Journal: Molecular Cell

Article Title: The ASC-1 Complex Disassembles Collided Ribosomes

doi: 10.1016/j.molcel.2020.06.006

Figure Lengend Snippet: ASCC Is Required for Aborting Translation at a Ribosome Stall (A) The dual-fluorescence reporter used to study translational stalling. (B) Cells were treated with control (gray shaded) or ASCC3-targeting (red traces) siRNAs for 72 h before induction of the stably integrated reporter with doxycycline for 20 h. The RFP:GFP ratio as determined by flow cytometry is plotted as a histogram. (C) Immunoblots of whole cell lysates after treatment with the indicated siRNAs for 72 h. A non-specific product detected by the ASCC1 antibody is indicated with an asterisk in this and subsequent figures. (D) Stalling assay as in (B) after treatment with the indicated siRNAs for 72 h. See also and .

Article Snippet: Rabbit polyclonal anti-ASCC1 , Bethyl , Cat. #A303-871A.

Techniques: Fluorescence, Stable Transfection, Flow Cytometry, Western Blot

Journal: Molecular Cell

Article Title: The ASC-1 Complex Disassembles Collided Ribosomes

doi: 10.1016/j.molcel.2020.06.006

Figure Lengend Snippet:

Article Snippet: Rabbit polyclonal anti-ASCC1 , Bethyl , Cat. #A303-871A.

Techniques: Recombinant, Protease Inhibitor, Plasmid Preparation, Sequencing, Mutagenesis, Software, Clone Assay

Journal: Neural Regeneration Research

Article Title: Mutual regulation of microglia and astrocytes after Gas6 inhibits spinal cord injury

doi: 10.4103/NRR.NRR-D-23-01130

Figure Lengend Snippet: Primary antibodies used in this study

Article Snippet: ASCC1 , 1:200 , Origene , Rockville, MD, USA , TA503721S , AB_11127958.

Techniques:

Journal: Neural Regeneration Research

Article Title: Mutual regulation of microglia and astrocytes after Gas6 inhibits spinal cord injury

doi: 10.4103/NRR.NRR-D-23-01130

Figure Lengend Snippet: Gas6/Axl signal pathway is inactive in reactive and scar-forming astrocyte after SCI. (A) The violin plot analyses were shown the change of the Gas6 and Axl expression in naive, reactive and scar-forming astrocytes clusters after SCI. (B) Immunofluorescence analysis of Ascc1 + (green, FITC) cells and Gas6 (red, Alexa Fluor 594) immunopositivity in the injured spinal cord. Ascc1 + cells and the immunopositivity of Gas6 were significantly decreased after SCI. (C) Immunofluorescence analysis of Nestin + (green, FITC) cells and Gas6 (red, Alexa Fluor 594) immunopositivity in the injured spinal cord. Nestin + cells were increased and the immunopositivity of Gas6 was significantly decreased after SCI. (D) Immunofluorescence analysis of Bcan + (green, FITC) cells and Gas6 (red, Alexa Fluor 594) immunopositivity in the injured spinal cord. Bcan + cells were increased and the immunopositivity of Gas6 was significantly decreased after SCI. (E) Immunofluorescence analysis of Ascc1 + (red, Alexa Fluor 594) cells and Axl (green, FITC) immunopositivity in the injured spinal cord. Ascc1 + cells and immunopositivity of Axl were significantly decreased after SCI. (F) Immunofluorescence analysis of Nestin + (red, Alexa Fluor 594) cells and Axl (green, FITC) immunopositivity in the injured spinal cord. Nestin + cells were increased and the immunopositivity of Axl was significantly decreased after SCI. (G) Immunofluorescence analysis of Bcan + (red, Alexa Fluor 594) cells and Axl (green, FITC) immunopositivity in the injured spinal cord. Bcan + cells were increased and the immunopositivity of Axl was significantly decreased after SCI. Scale bars: 100 μm (upper), 20 μm (lower). The data are presented as the means ± SD ( n = 3). ** P < 0.01, vs . sham group (unpaired t -test). A.U.: Arbitrary unit; Axl: AXL receptor tyrosine kinase; Bcan: brevican; DAPI: 4′,6-diamidino-2-phenylindole; FITC: fluorescein isothiocyanate isomer I; Gas6: growth arrest specific protein 6; SCI: spinal cord injury.

Article Snippet: ASCC1 , 1:200 , Origene , Rockville, MD, USA , TA503721S , AB_11127958.

Techniques: Expressing, Immunofluorescence

Journal: The Application of Clinical Genetics

Article Title: RAI1 gene mutations: mechanisms of Smith–Magenis syndrome

doi: 10.2147/TACG.S128455

Figure Lengend Snippet: Schematic representation of chromosome 17, common 17p11.2 deletion, and RAI1 . From left to right, the following are shown: the ideogram of G-band pattern of human chromosome 17; a schematic representation of the Smith–Magenis syndrome region with some representative genes; the RAI1 genomic and protein structure – glutamine-rich domain (Poly-Q), bipartite nuclear localization signals (NLS1 and NLS2), two serine-rich domains (Poly-S1 and Poly-S2), and C-terminal plant homeodomain (PHD); and the RAI1 mutations indexed in the HGMD™ Professional (version December 2015.4) known to date. * Indicates either frameshift or nonsense mutations.

Article Snippet: – A recent study by Thaker et al identified a de novo RAI1 mutation in a child with morbid obesity and a clinical diagnosis of the Rapid-onset Obesity with Hypothalamic dysfunction, Hypoventilation and Autonomic Dysregulation (ROHHAD) syndrome.

Techniques: