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anti id3 rabbit (Cell Signaling Technology Inc)

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Cell Signaling Technology Inc anti id3 rabbit
Anti Id3 Rabbit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti id3 rabbit/product/Cell Signaling Technology Inc
Average 86 stars, based on 1 article reviews

anti id3 rabbit - by Bioz Stars, 2026-05

86/100 stars

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ID3 is preferentially expressed in stem/eTA cell populations in the cornea. ( a ) The scRNA-seq identified three epithelial cell types in mouse cornea. ( b ) ID3 expression in limbal/corneal epithelial cells was plotted. The enclosed group represents stem/early TA cell populations. ID3 expression was higher in stem/early TA cell populations than other limbal/corneal epithelial cells. ( c ) Immunofluorescence staining of human cornea and limbus for K15 and ID3 showed that ID3 was predominantly expressed in the limbal basal layer. The arrows point to colocalization of K15 and ID3.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: ID3 is preferentially expressed in stem/eTA cell populations in the cornea. ( a ) The scRNA-seq identified three epithelial cell types in mouse cornea. ( b ) ID3 expression in limbal/corneal epithelial cells was plotted. The enclosed group represents stem/early TA cell populations. ID3 expression was higher in stem/early TA cell populations than other limbal/corneal epithelial cells. ( c ) Immunofluorescence staining of human cornea and limbus for K15 and ID3 showed that ID3 was predominantly expressed in the limbal basal layer. The arrows point to colocalization of K15 and ID3.

Article Snippet: The following primary antibodies were used: GAPDH (MAB374, 1:1000 dilution; Sigma-Aldrich), ID3 (9837, 1:500 dilution; Cell Signaling Technology), ERK1 (sc-94; 1:1000 dilution; Santa Cruz Biotechnology, Santa Cruz, CA, USA), p-ERK (sc-7383, 1:1000 dilution; Santa Cruz Biotechnology), Akt (4691, 1:1000 dilution; Cell Signaling Technology), p-Akt S473 (4060, 1:1000 dilution; Cell Signaling Technology), EphA2 (AF3035, 1:250 dilution; R&D Systems), and p-EphA2 S897 (6347, 1:1000 dilution; Cell Signaling Technology).

Techniques: Expressing, Immunofluorescence, Staining

Bulk RNA sequencing in human limbal epithelial cells suggests a role for ID3 in regulation of cell migration. ( a ) RT-qPCR demonstrated significant knockdown of ID3 expression with siRNA transfection ( n = 3). ** P < 0.01. ( b ) The PCA plot suggests that variance due to siRNA transfection was much higher than the occurrence of biological variance. ( c ) The heatmap shows dramatic transcriptome changes due to ID3 knockdown. ( d ) DEGs in HLECs transfected with either siID3 or siControl were subjected to GO enrichment analysis, which indicated that cell migration was the most significantly enriched GO term. This suggests a crucial involvement of ID3 in the regulation of limbal epithelial cell migration. The red rectangles indicate terms associated with migration.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: Bulk RNA sequencing in human limbal epithelial cells suggests a role for ID3 in regulation of cell migration. ( a ) RT-qPCR demonstrated significant knockdown of ID3 expression with siRNA transfection ( n = 3). ** P < 0.01. ( b ) The PCA plot suggests that variance due to siRNA transfection was much higher than the occurrence of biological variance. ( c ) The heatmap shows dramatic transcriptome changes due to ID3 knockdown. ( d ) DEGs in HLECs transfected with either siID3 or siControl were subjected to GO enrichment analysis, which indicated that cell migration was the most significantly enriched GO term. This suggests a crucial involvement of ID3 in the regulation of limbal epithelial cell migration. The red rectangles indicate terms associated with migration.

