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Proteintech notch1
Notch1, supplied by Proteintech, used in various techniques. Bioz Stars score: 97/100, based on 234 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+notch1/Notch1+Antibody/pm41905163-66-2-25
Average 97 stars, based on 234 article reviews

notch1 - by Bioz Stars, 2026-09

97/100 stars

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other:

Article Title: The Protective Effects of Dendrobine on LPS-Induced Neuroinflammation and Related Mechanisms Based on Microglial M1/M2 Polarization.
Article Snippet: Antibodies against Notch1, Hes1, and Hes5 were supplied by Proteintech (Rosemont, IL, USA), Abcam (Cambridge, UK), and Cell Signaling Technology (Danvers, MA, USA).

Article Title: The Protective Effects of Dendrobine on LPS-Induced Neuroinflammation and Related Mechanisms Based on Microglial M1/M2 Polarization
Article Snippet: Antibodies against Notch1, Hes1, and Hes5 were supplied by Proteintech (Rosemont, IL, USA), Abcam (Cambridge, UK), and Cell Signaling Technology (Danvers, MA, USA).

Membrane:

Article Title: Deciphering the crucial role of IGF2BP3 in modulating stemness traits of salivary adenoid cystic carcinoma
Article Snippet: .. After the membrane transfer, the blocking step was implemented, followed by incubation with anti-IGF2BP3 (Proteintech, IGF2BP3), anti-SOX2 (Abcam, ab97959), anti-BMI1 (Cell Signaling Technology, 6964S), anti-NOTCH1 (Proteintech, 20687-1), and anti-GAPDH antibodies (Abcam, ab181602). .. Subsequently, secondary antibodies (Cell Signaling Technology, 7076S) were used for detection, with chemiluminescence employed to assess the expression of IGF2BP3.

Article Title: Deciphering the crucial role of IGF2BP3 in modulating stemness traits of salivary adenoid cystic carcinoma.
Article Snippet: .. After the membrane transfer, the blocking step was implemented, followed by incubation with anti-IGF2BP3 (Proteintech, IGF2BP3), anti-SOX2 (Abcam, ab97959), anti-BMI1 (Cell Signaling Technology, 6964S), anti-NOTCH1 (Proteintech, 20687-1), and anti-GAPDH antibodies (Abcam, ab181602). .. Subsequently, secondary antibodies (Cell Signaling Technology, 7076S) were used for detection, with chemiluminescence employed to assess the expression of IGF2BP3.

Blocking Assay:

Article Title: MYT1L promotes autophagy to ameliorate amyloid-β pathology and cognitive deficits in Alzheimer's disease via Notch signaling pathway.
Article Snippet: Autophagy is essential in the growth and advancement of Alzheimer’s disease (AD).. Myelin transcription factor 1-like (MYT1L) has been reported to have neuroprotective properties; however, its precise role in AD is still unclear.. This study identified a reduction in MYT1L expression in the hippocampal neurons of AD model mice.

Incubation:

Image Search Results

Knockdown of LEF1 interferes with PAAD cell malignant progression and neovascularization by inhibiting Notch1 and NF-κB signaling pathways. A–F, Immunofluorescence experiments and fluorescence intensity analysis: the relative fluorescence level of Notch1 and P65 decreased in AsPC-1/LEF1 and BxPC-3/LEF1. G–M, WB assay results and quantitative analysis: the total Notch1, NICD, Hes1, Hey1, and Jagged1 protein levels and the p-P65/P65 ratio were decreased in AsPC-1/LEF1 and BxPC-3/LEF1 (n = 3, * P <0.05).

Journal: Pancreas

Article Title: Knockdown of Lymphoid Enhancer-binding Factor 1 Inhibits Pancreatic Adenocarcinoma Growth and Neoangiogenesis by Curbing Notch1 and Nuclear Factor Kappa B Signaling Pathways

doi: 10.1097/MPA.0000000000002562

Figure Lengend Snippet: Knockdown of LEF1 interferes with PAAD cell malignant progression and neovascularization by inhibiting Notch1 and NF-κB signaling pathways. A–F, Immunofluorescence experiments and fluorescence intensity analysis: the relative fluorescence level of Notch1 and P65 decreased in AsPC-1/LEF1 and BxPC-3/LEF1. G–M, WB assay results and quantitative analysis: the total Notch1, NICD, Hes1, Hey1, and Jagged1 protein levels and the p-P65/P65 ratio were decreased in AsPC-1/LEF1 and BxPC-3/LEF1 (n = 3, * P <0.05).

