e2f1  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Kaplan–Meier plot showing that overexpression of E2F1 is associated with shorter overall survival (A) and progression-free interval (B) in endometrial cancer cohort. (C, D) Kaplan–Meier plot showing that co-overexpression of LARP1 and E2F1 is associated with shorter overall survival (C) and progression-free interval (D) in endometrial cancer cohort. (E) Spearman correlation analysis shows a correlation between LARP1 and E2F1 in endometrial cancer patients.

Article Snippet: Cells were then incubated overnight at 4 °C with the following primary antibodies: LARP1 (Cat. No. sc-515873; 1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and E2F1 (Cat. No. 3742S; 1:400 dilution; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Over Expression

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Immunoblot analysis showing the protein expression of LARP1 and E2F1 after transfecting ISHI (A) and HEC-1A (B) cells with control or LARP1 siRNA. β-actin was used as a loading control. (C) Images representing immunofluorescence staining of LARP1 (green) and E2F1 (red) in HEC-1A cells after transfection with control or LARP1 siRNA. DAPI was used as a counter stain. Scale bar = 50 µm.

Article Snippet: Cells were then incubated overnight at 4 °C with the following primary antibodies: LARP1 (Cat. No. sc-515873; 1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and E2F1 (Cat. No. 3742S; 1:400 dilution; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Western Blot, Expressing, Control, Immunofluorescence, Staining, Transfection

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: Drosophila E2f1 is required for axon patterning and NMJs growth. A CNSaxons in stage 15–16 embryos of indicated genotypes were visualized with mAb BP102 staining. Scale bar = 10 μm. Broken commissures (arrowhead) and connectives (arrows) were observed in e2f1 07172/i2 ( n = 23), elav > e2f1 RNAi ( n = 20), elav ts > e2f1 ( n = 20), and elav > dp RNAi ( n = 18) flies, whereas axons are intact in wild-type w 1118 ( n = 15) and elav > + ( n = 15) and elav ts > + ( n = 15) control flies. Overexpression of the e2f1 by elav ts -Gal4 fully rescued disrupted axons in e2f1 07172/i2 mutant flies ( elav ts > e2f1 , e2f1 07172/i2 , n = 15). B Confocal images of NMJ boutons at muscles 6/7 in L3 larvae of indicated genotypes were visualized with anti-HRP (red) and anti-DLG (green) antibodies staining. Scale bar = 20 μm. The bouton number ( C ), branch length ( D ), and branch number ( E ) per M6/7 NMJ in ( B ) were quantified, they were all significantly increased in e2f1 07172/i2 mutant flies ( n = 18) compared with w 1118 flies ( n = 15), and elav > e2f1 RNAi flies ( n = 16) and elav > dp RNAi flies ( n = 18) compared with elav > + flies ( n = 15), and decreased in elav ts > e2f1 flies ( n = 25) compared with elav ts > + flies ( n = 12). Overexpression of the e2f1 by elav ts -Gal4 fully rescued abnormal growth of NMJs in e2f1 07172/i2 mutant flies ( elav ts > e2f1 , e2f1 07172/i2 , n = 16). Data are mean ± SEM, **** p < 0.0001, n.s., no significance. One-way ANOVA test with Tukey’s post hoc test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Staining, Control, Over Expression, Mutagenesis, Muscles