Techniques: RNA Sequencing, Migration, Quantitative RT-PCR, Knockdown, Expressing, Transfection

ID3 depletion in a limbal epithelial cell line enhances cell migration. ( a ) Western blot confirming ID3 knockdown and quantification ( n = 3). ( b ) Time-lapse images of representative samples at 0 hour, 3 hours, 6 hours, 9 hours, and 24 hours after scratch wounding. Dashed lines represent approximate borders of the wound edge. ( c ) Quantification of time-dependent wound closure displaying 3-hour intervals of wound closure during a 24-hour scratch wound assay showed that knockdown of ID3 significantly accelerated wound closure ( n = 3). * P < 0.05. Scale bar : 0.5 mm.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: ID3 depletion in a limbal epithelial cell line enhances cell migration. ( a ) Western blot confirming ID3 knockdown and quantification ( n = 3). ( b ) Time-lapse images of representative samples at 0 hour, 3 hours, 6 hours, 9 hours, and 24 hours after scratch wounding. Dashed lines represent approximate borders of the wound edge. ( c ) Quantification of time-dependent wound closure displaying 3-hour intervals of wound closure during a 24-hour scratch wound assay showed that knockdown of ID3 significantly accelerated wound closure ( n = 3). * P < 0.05. Scale bar : 0.5 mm.

Techniques: Migration, Western Blot, Knockdown, Scratch Wound Assay Assay

ID3 knockdown reveals increased expression of several genes related to migration. ( a ) RT-qPCR examined the relative gene expression changes of select DEGs associated with cell migration. The expression levels in cells transfected with siID3 were normalized to cells transfected with siControl. ( b , c ) Quantification ( b ) and representative images ( c ) at 6-hour migration after scratch wound of cells treated with GI254023X (GIX) showed with MMP9 inhibition and knockdown of ID3 still significantly enhanced cell migration compared to cells treated with siControl+GI254023X, suggesting that ID3 and MMP9 are two parallel pathways in terms of regulation of cell migration ( n = 3). * P < 0.05. Scale bar : 0.5 mm.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: ID3 knockdown reveals increased expression of several genes related to migration. ( a ) RT-qPCR examined the relative gene expression changes of select DEGs associated with cell migration. The expression levels in cells transfected with siID3 were normalized to cells transfected with siControl. ( b , c ) Quantification ( b ) and representative images ( c ) at 6-hour migration after scratch wound of cells treated with GI254023X (GIX) showed with MMP9 inhibition and knockdown of ID3 still significantly enhanced cell migration compared to cells treated with siControl+GI254023X, suggesting that ID3 and MMP9 are two parallel pathways in terms of regulation of cell migration ( n = 3). * P < 0.05. Scale bar : 0.5 mm.

Techniques: Knockdown, Expressing, Migration, Quantitative RT-PCR, Gene Expression, Transfection, Inhibition

ID3 knockdown increases phosphorylation of Akt and ligand-independent activation of EphA2. ( a , b ) After transfection with siControl or siID3, cells were treated with LY294002, an Akt inhibitor ( a ), or EphrinA1 peptide, a ligand of EphA2 that can block the ligand-independent activation of EphA2 ( b ). Protein lysates were subjected to western blot, and densitometry was conducted using Image Studio. It showed that knockdown of ID3 had no significant effect on phosphorylation of ERK. A significant increase of p-Akt, EphA2, and p-EphA2 (S897, a ligand-independent phosphorylation site) in cells transfected with siID3 was detected. Such increases were reversed by LY294002 or EphrinA1 peptide, respectively ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: ID3 knockdown increases phosphorylation of Akt and ligand-independent activation of EphA2. ( a , b ) After transfection with siControl or siID3, cells were treated with LY294002, an Akt inhibitor ( a ), or EphrinA1 peptide, a ligand of EphA2 that can block the ligand-independent activation of EphA2 ( b ). Protein lysates were subjected to western blot, and densitometry was conducted using Image Studio. It showed that knockdown of ID3 had no significant effect on phosphorylation of ERK. A significant increase of p-Akt, EphA2, and p-EphA2 (S897, a ligand-independent phosphorylation site) in cells transfected with siID3 was detected. Such increases were reversed by LY294002 or EphrinA1 peptide, respectively ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques: Knockdown, Phospho-proteomics, Activation Assay, Transfection, Blocking Assay, Western Blot