Article Snippet: The first antibodies were as follows: LEF1 (ab137872, 1:1000, Abcam), proliferating cell nuclear antigen (PCNA, ab29, 1:1000, Abcam), MMP-2 (4022S, 1:1000, CST), MMP-9 (3852S, 1:1000, CST), BAX (2772S, 1:1000, CST), Bcl-2 (15071S, 1:1000, CST), Cleaved caspase-3 (9661S, 1:1000, CST), Cleaved caspase-9 (9509S, 1:1000, CST), vascular endothelial growth factor-A (VEGFA, ab214424, 1:1000, Abcam), total Notch1 (ab52627, 1:1000, Abcam), NICD (4147, 1:1000, CST), Hes1 (ab71559, 1:1000, Abcam), Hey1 (ab235173, 1:1000, Abcam), Jagged1 (ab300561, 1:1000, Abcam), P65 (ab32536, 1:1000, Abcam), p-P65 (3033S, 1:1000, CST), GAPDH (5174S, 1:5000, CST), HRP-anti-Rabbit (A0362, 1:1000, Beyotime), HRP-anti-Mouse (A0350, 1:1000, Beyotime).

Techniques: Knockdown, Protein-Protein interactions, Immunofluorescence, Fluorescence

Knockdown of LEF1 enhances immune response in mice. A and B, Immunofluorescence results and percentage of positive cells: the fluorescence intensity of PD-L1 in tumor tissues of sh-LEF1 group decreased. C and D, HE staining results and necrotic cell count showed that the proportion of cell necrosis in sh-LEF1 tumor tissue was decreased. E–H, ELISA results and content statistics showed that knockdown of LEF1 downregulated the contents of TGF-β1, IL-10, PD-L1, and CCL2 in sh-LEF1 tumor tissues. I–O, WB assay results and quantitative analysis showed decreased levels of total Notch1, NICD, Hes1, Hey1, and Jagged1 proteins in tumor tissues, and a decreased p-P65/P65 ratio (n = 6, * P <0.05).

Journal: Pancreas

Article Title: Knockdown of Lymphoid Enhancer-binding Factor 1 Inhibits Pancreatic Adenocarcinoma Growth and Neoangiogenesis by Curbing Notch1 and Nuclear Factor Kappa B Signaling Pathways

doi: 10.1097/MPA.0000000000002562

Figure Lengend Snippet: Knockdown of LEF1 enhances immune response in mice. A and B, Immunofluorescence results and percentage of positive cells: the fluorescence intensity of PD-L1 in tumor tissues of sh-LEF1 group decreased. C and D, HE staining results and necrotic cell count showed that the proportion of cell necrosis in sh-LEF1 tumor tissue was decreased. E–H, ELISA results and content statistics showed that knockdown of LEF1 downregulated the contents of TGF-β1, IL-10, PD-L1, and CCL2 in sh-LEF1 tumor tissues. I–O, WB assay results and quantitative analysis showed decreased levels of total Notch1, NICD, Hes1, Hey1, and Jagged1 proteins in tumor tissues, and a decreased p-P65/P65 ratio (n = 6, * P <0.05).

Techniques: Knockdown, Immunofluorescence, Fluorescence, Staining, Cell Characterization, Enzyme-linked Immunosorbent Assay

