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Cell Signaling Technology Inc
rabbit polyclonal gli1 antibody  Rabbit Polyclonal Gli1 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/rabbit polyclonal gli1 antibody/product/Cell Signaling Technology Inc Average 96 stars, based on 1 article reviews
rabbit polyclonal gli1 antibody - by Bioz Stars,
2026-03
96/100 stars
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Cell Signaling Technology Inc
anti gli1 Anti Gli1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/anti gli1/product/Cell Signaling Technology Inc Average 95 stars, based on 1 article reviews
anti gli1 - by Bioz Stars,
2026-03
95/100 stars
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Granulocyte/macrophage - Colony-stimulating factor (GM-CSF) is a hematopoietic factor that is produced by activated T-cells, B-cells, mast cells, macrophages, fibroblasts, and endothelial cells. In addition to supporting colony formation of granulocyte/macrophage progenitors, GM-CSF is a
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Image Search Results
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) Overexpression of GLI1 increases BrdU incorporation of Huh7 cells and silencing GLI1 expression in SNU398 cells decreases BrdU incorporation. (B) As assessed by the MTT assay, cell viability is increased at 48, 72 and 96 hours by overexpression of GLI1 in Huh7 cells and decreased at 24, 48, 72 and 96 hours by knockdown of GLI1 in SNU398 cells. (C) As assessed by the wound-healing assay, at both 24 and 48 hours, cell migration rate is increased in Huh7 cells by overexpression of GLI1 and decreased in SNU398 cells by silencing GLI1 expression. (D) Cell invasion is increased by overexpression of GLI1 in Huh7 cells and decreased by knockdown of GLI1 in SNU398 cells. (E) Overexpression of GLI1 promotes colony formation of Huh7 cells; in contrast, knockdown of GLI1 represses colony formation of SNU398 cells.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Over Expression, BrdU Incorporation Assay, Expressing, MTT Assay, Knockdown, Wound Healing Assay, Migration
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) Tumor recurrence after surgical resection in 139 patients with HCCs. Differences between the Kaplan-Meier curves of patients in the GLI1 high expresser group and those in GLI1 low/non expresser group using the log rank test. (B) Tumor recurrence after surgical resection in the 35 patients from the high GLI1 group and in the 35 patients from the low GLI1 group. Increased GLI1 expression in HCC tissues was significantly correlated with more rapid tumor recurrence after surgical resection of the primary tumor.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Expressing
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) As measured by both qRT-PCR, SNAI1 expression is increased by overexpression of GLI1 in Huh7 cells and decreased by knockdown of GLI1 in SNU398 cells. (B) Western immunoblotting (lower panel) and immunofluorescence staining (upper panel) confirm that SNAI1 protein expression is increased by overexpression of GLI1 in Huh7 cells (left panel) and decreased by knockdown of GLI1 in SNU398 cells (right panel). (C) ChIP assay verifies that GLI1 protein binds to the SNAI1 promoter. PCR was performed using a specific set of primers as indicated in Methods. (D) Bioinformatics analysis of the SNAI1 promoter identified candidate GLI (G) binding sites; (TSS = transcription start site). The positive amplicon for the ChIP assay is marked −1,417/−1,214 bp upstream of transcription start site (E) Relative changes in luciferase activity in Huh7 (left) and SNU398 (right) cells transfected with the WT and GLI mutant SNAI1 promoter luciferase reporter and control vector or GLI1.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Quantitative RT-PCR, Expressing, Over Expression, Knockdown, Western Blot, Immunofluorescence, Staining, Binding Assay, Amplification, Luciferase, Activity Assay, Transfection, Mutagenesis, Control, Plasmid Preparation
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) As assessed by qRT-PCR, overexpression of GLI1 decreases E-cadherin mRNA expression and increases the mRNA expression of both N-cadherin and Vimentin in Huh7 cells, while knockdown of GLI1 increases E-cadherin mRNA expression and decreases the mRNA expression of both N-cadherin and Vimentin in SNU398 cells. (B) As assessed by Western immunoblotting followed by densitometry analysis, overexpression of GLI1 decreases E-cadherin expression and increases the expression of both N-cadherin and Vimentin in Huh7 cells, while knockdown of GLI1 increases E-cadherin expression and decreases the expression of both N-cadherin and Vimentin in SNU398 cells.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Quantitative RT-PCR, Over Expression, Expressing, Knockdown, Western Blot
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) As assessed by immunofluorescence staining and confocal microscopy, overexpression of GLI1 decreases E-cadherin protein expression and increases the protein expression of both N-cadherin and Vimentin in Huh7 cells. (B) As assessed by immunofluorescence staining and confocal microscopy, knockdown of GLI1 (GLI1 ASO) increases E-cadherin protein expression and decreases the protein expression of both N-cadherin and Vimentin in SNU398 cells. DAPI was used as nuclear staining.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Immunofluorescence, Staining, Confocal Microscopy, Over Expression, Expressing, Knockdown
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) SNAI1 siRNA decreases SNAI1 expression in Huh7 cells transfected stably with GLI1 expressing plasmid. SNAI1 siRNA increases E-cadherin expression (B) and decreases the expression of both N-cadherin (C) and Vimentin (D) in Huh7 cells transfected stably with GLI1 expressing plasmid.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Expressing, Transfection, Stable Transfection, Plasmid Preparation
Journal: PLoS ONE
Article Title: The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
doi: 10.1371/journal.pone.0049581
Figure Lengend Snippet: (A) TGFβ1 increases GLI1 expression in Huh7 cells. And TGFβ1 is also found to decrease E-cadherin expression, while increasing the expression of N-cadherin, Vimentin and SNAI1 in Huh7 cells. (B) Suppressing the TGFβ1 induced up-regulation of GLI1 in Huh7 cells by GLI1 ASO decreased the expression of both GLI1 and SNAI1 in Huh7 cells. (C) Suppressing the TGFβ1 induced up-regulation of GLI1 in Huh7 cells by GLI1 ASO increases E-cadherin expression and decreases the expression of both N-cadherin and Vimentin.
Article Snippet: After transfer to PVDF membrane, blots were probed overnight with the following anti-human primary antibodies:
Techniques: Expressing