mouse anti calnexin99a  (Developmental Studies Hybridoma Bank)

Journal: PLOS One

Article Title: Exosomal miR-320b regulates cardiomyocyte FOXM1 expression and may serve as an early-stage compensatory mechanism in obstructive sleep apnea

doi: 10.1371/journal.pone.0332862

Figure Lengend Snippet: (a) Representative transmission electron microscopy (TEM) images of exosomes isolated from plasma samples. The images depict the cup-shaped morphology of Ctrl -exo (left panel) and OSA-exo (right panel). Scale bars = 100 nm. (b) WB analysis showing the presence of the exosomal markers TSG101 and CD9 and the absence of Calnexin, a common exosomal contaminant, indicating high purity of the exosomes. HEK293T cell lysate was used as a control to verify the specificity of exosomal markers and rule out contamination. (c) Nano-flow cytometry (nFCM) analysis showing the presence of the exosome surface markers CD9 and CD81 and the absence of IgG, a negative control, in both Ctrl-exo (upper panel) and OSA-exo (lower panel). (d) Particle size distribution of exosomes as determined by nFCM. Both Ctrl-exo (left panel) and OSA-exo (right panel) displayed a typical size range of 30–150 nm.

Article Snippet: After blocking in 5% non-fat dry milk in TBST for 30 min, the membranes were incubated overnight at 4°C with primary antibodies (1:1000, Abcam) toward TSG101 (ab125011), CD9 (BOSTER, BM4212), Calnexin (ab22595), FOXM1 (ab207298), and β-Tubulin (Sinobiological, 100109-MM05T), respectively.

Techniques: Transmission Assay, Electron Microscopy, Isolation, Clinical Proteomics, Control, Flow Cytometry, Negative Control

Journal: eLife

Article Title: Loss of dihydroceramide desaturase drives neurodegeneration by disrupting endoplasmic reticulum and lipid droplet homeostasis in glial cells

doi: 10.7554/eLife.99344

Figure Lengend Snippet: ( A, B ) Abdominal segments of dissected ventral nerve cords from late-third instar larvae of the indicated genotype labeled for fatty acid binding protein (FABP) to label cortex glia and ELAV to label neurons ( A–A’’ ) or FABP and the ER-marker Calnexin-99A (CNX99A; B–B’’ ). As observed in ifc js3 / ifc-KO larvae, ifc js1 and ifc js2 larvae exhibited swollen cortex glia ( A, B ) and an expanded ER phenotype in cortex glia as indicated by elevated CNX99A expression ( B ). ( C–C’’’ ) ifc js1 and ifc js1 / ifc js2 larvae also exhibit enhanced presence of the neuronal cell death marker Cleaved Caspase-3 (CC3). Note that the chromosome that harbors the ifc js2 chromosome also harbors a mutation in the pro-apoptotic gene, Dark . Therefore, to track the impact of ifc js2 on neuronal cell death, we assessed neuronal cell death in larvae trans-heterozygous for ifc js1 and ifc js2 (Civ). Scale bar is 50 µm.

Article Snippet: Antibody , Mouse anti-CNX 99A monoclonal , DSHB , RRID: AB_2722011 , 1:20.

Techniques: Labeling, Binding Assay, Marker, Expressing, Mutagenesis