A. Schematic of the two SCLC mouse models: the RPR2;Hes1 GFP model ( RPR2 ) ( Rb1 Δ/Δ ;p53 Δ/Δ ;Rbl2 Δ/Δ ;Hes1G FP/+ mutant tumors), in which non-neuroendocrine (non-NE, ASCL1 low YAP1 high ) SCLC cells can be separated from NE ASCL1 high SCLC cells using GFP expression, and the RP model ( Rb1 Δ/Δ ;p53 Δ/Δ ), in which non-NE “stickers” (ST, ASCL1 low YAP1 high ) can be separated from NE “floaters” (FL, ASCL1 high ) in culture. B. Hierarchical clustering analysis of statistically significant (P<0.005) metabolites with a fold-change of at least 2 in the RPR2 model comparing ASCL1 high and ASCL1 low SCLC cells. C. Venn diagram showing overlapping pathways identified in overrepresentation analysis of untargeted metabolomics in the two mouse models as in (A). See Tables S1,2. D. Selected pathways differentially regulated transcriptionally (adjusted P-value>0.05, n=4) and metabolically (with n≥3 matched metabolites) in the RPR2 model comparing ASCL1 high and ASCL1 low SCLC cells. Purple: glutathione-associated pathways. E. Relative abundance (peak area) of selected metabolites detected by LC/MS in ASCL1 high and ASCL1 low SCLC cells (n=3) from the RPR2 model. F. Representative fluorescent imaging (left) of HES1 (anti-HES1, green) and mass spectrometry imaging (right) of GSH (red) in a representative section from RPR2 mutant mouse lungs. DAPI marks the DNA in blue. Scale bar, 1 mm. G. Average peak area (5 × 5 pixels) of GSH and HES1 fluorescence signal intensity in randomly chosen tumor regions as in (F) (n=45 points, n=2 RPR2 mutant mouse lungs). H. ASCL1 high mouse SCLC cells were transduced with a lentiviral vector expressing the NOTCH1 intracellular domain (N1ICD) and chromatin immunoprecipitation (ChIP) was performed, followed by qPCR around a consensus sequence for RBP-J binding (the partner of NICD) in the Nfe2l2 promoter (n=4). I. Average levels of total glutathione (GSH) in ASCL1 high and ASCL1 low mouse SCLC cells (mSCLC) quantified as percent of glutathione colorimetric assay readout in control wild-type cells. Two independent shRNAs were used to knock-down Nfe2l2 (coding for NRF2) (n=3). The P-values for (D) were calculated from pathway analysis using the RNA-seq data. P-values for (E) and (H) were calculated by the unpaired Student’s t-test. The P-value for (G) was calculated using the F-test. Sidak test following one-way analysis of variance (ANOVA) were performed in (I) (P<0.0001). Error bars indicate mean ± SEM.

Journal: bioRxiv

Article Title: Cell state-specific metabolic networks govern ferroptosis versus apoptosis in small cell lung cancer

doi: 10.64898/2026.03.27.714827

Figure Lengend Snippet: A. Schematic of the two SCLC mouse models: the RPR2;Hes1 GFP model ( RPR2 ) ( Rb1 Δ/Δ ;p53 Δ/Δ ;Rbl2 Δ/Δ ;Hes1G FP/+ mutant tumors), in which non-neuroendocrine (non-NE, ASCL1 low YAP1 high ) SCLC cells can be separated from NE ASCL1 high SCLC cells using GFP expression, and the RP model ( Rb1 Δ/Δ ;p53 Δ/Δ ), in which non-NE “stickers” (ST, ASCL1 low YAP1 high ) can be separated from NE “floaters” (FL, ASCL1 high ) in culture. B. Hierarchical clustering analysis of statistically significant (P<0.005) metabolites with a fold-change of at least 2 in the RPR2 model comparing ASCL1 high and ASCL1 low SCLC cells. C. Venn diagram showing overlapping pathways identified in overrepresentation analysis of untargeted metabolomics in the two mouse models as in (A). See Tables S1,2. D. Selected pathways differentially regulated transcriptionally (adjusted P-value>0.05, n=4) and metabolically (with n≥3 matched metabolites) in the RPR2 model comparing ASCL1 high and ASCL1 low SCLC cells. Purple: glutathione-associated pathways. E. Relative abundance (peak area) of selected metabolites detected by LC/MS in ASCL1 high and ASCL1 low SCLC cells (n=3) from the RPR2 model. F. Representative fluorescent imaging (left) of HES1 (anti-HES1, green) and mass spectrometry imaging (right) of GSH (red) in a representative section from RPR2 mutant mouse lungs. DAPI marks the DNA in blue. Scale bar, 1 mm. G. Average peak area (5 × 5 pixels) of GSH and HES1 fluorescence signal intensity in randomly chosen tumor regions as in (F) (n=45 points, n=2 RPR2 mutant mouse lungs). H. ASCL1 high mouse SCLC cells were transduced with a lentiviral vector expressing the NOTCH1 intracellular domain (N1ICD) and chromatin immunoprecipitation (ChIP) was performed, followed by qPCR around a consensus sequence for RBP-J binding (the partner of NICD) in the Nfe2l2 promoter (n=4). I. Average levels of total glutathione (GSH) in ASCL1 high and ASCL1 low mouse SCLC cells (mSCLC) quantified as percent of glutathione colorimetric assay readout in control wild-type cells. Two independent shRNAs were used to knock-down Nfe2l2 (coding for NRF2) (n=3). The P-values for (D) were calculated from pathway analysis using the RNA-seq data. P-values for (E) and (H) were calculated by the unpaired Student’s t-test. The P-value for (G) was calculated using the F-test. Sidak test following one-way analysis of variance (ANOVA) were performed in (I) (P<0.0001). Error bars indicate mean ± SEM.

