mouse α tuj1 (Cell Signaling Technology Inc)
Structured Review

Mouse α Tuj1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 194 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse α tuj1/product/Cell Signaling Technology Inc
Average 96 stars, based on 194 article reviews
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1) Product Images from "Activation of pro-survival autophagy by a small molecule promoting p62 oligomerisation"
Article Title: Activation of pro-survival autophagy by a small molecule promoting p62 oligomerisation
Journal: bioRxiv
doi: 10.1101/2025.05.27.656309
Figure Legend Snippet: A, Fluorescence microscopy images and quantification of mitophagy in Npc1 +/+ and Npc1 -/- MEFs expressing mt-mKeima cultured for 24 h in galactose medium supplemented with 50 nM rapamycin or 10 µM SQ-1. B , Fluorescence microscopy images and quantification of MitoSOX staining of Npc1 +/+ and Npc1 -/- MEFs cultured for 24 h in galactose medium supplemented with 50 nM rapamycin or 10 µM SQ-1. C , Phase-contrast images and cytotoxicity assay in Npc1 +/+ and Npc1 -/- MEFs cultured in galactose medium supplemented with 50 nM rapamycin or 10 µM SQ-1 for 72 h (phase contrast image) or 144 h (cytotoxicity assay). D , Cytotoxicity assay in control and NPC1 patient iPSC-derived cortical neurons after 4 weeks of neuronal differentiation, where neurons were treated with 50 nM rapamycin or 1-100 µM SQ-1 for 6 days. E , Fluorescence images and quantification of TUNEL + apoptotic nuclei in TUJ1 + cells treated as in D. F , Fluorescence images and quantification of LC3B and p62 puncta in TUJ1 + treated as in D. G , Schematic representation of the proposed mechanism by which SQ-1 sensitises p62 to mitochondria-generated ROS, leading to p62 oligomer formation, selective autophagy/mitophagy rescue, reduction in mitochondria with elevated ROS levels, and rescue of cell death. Data are mean ± SEM of n = 3 biological replicates. P values were calculated by one-way ANOVA followed by multiple comparisons with Dunnett’s test (A) or two-way ANOVA followed by multiple comparisons with Dunnett’s test (B, C, D). *P< 0.05; **P<0.01; ***P<0.001; ns (non-significant).
Techniques Used: Fluorescence, Microscopy, Expressing, Cell Culture, Staining, Cytotoxicity Assay, Control, Derivative Assay, TUNEL Assay, Generated


![Analysis of NEUROG1-deficient ears indicates that the nonsensory defects are not caused secondarily from reductions in the otic ganglion. (A-C) Low-power midmodiolar sections from control (A), Neurog1−/− (B) and E8.5 Sox2-deleted cochleae (C). The nonsensory phenotype was more severe in the absence of E8.5 SOX2 than of NEUROG1, and some neuronal formation still occurred [arrows mark neuronal expression <t>(TUJ1;</t> white) in C,F,I]. (D-K) Higher magnification views of the boxed regions in A-C highlight that sensory formation occurred fairly normally in the Neurog1-deficient mutant. (L-T) Examples of cross-sections through each vestibular organ in control (L-O), Neurog1−/− mutant (P-S) and E8.5 SOX2-deleted inner ears (T). The vestibule forms relatively normally in Neurog1-deficient mutants, with the exception of a smaller saccule devoid of sensory markers (arrow, P). By contrast, the only vestibular structure seen in E8.5 SOX2-deficient inner ears was an underdeveloped saccule (T). Scale bars: 50 µm.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_3603/pmc06633603/pmc06633603__develop-146-170522-g8.jpg)