ID3 negatively regulates limbal epithelial cell migration through EphA2/Akt signaling. After transfection with siControl or siID3, cells were treated with LY294002, an Akt inhibitor, or EphrinA1 peptide, a ligand of EphA2 that can block the ligand-independent activation of EphA2. These cells were subjected to scratch wound assays ( n = 9). ( a ) Representative images of scratch wound assays at 6 hours after wounding. Prior to wounding, cells were treated with the PI3K/Akt inhibitor LY294002. Wound closures were quantified using ImageJ. Quantification is shown on the right. ( b ) Representative images of scratch wound assays at 6 hours after wounding. Prior to wounding, cells were treated with EphrinA1 peptide. Quantification is shown on the right. Scale bar : 0.5 mm. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway

doi: 10.1167/iovs.66.9.2

Figure Lengend Snippet: ID3 negatively regulates limbal epithelial cell migration through EphA2/Akt signaling. After transfection with siControl or siID3, cells were treated with LY294002, an Akt inhibitor, or EphrinA1 peptide, a ligand of EphA2 that can block the ligand-independent activation of EphA2. These cells were subjected to scratch wound assays ( n = 9). ( a ) Representative images of scratch wound assays at 6 hours after wounding. Prior to wounding, cells were treated with the PI3K/Akt inhibitor LY294002. Wound closures were quantified using ImageJ. Quantification is shown on the right. ( b ) Representative images of scratch wound assays at 6 hours after wounding. Prior to wounding, cells were treated with EphrinA1 peptide. Quantification is shown on the right. Scale bar : 0.5 mm. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques: Migration, Transfection, Blocking Assay, Activation Assay

Figure 4. Single-cell analysis highlighting differential gene expression and cellular distribution among speciﬁc clusters of interest (A) A series of UMAPs showing the spatial reduction of cells included from the 20 samples in the scRNA-seq analysis including (i) stratiﬁed by cell types, (ii) time in the treatment cycle, (iii) sample number, (iv) response to neoadjuvant therapy, and (v) cell type allocation: CTL (CD8+GZMB+), TREG (CD4+FOXP3+), and M2- TAM (CD68+CD163+/CD206+) cells from all collected samples (n = 20). (B) A heatmap showing the top 10 genes (weighted by lowest adjusted p value) per cluster of M2-TAM, TREG, and CTL cell clusters among all samples (n = 20). (C) A bar plot showing the percentage distribution of M2-TAM, TREG, and CTL cells stratiﬁed by sample, response to treatment, and stage in the treatment cycle (treatment pre n = 10, treatment mid n = 2, and treatment post n = 5) with the corresponding number of cells per sample. (D) A transposition of the same data showing the combined cell distribution across all samples stratiﬁed by cell type and response to therapy.

Journal: Cell reports. Medicine

Article Title: Phase 2 trial of perioperative chemo-immunotherapy for gastro-esophageal adenocarcinoma: The role of M2 macrophage landscape in predicting response.

doi: 10.1016/j.xcrm.2025.102045

Figure Lengend Snippet: Figure 4. Single-cell analysis highlighting differential gene expression and cellular distribution among speciﬁc clusters of interest (A) A series of UMAPs showing the spatial reduction of cells included from the 20 samples in the scRNA-seq analysis including (i) stratiﬁed by cell types, (ii) time in the treatment cycle, (iii) sample number, (iv) response to neoadjuvant therapy, and (v) cell type allocation: CTL (CD8+GZMB+), TREG (CD4+FOXP3+), and M2- TAM (CD68+CD163+/CD206+) cells from all collected samples (n = 20). (B) A heatmap showing the top 10 genes (weighted by lowest adjusted p value) per cluster of M2-TAM, TREG, and CTL cell clusters among all samples (n = 20). (C) A bar plot showing the percentage distribution of M2-TAM, TREG, and CTL cells stratiﬁed by sample, response to treatment, and stage in the treatment cycle (treatment pre n = 10, treatment mid n = 2, and treatment post n = 5) with the corresponding number of cells per sample. (D) A transposition of the same data showing the combined cell distribution across all samples stratiﬁed by cell type and response to therapy.

Article Snippet: The labeling for various primary antibodies included CK7 (Roche, #790–4462), CD8 (DAKO, #M7103), granzyme B (Roche, #760–4283), CD68 (Roche #790–2931), CD163 (Roche #760–4437) and FoxP3 (CST, #9837).

Techniques: Single-cell Analysis, Gene Expression

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