Article Snippet: The antibodies used were Notch1 (CST, 3608) and rabbit IgG (CST, 2729).

Techniques: Mutagenesis, Expressing, Metabolic Labelling, Liquid Chromatography with Mass Spectroscopy, Imaging, Mass Spectrometry, Fluorescence, Transduction, Plasmid Preparation, Chromatin Immunoprecipitation, Sequencing, Binding Assay, Colorimetric Assay, Control, Knockdown, RNA Sequencing

a , b Flow cytometric analysis comparing Notch1 expression in the GE and the cortex ( a ), and in the transient VPA-treated forebrain primary culture (in vitro ASD model) and untreated culture ( b ). c Quantification of active NOTCH1 intracellular domain (ICN) protein levels in the in vitro ASD model, with or without pharmacological inhibition of Notch activity by DAPT treatment (Control= 7, VPA = 9, VPA + DAPT = 9, DAPT = 5). P = 0.0087 (Control vs. VPA), p < 0.0001 (VPA vs. VPA + DAPT). d Experimental scheme for genetic and pharmacological manipulation of Notch signaling in forebrain culture. Notch inhibition or activation was induced on DIV3–4, and maintained until DIV22–26. e , f Effects of Notch gain-of-function and loss-of-function on Vip transcript levels using the in vitro ASD models. e Overexpression of Notch1 ICN via retroviral infection reduced Vip transcript levels in forebrain cultures (Control = 9, ICN = 15). P = 0.0017 ( Vip ), p = 0.2867 ( Sst ). f Genome editing-mediated Notch1 gene disruption or DAPT treatment increased Vip transcript levels (Control = 5, sgN1 = 6; Control = 6, DAPT = 3). Single-guide RNAs of Notch1 (sgN1) was introduced with retrovirus vectors into forebrain cultures. The cultures used in the genome-editing experiments were prepared from embryos of Cas9-expressing mice. P = 0.0066 ( Vip , sgN1), p = 0.6345 ( Sst , sgN1), p < 0.0001 ( Vip , DAPT), p = 0.0736 ( Sst , DAPT). g Rescue of VPA-induced reduction in Vip transcript through Notch1 gene disruption (sgN1) or DAPT treatment (Control = 11, VPA = 21, VPA+sgN1 = 12; Control = 14, VPA = 15, VPA + DAPT = 4). P < 0.0001. h , i Representative images and quantification of VIP-IN density in forebrain cultures, showing significant reduction following overexpression of Notch1 ICN (Control = 9, ICN = 7). Arrowheads indicate VIP-stained cells. P = 0.0027. Scale bar: 50 µm. j , k Representative images and quantification of VIP-IN density showing restoration by gene disruption of Notch1 in VPA-exposed forebrain cultures prepared from Cas9-expressing embryos (Control = 7, VPA = 7, VPA+sgN1 = 15). P < 0.0001 (Control vs. VPA), p = 0.0003 (VPA vs. VPA+ sgN1). Scale bar: 50 µm. c , e , f , g , k , i Data are presented as mean values +/− SEM. c , g , k One-way ANOVA with Bonferroni’s multiple comparisons test. e , f , i Two-tailed unpaired t-test. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting notch signaling to restore neural development and behavior in mouse models of ASD