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: miR-33 works downstream of E2f1 to regulate axon patterning and NMJs growth. Relative expression of the miR-33 in L3 larvae brains of w 1118 and e2f1 07172/i2 mutant flies ( A ), and elav ts > + flies and elav ts > e2f1 flies ( B ) was detected via RT-qPCR. Data were normalized with U6 as an internal control. Expression of the miR-33 was decreased in e2f1 mutant flies compared with w 1118 flies ( A ), and increased in elav ts > e2f1 flies compared with elav ts > + flies ( B ). **** p < 0.0001, two-tailed two-sample t test. C CNS axons in stage 15–16 embryos of indicated genotypes were visualized with mAb BP102 staining. Scale bar = 10 μm. Overexpression of the miR-33 by elav-Gal4 fully rescued disrupted axons in e2f1 07172/i2 mutant flies ( elav > miR-33 , e2f1 07172/i2 , n = 17). D Confocal images of NMJ boutons at muscles 6/7 in L3 larvae of indicated genotypes were visualized with anti-HRP (red) and anti-DLG (green) antibodies staining. Scale bar = 20 μm. The bouton number ( E ), branch length ( F ), and branch number ( G ) per M6/7 NMJ in ( D ) were quantified. Overexpression of the miR-33 by elav-Gal4 fully rescued abnormal growth of NMJs in e2f1 07172/i2 mutant flies ( elav > miR-33 , e2f1 07172/i2 , n = 17). Data are mean ± SEM, **** p < 0.0001, n.s., no significance. One-way ANOVA test with Tukey’s post hoc test. H Scheme of the miR-33 promoter region. Putative E2f-sites are depicted, and nucleotide positions of E2f-sites are provided with respect to the miR-33 transcription start site. I ChIP-qPCR analysis revealed significant binding of the E2f1 protein to site #1 and #2 in the miR-33 promoter region, and the PCNA promoter region as a positive control, and no binding to site #3 in the miR-33 promoter region and the negative control rp49 promoter region. * p < 0.05, *** p < 0.001, **** p < 0.0001, n.s., no significance. Two-tailed two-sample t test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Expressing, Mutagenesis, Quantitative RT-PCR, Control, Two Tailed Test, Staining, Over Expression, Muscles, ChIP-qPCR, Binding Assay, Positive Control, Negative Control

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: Trio works as the effector of E2f1 signaling in neuron development. A CNS axons in stage 15–16 embryos of indicated genotypes were visualized with mAb BP102 staining. Scale bar = 10 μm. Knockdown of the trio expression by elav > trio RNAi fully rescued disrupted axons in e2f1 07172/i2 mutant flies ( elav > trio RNAi , e2f1 07172/i2 , n = 17), and overexpression of the trio gene by elav ts -Gal4 greatly rescued disrupted axons in elav ts > e2f1 flies ( elav ts > e2f1/trio , n = 17). B Confocal images of NMJ boutons at muscles 6/7 in L3 larvae of indicated genotypes were visualized with anti-HRP (red) and anti-DLG (green) antibodies staining. Scale bar = 20 μm. The bouton number ( C ), branch length ( D ), and branch number ( E ) per M6/7 NMJ in ( B ) were quantified. Knockdown of the trio expression by elav > trio RNAi fully rescued abnormal growth of NMJs in e2f1 07172/i2 mutant flies ( elav > trio RNAi , e2f1 07172/i2 , n = 16), and overexpression of the trio gene by elav ts -Gal4 greatly rescued abnormal growth of NMJs in elav ts > e2f1 flies ( elav ts > e2f1/trio , n = 18). Data are mean ± SEM, * p < 0.05, **** p < 0.0001. One-way ANOVA test with Tukey’s post hoc test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Staining, Knockdown, Expressing, Mutagenesis, Over Expression, Muscles

