Journal: bioRxiv

Article Title: Single-cell transcriptional landscape of temporal neutrophil response to burn wound in larval zebrafish

doi: 10.1101/2024.04.01.587641

Figure Lengend Snippet: (A) Schematic view of validating signatures identified from zebrafish myeloid subsets in human burn patient expression profile. (B) Expression level distribution of Immature_Neuts signatures (top panel) and lgals3bpb_Mac1 (bottom panel) by patient TBSA shown as raincloud plots. Paired T-tests were performed between the Low and the Very High TBSA groups. (C) Expression distribution of GPR84 and GYG1 in patients by TBSA level. Spearman correlation (ρ) is calculated between gene expression and TBSA level. (D) Representative flow plots (left) and quantifications of frequencies shown as percentages (right) of GPR84+ neutrophils in burn (n = 6) and healthy (n = 4) blood. Paired samples t-test, p = 0.022.

Article Snippet: Protein-targeted staining was done with the following antibodies in Cell Staining Buffer: Alexa Fluor 700-conjugated anti-human CD16 at 1:400, PE/Fire-640-conjugated anti-human CD66b at 1:400, PerCP-conjugated anti-human CD3 at 1:200, PerCP-conjugated anti-human CD19 at 1:200, PerCP-conjugated anti-human CD56 at 1:400, PerCP-conjugated anti-human CD203c at 1:100 (BioLegend), BUV395-conjugated mouse anti-human CD45 at 1:100 (BD Biosciences), and PE-conjugated GPR84 at 1:200 (Alomone Labs).

Techniques: Expressing, Gene Expression

Journal: Cancer cell

Article Title: Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

doi: 10.1016/j.ccell.2019.08.006

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: After removing the Cell Stripper and washing the cell pellet with ice cold PBS, the cells were stained on ice for 30 minutes in 100 µL DMEM/F12 (without phenol red) with an APC mouse anti-human CD44 (559942, BD Biosciences) and FITC mouse anti-human CD24 (555427, BD Biosciences) or an APC mouse IgG2b (555745, BD Biosciences) and FITC mouse IgG2a (553456, BD Biosciences) as isotype controls.

Techniques: Magnetic Beads, Recombinant, Electron Microscopy, Protease Inhibitor, Transfection, DC Protein Assay, Blocking Assay, Mutagenesis, SYBR Green Assay, Sample Prep, Purification, Chromatin Immunoprecipitation, DNA Purification, Amplification, Mass Spectrometry, Expressing, Binding Assay, Plasmid Preparation, Construct, Software, Real-time Polymerase Chain Reaction

Journal: American Journal of Human Genetics

Article Title: Identification of a Kir3.4 Mutation in Congenital Long QT Syndrome

doi: 10.1016/j.ajhg.2010.04.017

Figure Lengend Snippet: The Kir3.4-Gly387Arg Mutation Is Associated with Congenital Long QT Syndrome

Article Snippet: Proteins were transferred onto Hybond-P polyvinylidene difluoride transfer membranes (Amersham Biosciences, 0.45 μm), and membranes were blocked in 5% nonfat milk in TBST (0.1% Tween 20 in Tris-buffered saline solution) for 2 hr at room temperature and then incubated with primary antibody against Kir3.1 (1:1,000; Alomone Labs), Kir3.4 (1:1,000; Alomone Labs), calnexin (1:2,000; Nordic Biosite), or Na + /K+-ATPase α1 (1:500; Santa Cruz Biotechnology) overnight.

Techniques: Mutagenesis

Journal: American Journal of Human Genetics

Article Title: Identification of a Kir3.4 Mutation in Congenital Long QT Syndrome

doi: 10.1016/j.ajhg.2010.04.017

Figure Lengend Snippet: Clinical Characteristics of the Pedigree Members with Kir3.4-Gly387Arg or Sudden Death

Article Snippet: Proteins were transferred onto Hybond-P polyvinylidene difluoride transfer membranes (Amersham Biosciences, 0.45 μm), and membranes were blocked in 5% nonfat milk in TBST (0.1% Tween 20 in Tris-buffered saline solution) for 2 hr at room temperature and then incubated with primary antibody against Kir3.1 (1:1,000; Alomone Labs), Kir3.4 (1:1,000; Alomone Labs), calnexin (1:2,000; Nordic Biosite), or Na + /K+-ATPase α1 (1:500; Santa Cruz Biotechnology) overnight.