doi: 10.1038/s41467-026-70321-6

Figure Lengend Snippet: a , b Flow cytometric analysis comparing Notch1 expression in the GE and the cortex ( a ), and in the transient VPA-treated forebrain primary culture (in vitro ASD model) and untreated culture ( b ). c Quantification of active NOTCH1 intracellular domain (ICN) protein levels in the in vitro ASD model, with or without pharmacological inhibition of Notch activity by DAPT treatment (Control= 7, VPA = 9, VPA + DAPT = 9, DAPT = 5). P = 0.0087 (Control vs. VPA), p < 0.0001 (VPA vs. VPA + DAPT). d Experimental scheme for genetic and pharmacological manipulation of Notch signaling in forebrain culture. Notch inhibition or activation was induced on DIV3–4, and maintained until DIV22–26. e , f Effects of Notch gain-of-function and loss-of-function on Vip transcript levels using the in vitro ASD models. e Overexpression of Notch1 ICN via retroviral infection reduced Vip transcript levels in forebrain cultures (Control = 9, ICN = 15). P = 0.0017 ( Vip ), p = 0.2867 ( Sst ). f Genome editing-mediated Notch1 gene disruption or DAPT treatment increased Vip transcript levels (Control = 5, sgN1 = 6; Control = 6, DAPT = 3). Single-guide RNAs of Notch1 (sgN1) was introduced with retrovirus vectors into forebrain cultures. The cultures used in the genome-editing experiments were prepared from embryos of Cas9-expressing mice. P = 0.0066 ( Vip , sgN1), p = 0.6345 ( Sst , sgN1), p < 0.0001 ( Vip , DAPT), p = 0.0736 ( Sst , DAPT). g Rescue of VPA-induced reduction in Vip transcript through Notch1 gene disruption (sgN1) or DAPT treatment (Control = 11, VPA = 21, VPA+sgN1 = 12; Control = 14, VPA = 15, VPA + DAPT = 4). P < 0.0001. h , i Representative images and quantification of VIP-IN density in forebrain cultures, showing significant reduction following overexpression of Notch1 ICN (Control = 9, ICN = 7). Arrowheads indicate VIP-stained cells. P = 0.0027. Scale bar: 50 µm. j , k Representative images and quantification of VIP-IN density showing restoration by gene disruption of Notch1 in VPA-exposed forebrain cultures prepared from Cas9-expressing embryos (Control = 7, VPA = 7, VPA+sgN1 = 15). P < 0.0001 (Control vs. VPA), p = 0.0003 (VPA vs. VPA+ sgN1). Scale bar: 50 µm. c , e , f , g , k , i Data are presented as mean values +/− SEM. c , g , k One-way ANOVA with Bonferroni’s multiple comparisons test. e , f , i Two-tailed unpaired t-test. Source data are provided as a Source Data file.

Article Snippet: The following commercially available primary antibodies were used: Rabbit anti-VIP (1:1000, 20077, ImmunoStar) Mouse anti-Reelin (1:500, D223-3 (CR-50), MBL) Rat anti-Somatostatin (1:300, MAB354 (YC7), Merck Millipore) Rabbit anti-Parvalbumin (1:1000, MSFR105210, Nittobo Medical) Rabbit anti-Calretinin (1:1000, MSFR100440, Nittobo Medical) Mouse anti-Calretinin (1:1000, MAB1568 (6B8.2), Merck Millipore) Mouse anti-GAD67 (1:1000, MAB5406 (1G10.2), Merck Millipore) Rabbit anti-PROX1 (1:1000, ab199359, Abcam) Mouse anti-COUP-TFII (1:1000, PP-H7147-00 (H7147), Perseus Proteomics) Rabbit anti-SOX6 (1:1000, ab30455, Abcam) Mouse anti-LHX6 (1:1000, H00026468-M02 (1B11), Abnova) Mouse anti-HDAC3 (1:1000, #3949 (7G6C5), Cell Signaling) Rabbit anti-cleaved NOTCH1 (1:1000, #4147 (Val1744) (D3D8), Cell Signaling,) Mouse anti-GAPDH (1:1000, Santa Cruz Biotechnology) For immunostaining, Alexa Fluor 488- or 546-conjugated secondary antibodies (Molecular Probes) were used.

