rbpj inhibitor rin1  (MedChemExpress)

Journal: PLOS Biology

Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking

doi: 10.1371/journal.pbio.3003516

Figure Lengend Snippet: (A and B) Immunohistochemistry for RIN1 (green) in spinal sections of SOM-tdTomato mice at postnatal day 1 (P1) to P28. ***P < 0.001 (Kruskal–Wallis test). n = 30 neurons from 3 mice per group. Scale bar, 5 µm. (C) Distribution of RIN1 (green) in the soma (arrow) and dendrites (arrowhead) of tdTomato + neurons in the superficial dorsal horn of adult SOM-tdTomato mice. The area enclosed in the white square ( up ) was enlarged ( down ). Scale bar, 100 µm ( up ) and 10 µm ( down ). (D) Immunohistochemistry for RIN1 (red) and PSD-95 (green) in SOM + neurons (blue) labelled by intraspinal injection of AAV2/9-DIO-EGFP in SOM-Cre mice. Arrows indicated the colocalization. Scale bar, 10 µm. The data underlying this Figure can be found in .

Article Snippet: Primary antibodies used in this study included the mouse anti-RIN1 antibody (1:200; #H00009610-B01P, Novus Biologicals, Littleton, CO), rabbit anti-RIN1 antibody (1:200; #bs-6094R, Biosynthesis Biotechnology, Beijing, China), and mouse anti-PSD-95 antibody (1:200; #51-6900, Invitrogen).

Techniques: Immunohistochemistry, Injection

Journal: PLOS Biology

Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking

doi: 10.1371/journal.pbio.3003516

Figure Lengend Snippet: (A) Representative NMDAR-EPSCs and AMPAR-EPSCs recorded from P7 to P28. (B and C) Comparisons of NMDAR/AMPAR ratios (B) and decay kinetics of NMDAR-EPSCs (C) recorded from male and female mice. *P = 0.035, **P = 0.005, ## P = 0.002 (Mann-Whitney U test). n = 6 neurons (B) and 6-10 neurons (C) from 4-5 mice per group. (D) Changes of NMDAR-EPSCs recorded in spinal slices prepared from control and cKO-RIN1 mice at P5-P7 after bath perfusion of ifenprodil ( left ; F(31, 310) = 0.997, P = 0.475, repeated measurement, n = 6 neurons/group from 3-4 mice) or TCN-201 ( right ; F(31, 310) = 0.491, P = 0.991, repeated measurement, n = 6 neurons/group from 3-4 mice). (E) Changes of NMDAR-EPSCs recorded in control and cKO-RIN1 mice at P28-P35 after bath perfusion of ifenprodil ( left ; F(31, 310) = 7.877, P < 0.001, repeated measurement) or TCN-201 ( right ; F(31, 310) = 6.514, P < 0.001, repeated measurement). *P < 0.05 (post hoc Bonferroni test). n = 6 neurons/group from 3-4 mice. (F) Scheme for the injection of an adenoviral vector carrying RIN1 and/or EGFP in spinal cord dorsal horn of SOM-tdTomato mice at P5-P7 and electrophysiological recordings after 3-5 days. (G and H) Effects of RIN1 expression on the decay kinetics of NMDAR-EPSCs (G) and ifenprodil sensitivity (H) . **P = 0.004, ***P < 0.001 (Mann-Whitney U test). n = 15 neurons/group (G) and 6 neurons/group (H) from 4-5 mice. (I) Effect of ifenprodil on NMDAR-EPSCs recorded on SOM + interneurons expressing RIN1 or EGFP at P28-P35. n = 6 neurons from 2–3 mice/group. The data underlying this Figure can be found in .

Article Snippet: Primary antibodies used in this study included the mouse anti-RIN1 antibody (1:200; #H00009610-B01P, Novus Biologicals, Littleton, CO), rabbit anti-RIN1 antibody (1:200; #bs-6094R, Biosynthesis Biotechnology, Beijing, China), and mouse anti-PSD-95 antibody (1:200; #51-6900, Invitrogen).

Techniques: MANN-WHITNEY, Control, Injection, Plasmid Preparation, Expressing

Journal: PLOS Biology

Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking

doi: 10.1371/journal.pbio.3003516

Figure Lengend Snippet: (A) RIN1 immunoprecipitates from spinal cord dorsal horn of mice were probed with the antibodies indicated on the left of panels. The experiments were replicated for 3 times and each obtained a similar result. IgG, immunoglobulin G; IP, immunoprecipitation. (B) PLA detection of RIN1-GluN2A complex ( up ) or RIN1-GluN2B complex ( down ) in EGFP-labeled SOM + interneurons. Scale bar, 5 µm. (C and D) GST fusion of wild-type RIN1 [RIN1(WT)] or RIN1(1-221) mutant (C) pulled down GluN2A from the lysates of spinal cord (D) . Arrowheads indicated the apparent molecular size of GST-RIN1(WT) or GST-RIN1(1-221) (D) . The experiments were replicated for 3 times and each obtained a similar result. (E) Scheme for the viral injection in the spinal cord of SOM-Cre::RIN1 fl/fl mice at P7-P8 and electrophysiological recordings or immunostaining after 21 days. (F) Effects of RIN1(WT) and its mutants on the surface expression of GluN2A and GluN2B. *** P < 0.001, ** P = 0.003, ## P = 0.006, && P = 0.002 (Kruskal–Wallis test). n = 16 neurons (GluN2A) and 15 neurons (GluN2B) from 5 mice. Scale bar, 4 µm. (G-I) Effects of RIN1(WT) and its mutants on NMDAR/AMPAR ratios (G, H; **P = 0.008, ## P = 0.006; Kruskal–Wallis test; n = 10–11 neurons/group from 5-7 mice) and NMDAR-EPSC decay kinetics (G, I; ***P < 0.001, *P = 0.018, # P = 0.042, & P = 0.032, $ P = 0.022; Kruskal–Wallis test; n = 18-20 neurons/group from 5-7 mice). The data underlying this Figure can be found in .

