igf 1r  (Bioss)

Journal: Journal of Nanobiotechnology

Article Title: RVG-targeted extracellular vesicles loaded with echinatin attenuate dopaminergic neurodegeneration via the IGF-2/PI3K/Akt pathway in Parkinson’s disease mice

doi: 10.1186/s12951-025-03997-5

Figure Lengend Snippet: RVG-EVs@Echi attenuate oxidative stress in the in vitro PD models. ( a ) Representative blots and ( b ) quantification of the expression levels of IGF2, P-PI3K, PI3K, P-Akt, Akt, and Nrf2 in MN9D cells. ( c ) Representative blots and ( d ) quantification of Bcl-2, Bax, and the resulting Bcl-2/Bax ratio in MN9D cells. ( e , g ) Representative blots and ( f , h ) quantification showing the effects of the IGF-1R/IR inhibitor NVP-AEW541 in MN9D cells. ( i ) Representative graphs of ROS generation in control or MPP+-treated cells upon RVG-EVs@Echi treatment. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( k ) MitoSOX was used to stain live control or MPP+-treated cells upon treatment with RVG-EVs@Echi. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( j , l ) Quantification of the relative ROS and MitoSOX fluorescence intensity. n = 6 per group. ( m ) Representative flow cytometry histograms and ( n ) quantification of mean fluorescence intensity (MFI) showing intracellular ROS levels in MN9D cells. n = 3 per group. Statistical Analysis: For (a-d): Groups are Control, MPP+, and MPP + + RVG-EVs@Echi. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + group. For (e-h): Groups are Control, MPP + + RVG-EVs@Echi, and MPP + + RVG-EVs@Echi + NVP-AEW541. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + + RVG-EVs@Echi group. For (i-n): Groups are Control, RVG-EVs@Echi, MPP+, and MPP + + RVG-EVs@Echi. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. RVG-EVs@Echi group; & p < 0.05, && p < 0.01 vs. MPP + group

Article Snippet: To assess the effects of RVG-EVs@Echi, MN9D cells were treated with MPP+ (600 μM) or RVG-EVs@Echi (1 μM) for 24 h. For the IGF-1R inhibition experiment, cells were pre-treated with the IGF-1R/IR inhibitor NVP-AEW541 (0.2 μM; MCE, HY-50866) [ ] for 2 h, followed by co-incubation with MPP + and RVG-EVs@Echi for 24 h.

Techniques: In Vitro, Expressing, Control, Staining, Fluorescence, Flow Cytometry

Journal: Cancer Medicine

Article Title: Detection of Genome‐Wide IGF ‐ 1R Recruitment to Enhancer and Promoter Regions of Chromatin in Clinical Prostate Cancers

doi: 10.1002/cam4.71257

Figure Lengend Snippet: Characterisation of sites of IGF‐1R enrichment in clinical prostate tissues. (A) UCSC Genome Browser images showing IGF1R and H3K4me1 binding sites at the RRM2 TSS in RP3 (left) and RP5 (right) from ChIP‐seq data. Chromosome location is shown at the top of the image, with the location of RRM2 highlighted in blue. H3K27Ac mark, often found near active regulatory elements, from ENCODE ( https://genome.ucsc.edu/ENCODE/ ), is also shown. (B) IGF‐1R ChIP in DU145 cells showing significantly increased recruitment of IGF‐1R to the RRM2 TSS (as shown in B). Graphs represent mean ± SEM fold enrichment over control (* p < 0.05, unpaired t ‐test).

Article Snippet: IHC was performed on freshly cut 4 μm FFPE tissue sections using antibody to IGF‐1R (#9750, Cell Signalling Technology) as in [ ] and phospho‐Y1161 IGF‐1R (orb644426, Biorbyt Ltd., Cambridge UK) on a Leica‐Bond autostainer with antigen retrieval in Tris‐EDTA pH 9.

Techniques: Binding Assay, ChIP-sequencing, Control