Techniques: Expressing, In Vitro, Inhibition, Activity Assay, Control, Activation Assay, Over Expression, Retroviral, Infection, Disruption, Staining, Two Tailed Test

a Generation of CGE-specific Notch1/2 cKO mice. Htr3a -Cre mice were used to delete Notch1/2 genes in CGE progenitors exposed to VPA. b Restoration of VIP-IN density in VPA-exposed cKO mice. Representative coronal images of the somatosensory cortex and quantification of VIP-IN density (control=46, cKO=45, WT-VPA = 45, cKO-VPA = 46 images). P < 0.0001 (WT vs. WT-VPA, cKO vs. WT-VPA, WT-VPA vs. cKO-VPA). Scale bar: 100 µm. c – g Behavioral rescue in VPA-exposed cKO mice. c Duration of self-grooming (control=30, cKO=23, WT-VPA = 44, cKO-VPA = 36). P > 0.9999 (WT vs. cKO), p = 0.0018 (WT vs. WT-VPA), p = 0.0047 (WT vs. cKO-VPA), p > 0.9999 (WT-VPA vs. cKO-VPA). d Contact time in the reciprocal social interaction test (control=29, cKO=25, WT-VPA = 32, cKO-VPA = 26). P = 0.0006 (WT vs. WT-VPA), p < 0.0001 (cKO vs. WT-VPA), p = 0.0476 (WT-VPA vs. cKO-VPA). e – g Three-chamber social interaction test (control = 57, cKO=54, WT-VPA = 63, cKO-VPA = 51). e Time spent in each chamber. Increased time in the familiar chamber by VPA-exposure, p = 0.0447 (WT vs. WT-VPA), p = 0.0128 (cKO vs. WT-VPA), p = 0.0004 (WT-VPA vs. cKO-VPA). Decreased time in the centre chamber. p = 0.0154 (cKO vs. WT-VPA), p = 0.0252 (WT-VPA vs. cKO-VPA). f Representative heatmaps of each test mouse. g SNI in the social novelty session. P = 0.0378 (WT vs. WT-VPA), p = 0.0205 (cKO vs. WT-VPA), p = 0.0021 (WT-VPA vs. cKO-VPA). b , c , d , e , g Data are presented as mean values +/−SEM. b , c , d , g One-way ANOVA with Bonferroni’s multiple comparisons test. e Two-tailed unpaired t-test. h – m Transcriptomic changes analyzed by RNA-seq of the adult forebrain ( n = 3) exhibited gene expression profiles between four groups (WT, WT-VPA, cKO, and cKO-VPA). h Number of differentially altered genes across genotypes and/or condition. i PCA showed distinct clustering of cKO-VPA mice from WT-VPA mice. j Gene enrichment analysis by STRING revealed increased glutamatergic synaptic transmission in WT-VPA, restored in cKO-VPA. k – m Volcano plots illustrating differential gene expression in comparisons: WT vs. cKO ( k ), WT vs. WT-VPA ( l ), and WT-VPA vs. cKO-VPA ( m ), highlighting the selective downregulation of Glutamatergic neuron-related genes in the cKO-VPA mice. j – m Two-sided unpaired t-test with Benjamini–Hochberg multiple testing correction. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting notch signaling to restore neural development and behavior in mouse models of ASD