Techniques:

Journal: American Journal of Human Genetics

Article Title: Identification of a Kir3.4 Mutation in Congenital Long QT Syndrome

doi: 10.1016/j.ajhg.2010.04.017

Figure Lengend Snippet: Electrophysiological Analyses of Kir3.4-Gly387Arg

Article Snippet: Proteins were transferred onto Hybond-P polyvinylidene difluoride transfer membranes (Amersham Biosciences, 0.45 μm), and membranes were blocked in 5% nonfat milk in TBST (0.1% Tween 20 in Tris-buffered saline solution) for 2 hr at room temperature and then incubated with primary antibody against Kir3.1 (1:1,000; Alomone Labs), Kir3.4 (1:1,000; Alomone Labs), calnexin (1:2,000; Nordic Biosite), or Na + /K+-ATPase α1 (1:500; Santa Cruz Biotechnology) overnight.

Techniques:

Journal: American Journal of Human Genetics

Article Title: Identification of a Kir3.4 Mutation in Congenital Long QT Syndrome

doi: 10.1016/j.ajhg.2010.04.017

Figure Lengend Snippet: Cell Surface Expression of Kir3.4-Gly387Arg and Kir3.1

Article Snippet: Proteins were transferred onto Hybond-P polyvinylidene difluoride transfer membranes (Amersham Biosciences, 0.45 μm), and membranes were blocked in 5% nonfat milk in TBST (0.1% Tween 20 in Tris-buffered saline solution) for 2 hr at room temperature and then incubated with primary antibody against Kir3.1 (1:1,000; Alomone Labs), Kir3.4 (1:1,000; Alomone Labs), calnexin (1:2,000; Nordic Biosite), or Na + /K+-ATPase α1 (1:500; Santa Cruz Biotechnology) overnight.

Techniques: Expressing

Journal: American Journal of Human Genetics

Article Title: Identification of a Kir3.4 Mutation in Congenital Long QT Syndrome

doi: 10.1016/j.ajhg.2010.04.017

Figure Lengend Snippet: Human Atrial and Ventricular Expression of Kir3.1 and Kir3.4

Article Snippet: Proteins were transferred onto Hybond-P polyvinylidene difluoride transfer membranes (Amersham Biosciences, 0.45 μm), and membranes were blocked in 5% nonfat milk in TBST (0.1% Tween 20 in Tris-buffered saline solution) for 2 hr at room temperature and then incubated with primary antibody against Kir3.1 (1:1,000; Alomone Labs), Kir3.4 (1:1,000; Alomone Labs), calnexin (1:2,000; Nordic Biosite), or Na + /K+-ATPase α1 (1:500; Santa Cruz Biotechnology) overnight.

Techniques: Expressing

Journal: American Journal of Physiology - Heart and Circulatory Physiology

Article Title: Enhanced large conductance K + channel activity contributes to the impaired myogenic response in the cerebral vasculature of Fawn Hooded Hypertensive rats

doi: 10.1152/ajpheart.00636.2013

Figure Lengend Snippet: Comparison of BK-α- and BK-β-subunit expression in cerebral vessel homogenates isolated from FHH and FHH.1BN rats. BK-α- and BK-β-subunits were probed on different blots. The same blots were then reprobed for β-actin. A: representative bands corresponding to the molecular weight of the BK-α-subunit (∼100 kDa), BK-β-subunit (∼25 kDa), and β-actin (∼42 kDa) in cerebral vessels obtained from FHH and FHH.1BN rats (n = 8 animals each; 3 sets of experiments). B: a comparison of the expression of α- and β-subunits. Numbers in parentheses indicate the number of samples studied.

Article Snippet: After transfer, the membrane was blocked with TBS-T buffer containing 20 mM Tris pH 7.5, 150 mM NaCl, 0.05% Tween, and a 5% blocking powder (Bio-Rad) at 4°C for 1 h. The blot was probed with primary antibody against BK α- and β-subunit [1:500 and 1:200, respectively; polyclonal rabbit Anti-K Ca 1.1, to amino acids 1184–1200 and Anti-sloβ1 (KCNMB1); Alomone Labs, Jerusalem, Israel] overnight at 4°C.

Techniques: Expressing, Isolation, Molecular Weight