Article Snippet: Primary antibodies used in this study included the mouse anti-RIN1 antibody (1:200; #H00009610-B01P, Novus Biologicals, Littleton, CO), rabbit anti-RIN1 antibody (1:200; #bs-6094R, Biosynthesis Biotechnology, Beijing, China), and mouse anti-PSD-95 antibody (1:200; #51-6900, Invitrogen).

Techniques: Immunoprecipitation, Labeling, Mutagenesis, Injection, Immunostaining, Expressing

Journal: PLOS Biology

Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking

doi: 10.1371/journal.pbio.3003516

Figure Lengend Snippet: (A) Changes in the paw withdrawal thresholds (PWTs) of male and female mice after spared nerve injury (SNI) on the left sciatic nerves and sham surgery on the right nerves. ***P < 0.001 (paired Student t t est). n = 15 mice/group. (B) Changes in the decay kinetics of NMDAR-EPSC recorded in spinal slices from male mice ( left ; **P = 0.002, *P = 0.03, Paired Student t t est, n = 9-11 neurons from 3–5 mice per group) and female mice ( right ; *P = 0.01, # P = 0.035, Paired Student t t est, n = 7–9 neurons from 3-4 mice per group). (C) NMDAR/AMPAR ratios recorded at days 7 (D7) and 28 (D28) after surgery in male and female mice. *P = 0.028, **P = 0.002, ns P = 1.00 (Kruskal–Wallis test). n = 10 neurons from 3–4 mice per group. (D) Inhibition by ifenprodil of NMDAR-EPSCs recorded at day 7 after surgery in male and female mice. F(30, 270) = 1.932, P = 0.003 (repeated measurement). *P < 0.05 (Post hoc Bonferroni test). n = 6 neurons/group from 3-4 mice. (E) Inhibition by ifenprodil of NMDAR-EPSCs recorded at day 28 after surgery in male and female mice. F(31, 310) = 0.421, P = 0.998 (repeated measurement). n = 6 neurons per group from 3–4 mice. (F) Immunohistochemistry for RIN1 (green) in spinal SOM + interneurons at days 7 and 28 after surgery in male and female mice. ***P < 0.001 (Kruskal–Wallis test). n = 30 neurons from 3 mice per group. The data underlying this figure can be found in .

Article Snippet: Primary antibodies used in this study included the mouse anti-RIN1 antibody (1:200; #H00009610-B01P, Novus Biologicals, Littleton, CO), rabbit anti-RIN1 antibody (1:200; #bs-6094R, Biosynthesis Biotechnology, Beijing, China), and mouse anti-PSD-95 antibody (1:200; #51-6900, Invitrogen).

Techniques: Inhibition, Immunohistochemistry

Journal: PLOS Biology

Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking

doi: 10.1371/journal.pbio.3003516

Figure Lengend Snippet: (A) Comparison of NMDAR-EPSC decay kinetics at days 7-28 after sham and SNI surgery in male ( *P = 0.014, # P = 0.036, & P = 0.03, % P = 0.026, Paired Student t test) and female cKO-RIN1 mice ( *P = 0.024, # P = 0.034, & P = 0.048, % P = 0.038, paired Student t test). n = 6-9 neurons from 2-3 mice per group. (B) Targeted deletion of RIN1 by intraspinal injection of AAV2/9-SOM-Cre and AAV2/9-SOM-EGFP in RIN1 fl/fl mice. Arrows indicated EGFP + neurons with RIN1 deleted. Scale bar, 10 µm. (C and D) Ifenprodil was more effective than TCN-201 in elevating PWTs of RIN1-deficient mice at day 7 (C) and day 28 (D) after SNI. **P = 0.003, ***P < 0.001 (repeated measurement with post hoc Bonferroni test). n = 10 male and female mice per group. (E and F) Ifenprodil was more effective than TCN-201 in alleviating spontaneous pain behaviors of RIN1-deficient mice at day 7 (E) and day 28 (F) after SNI surgery. *P = 0.018, **P = 0.002, ## P = 0.001, ***P < 0.001 (Kruskal–Wallis test). n = 10 male and female mice per group. The data underlying this figure can be found in .

Article Snippet: Primary antibodies used in this study included the mouse anti-RIN1 antibody (1:200; #H00009610-B01P, Novus Biologicals, Littleton, CO), rabbit anti-RIN1 antibody (1:200; #bs-6094R, Biosynthesis Biotechnology, Beijing, China), and mouse anti-PSD-95 antibody (1:200; #51-6900, Invitrogen).

Techniques: Comparison, Injection

Journal: bioRxiv

Article Title: Graded Notch Signaling Functions as a Rheostat of Lineage Plasticity and Therapy Resistance in Prostate Cancer

doi: 10.1101/2025.11.23.690056

Figure Lengend Snippet: (A, B) Relative gene expression of Notch pathway components and lineage markers in enzalutamide-resistant cell lines, (A) gTP53/RB1-R and (B) PC3, after treatment with a gamma-secretase inhibitor (DAPT), an RBPJ inhibitor (RIN1), or DMSO vehicle control. Significance is denoted as *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: DMSO (vehicle control), 10 μM DAPT (MedChemExpress, HY-13027), or 5 μM RIN1 (MedChemExpress, HY-137471) were added to 3 biological replicates each.

Techniques: Gene Expression, Control