doi: 10.1038/s41467-026-70321-6

Figure Lengend Snippet: a Generation of CGE-specific Notch1/2 cKO mice. Htr3a -Cre mice were used to delete Notch1/2 genes in CGE progenitors exposed to VPA. b Restoration of VIP-IN density in VPA-exposed cKO mice. Representative coronal images of the somatosensory cortex and quantification of VIP-IN density (control=46, cKO=45, WT-VPA = 45, cKO-VPA = 46 images). P < 0.0001 (WT vs. WT-VPA, cKO vs. WT-VPA, WT-VPA vs. cKO-VPA). Scale bar: 100 µm. c – g Behavioral rescue in VPA-exposed cKO mice. c Duration of self-grooming (control=30, cKO=23, WT-VPA = 44, cKO-VPA = 36). P > 0.9999 (WT vs. cKO), p = 0.0018 (WT vs. WT-VPA), p = 0.0047 (WT vs. cKO-VPA), p > 0.9999 (WT-VPA vs. cKO-VPA). d Contact time in the reciprocal social interaction test (control=29, cKO=25, WT-VPA = 32, cKO-VPA = 26). P = 0.0006 (WT vs. WT-VPA), p < 0.0001 (cKO vs. WT-VPA), p = 0.0476 (WT-VPA vs. cKO-VPA). e – g Three-chamber social interaction test (control = 57, cKO=54, WT-VPA = 63, cKO-VPA = 51). e Time spent in each chamber. Increased time in the familiar chamber by VPA-exposure, p = 0.0447 (WT vs. WT-VPA), p = 0.0128 (cKO vs. WT-VPA), p = 0.0004 (WT-VPA vs. cKO-VPA). Decreased time in the centre chamber. p = 0.0154 (cKO vs. WT-VPA), p = 0.0252 (WT-VPA vs. cKO-VPA). f Representative heatmaps of each test mouse. g SNI in the social novelty session. P = 0.0378 (WT vs. WT-VPA), p = 0.0205 (cKO vs. WT-VPA), p = 0.0021 (WT-VPA vs. cKO-VPA). b , c , d , e , g Data are presented as mean values +/−SEM. b , c , d , g One-way ANOVA with Bonferroni’s multiple comparisons test. e Two-tailed unpaired t-test. h – m Transcriptomic changes analyzed by RNA-seq of the adult forebrain ( n = 3) exhibited gene expression profiles between four groups (WT, WT-VPA, cKO, and cKO-VPA). h Number of differentially altered genes across genotypes and/or condition. i PCA showed distinct clustering of cKO-VPA mice from WT-VPA mice. j Gene enrichment analysis by STRING revealed increased glutamatergic synaptic transmission in WT-VPA, restored in cKO-VPA. k – m Volcano plots illustrating differential gene expression in comparisons: WT vs. cKO ( k ), WT vs. WT-VPA ( l ), and WT-VPA vs. cKO-VPA ( m ), highlighting the selective downregulation of Glutamatergic neuron-related genes in the cKO-VPA mice. j – m Two-sided unpaired t-test with Benjamini–Hochberg multiple testing correction. Source data are provided as a Source Data file.

Techniques: Control, Two Tailed Test, RNA Sequencing, Gene Expression, Transmission Assay

a Experimental scheme showing the in vivo rescue of Notch signaling by a single dose of γ-secretase inhibitor Ro4929097 (Ro) in the ASD-model mice exposure to VPA. b Normalized protein level of active Notch1 in the VPA-exposed mouse embryos by Ro treatment. c , d Rescue of VIP-IN density in Ro-treated VPA-exposed mice. c Representative coronal images of the somatosensory cortex. d Quantification of VIP-IN density showed a significant increase by Ro injection in VPA-exposed mice (control = 48, VPA = 68, VPA+Ro = 86 images). P < 0.0001 (Control vs. VPA, VPA vs. VPA+Ro). Scale bar: 100 µm. e – i Behavioral improvements in Ro-treated VPA-exposed mice. e Hair loss observed in 27% of VPA-exposed mice rescued by Ro exposure (control = 30, VPA = 34, VPA+Ro=29). P = 0.0024 (Control vs. VPA), p = 0.0414 (VPA vs. VPA+Ro). f Total grooming duration (control=70, VPA = 72, VPA+Ro=66). P < 0.0001 (Control vs. VPA), p = 0.0008 (VPA vs. VPA+Ro). g – i Reciprocal social interaction test (control=29, VPA = 41, VPA+Ro = 45). g Contact number, p = 0.0028 (Control vs. VPA), p = 0.0438 (VPA vs. VPA+Ro). h Contact time, p = 0.0034 (Control vs. VPA), p = 0.0375 (VPA vs. VPA+Ro). i Resting time, p < 0.0001 (Control vs. VPA, VPA vs. VPA+Ro). d , f , g – i Data are presented as mean values +/−SEM. One-way ANOVA with Bonferroni’s multiple comparisons test. e Two-sided Pearson’s chi-square test. j – o Single-cell RNA sequencing (scRNA-seq) analysis of whole brain (P2) from VPA-exposed mice revealed cellular and transcriptomic rescue by Ro. j UMAP plot of 20 clusters in whole-brain cells. k Restored perturbations in the whole cell compositions in VPA-exposed mouse with Ro exposure. l Heatmap of residuals and Pearson’s coefficients for cell-type distributions. Combined heatmap showing standardized residuals from chi-square tests and Pearson’s coefficients between groups (control, VPA, VPA+Ro). Ro treatment shifted the VPA-induced distribution pattern toward that of control mouse. m Sub-clustering of NSC/NP-enriched populations (clusters #6 and #7) and the normalized cellular composition of Htr3a + CGE-enriched cell populations in VPA-exposed mouse after Ro treatment. n Normalized cell composition of oligodendrocyte-enriched clusters (clusters #5, #8, #12, #14, and #18) with Ro exposure. ovgy Cell composition of astrocyte-enriched clusters (clusters #2, #3, and #13) with Ro exposure. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting notch signaling to restore neural development and behavior in mouse models of ASD

