins in neonatal rat cardiomyocytes transfected with Si- MacroD1 (Si-M) or scrambled control (NC) for 36 h and administered ATP (3 mM) 18 h after LPS (1 μg/ml) treatment for 2 h ( n = 4). S Representative fluorescence images examining co-localization of ASC (green), NLRP3 (red), and DAPI (blue) staining in NRCMs transfected with Si- MacroD1 (Si-M) or scrambled control (NC) for 36 h and administered ATP (3 mM) 18 h after saline or LPS (1 μg/ml) treatment for 2 h. Flox: MacroD1 flox/flox controls; cKO: MacroD1 flox/flox /αMHC MerCreMer mice. The three lines in the violin plot represent the third quartile, median, and first quartile, respectively, while other data are shown as mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test ( B – D , N ). Data analysis was conducted using a two-tailed unpaired Student t test ( F , G , J, K , P – R ). Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Expressing, Injection, Sequencing, Isolation, Co-Immunoprecipitation Assay, Proximity Ligation Assay, Fluorescence, Transfection, Control, Staining, Saline, Comparison, Two Tailed Test

Journal: Nature Communications

Article Title: Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice

doi: 10.1038/s41467-025-62384-8

Figure Lengend Snippet: A Schematics for the application of the MacroD1 inhibitor in mice subjected to LPS challenge (MRS: MRS2578; Veh: vehicle; Echo: Echocardiography). B Kaplan-Meier survival analysis of wild-type mice with LPS and MRS2578 or vehicle administration ( n = 15). C – E Representative echocardiography ( C ) and echocardiographic analysis ( D and E ) in mice (LVEF: left ventricular ejection fraction; LVFS: left ventricular fractional shortening; n = 6). F and G , Serum levels of LDH and cTnT in mice ( n = 7). H – K Immunofluorescent analysis of Myeloperoxidase (MPO) ( H and I ; n = 7), dihydroethidium (DHE) ( H and J ; n = 7), and Masson’s staining analysis ( H and K ; n = 6) in the heart of mice. L ATP levels in mice hearts ( n = 6). M Schematic illustration displaying the action modality by which MacroD1 modulates heart function in sepsis. Under septic insults, cardiomyocyte MacroD1 inhibits mitochondrial complex I activity via de-monoADP-ribosylating (de-MARylation) Ndufb9, leading to aggravating mitochondrial dysfunction, inflammasome activation-coupled cardiomyocyte pyroptosis, and cardiac dysfunction. In contrast, genetic and pharmacological inhibition of MacroD1 preserves cardiac function by enhancing Ndufb9 MARylation-dependent bioenergetic reserve. Data are shown as the mean ± SD. Data analysis was conducted utilizing one-way ANOVA with Tukey’s multiple comparison test. The log-rank test was employed to analyze survival data. Source data are provided as a Source Data file.

Article Snippet: The mouse strain of cardiac-specific inducible knockout of the MacroD1 gene (cKO) was generated from Cyagen Biosciences (Shanghai, China) by crossing α-myosin heavy chain promoter-driven Cre mice ( αMHC MerCreMer ) with floxed MacroD1 ( MacroD1 flox/flox ) mice.

Techniques: Staining, Activity Assay, Activation Assay, Inhibition, Comparison

Journal: Scientific Reports

Article Title: A comparative study of five physiological key parameters between four different human trophoblast-derived cell lines

doi: 10.1038/s41598-017-06364-z

Figure Lengend Snippet: Evaluation of barrier function: Transport of nanoparticles through placental cell barriers. ( a ) Cytotoxicity of fluorescently-labelled 50 nm and 490 nm polystyrene nanoparticles. ( b ) Influence of adhesion promoters on the transport of fluorescently-labelled 50 nm polystyrene nanoparticles through 3 µm transwell membranes. Values for transwell inserts without cells were set to 100% of membrane-less wells. ( c ) Time-trace of transcellular transport after 6 h, 12 h and 24 h of transport of 50 nm fluorescently-labelled polystyrene nanoparticles through BeWo, ACH-3P, Jeg-3 and JAR cell barriers. ( d ) Apical-to-basal transport ratio after 24 h for 50 nm and 490 nm fluorescently-labelled polystyrene nanoparticles through BeWo, ACH-3P, Jeg-3 and JAR cell barriers. Data points are mean values ± SD for n = 3 .

Article Snippet: For evaluation of the cytotoxic potential of non-toxic 50 nm and 490 nm polystyrene nanoparticles (Kisker Biotech, PFP-00552), an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was performed in 96-well microtiter plates to determine placental cell viability.

Techniques: Membrane

Journal: Scientific Reports

Article Title: A comparative study of five physiological key parameters between four different human trophoblast-derived cell lines

doi: 10.1038/s41598-017-06364-z

Figure Lengend Snippet: Functional evaluation matrix for BeWo, ACH-3P, JAR and Jeg-3 cell models.

Article Snippet: For evaluation of the cytotoxic potential of non-toxic 50 nm and 490 nm polystyrene nanoparticles (Kisker Biotech, PFP-00552), an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was performed in 96-well microtiter plates to determine placental cell viability.

Techniques: Functional Assay, Permeability