doi: 10.1038/s41467-026-70321-6

Figure Lengend Snippet: a Experimental scheme showing the in vivo rescue of Notch signaling by a single dose of γ-secretase inhibitor Ro4929097 (Ro) in the ASD-model mice exposure to VPA. b Normalized protein level of active Notch1 in the VPA-exposed mouse embryos by Ro treatment. c , d Rescue of VIP-IN density in Ro-treated VPA-exposed mice. c Representative coronal images of the somatosensory cortex. d Quantification of VIP-IN density showed a significant increase by Ro injection in VPA-exposed mice (control = 48, VPA = 68, VPA+Ro = 86 images). P < 0.0001 (Control vs. VPA, VPA vs. VPA+Ro). Scale bar: 100 µm. e – i Behavioral improvements in Ro-treated VPA-exposed mice. e Hair loss observed in 27% of VPA-exposed mice rescued by Ro exposure (control = 30, VPA = 34, VPA+Ro=29). P = 0.0024 (Control vs. VPA), p = 0.0414 (VPA vs. VPA+Ro). f Total grooming duration (control=70, VPA = 72, VPA+Ro=66). P < 0.0001 (Control vs. VPA), p = 0.0008 (VPA vs. VPA+Ro). g – i Reciprocal social interaction test (control=29, VPA = 41, VPA+Ro = 45). g Contact number, p = 0.0028 (Control vs. VPA), p = 0.0438 (VPA vs. VPA+Ro). h Contact time, p = 0.0034 (Control vs. VPA), p = 0.0375 (VPA vs. VPA+Ro). i Resting time, p < 0.0001 (Control vs. VPA, VPA vs. VPA+Ro). d , f , g – i Data are presented as mean values +/−SEM. One-way ANOVA with Bonferroni’s multiple comparisons test. e Two-sided Pearson’s chi-square test. j – o Single-cell RNA sequencing (scRNA-seq) analysis of whole brain (P2) from VPA-exposed mice revealed cellular and transcriptomic rescue by Ro. j UMAP plot of 20 clusters in whole-brain cells. k Restored perturbations in the whole cell compositions in VPA-exposed mouse with Ro exposure. l Heatmap of residuals and Pearson’s coefficients for cell-type distributions. Combined heatmap showing standardized residuals from chi-square tests and Pearson’s coefficients between groups (control, VPA, VPA+Ro). Ro treatment shifted the VPA-induced distribution pattern toward that of control mouse. m Sub-clustering of NSC/NP-enriched populations (clusters #6 and #7) and the normalized cellular composition of Htr3a + CGE-enriched cell populations in VPA-exposed mouse after Ro treatment. n Normalized cell composition of oligodendrocyte-enriched clusters (clusters #5, #8, #12, #14, and #18) with Ro exposure. ovgy Cell composition of astrocyte-enriched clusters (clusters #2, #3, and #13) with Ro exposure. Source data are provided as a Source Data file.

Techniques: In Vivo, Injection, Control, Single Cell, RNA Sequencing

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