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: Conserved regulations among human homologs of E2f1, miR-33 and Trio. A Scheme of the miR-33 sequence embedded in its host-gene SREBP and conservation in multiple species during evolution. B - C Relative expression of the hmiR-33 in HEK-293T cells transfected with shRNA sh- he2f1 or the control sh- NC ( B ), and transfected with pCDH-CMV-MCS-EF1-he2f1 or with the control pCDH-CMV-MCS-EF1 vector ( C ), was detected via RT-qPCR. Data were normalized with hU6 as an internal control. Expression of the hmiR-33 was decreased in sh- he2f1 treated cells compared with the control sh- NC ( B ), and increased in pCDH-CMV-MCS-EF1-he2f1 transfected cells compared with the control pCDH-CMV-MCS-EF1 vector transfected cells ( C ). ** p < 0.01, two-tailed two-sample t test. D Scheme of the hmiR-33 promoter region. Putative E2f-sites are depicted, and nucleotide positions of E2f-sites are provided with respect to the hmiR-33 transcription start site. E ChIP-qPCR analysis revealed significant binding of the hE2f1 protein to site #4 in the hmiR-33 promoter region, and the hPCNA promoter region as a positive control, and no binding to site #1, #2 or #3 in the hmiR-33 promoter region and the negative control hGAPDH promoter region. *** p < 0.001, **** p < 0.0001, n.s., no significance. Two-tailed two-sample t test. F Predicted binding-site for the miR-33 seed-sequence in the trio 3’ UTR in multiple species. G The binding-site of the hmiR-33 seed-sequence in the htrio 3’ UTR and mutagenesis of the binding-site are shown in red and blue, respectively. H Luciferase assay showing activity of a luciferase reporter containing htrio 3’ UTR ( htrio 3’ UTR wt ) or mutated htrio 3’ UTR ( htrio 3’ UTR mut ) treated with hmiR-33 mimics, or a negative control NC mimics. Data are mean ± SEM from three independent experiments. *** p < 0.001, n.s., no significance. Two-tailed two-sample t test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Sequencing, Expressing, Transfection, shRNA, Control, Plasmid Preparation, Quantitative RT-PCR, Two Tailed Test, ChIP-qPCR, Binding Assay, Positive Control, Negative Control, Mutagenesis, Luciferase, Activity Assay

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: Conserved functions of human miR-33 and Trio in neuron development. A and F CNS axons in stage 15–16 embryos of indicated genotypes were visualized with mAb BP102 staining. Scale bar = 10 μm. B and G Confocal images of NMJ boutons at muscles 6/7 in L3 larvae of indicated genotypes were visualized with anti-HRP (red) and anti-DLG (green) antibodies staining. Scale bar = 20 μm. A Broken commissures (arrowhead) and connectives (arrows) in e2f1 07172/i2 flies were greatly rescued by overexpression of a human homolog of the miR-33 ( elav > hmiR-33 , e2f1 07172/i2 , n = 15), and broken commissures (arrowhead) and connectives (arrows) in miR-33 KO flies were fully rescued by overexpression of the hmiR-33 ( elav > hmiR-33 , miR-33 KO , n = 15). Overexpression of the hmiR-33 ( elav > hmiR-33 , n = 20) caused broken commissures and connectives in flies. The bouton number ( C ), branch length ( D ), and branch number ( E ) per M6/7 NMJ in ( B ) were quantified. Increased bouton number, branch length and branch number in e2f1 07172/i2 mutant flies were fully rescued by overexpression of the hmiR-33 ( elav > hmiR-33 , e2f1 07172/i2 , n = 16), and increased bouton number, branch length and branch number in miR-33 KO flies were fully rescued by overexpression of the hmiR-33 ( elav > hmiR-33 , miR-33 KO , n = 15). Overexpression of the hmiR-33 ( elav > hmiR-33 , n = 24) decreased bouton number, branch length and branch number compared with elav > + control flies. Data are mean ± SEM, **** p < 0.0001, n.s., no significance. One-way ANOVA test with Tukey’s post hoc test. F Broken commissures (arrowhead) and connectives (arrows) in elav > miR-33 flies were greatly rescued by overexpression of a human homolog of the trio gene ( elav > miR-33/htrio , n = 15), and broken commissures (arrowhead) and connectives (arrows) in trio mutant flies were greatly rescued by overexpression of the htrio gene ( elav > htrio , trio 1/s137203 , n = 15). Overexpression of the htrio gene ( elav > htrio , n = 24) caused broken commissures and connectives in flies. The bouton number ( H ), branch length ( I ), and branch number ( J ) per M6/7 NMJ in ( G ) were quantified. Decreased bouton number, branch length and branch number in elav > miR-33 flies were fully rescued by overexpression of the htrio gene ( elav > miR-33/htrio , n = 17), and decreased bouton number, branch length and branch number in trio mutant flies were fully rescued by overexpression of the htrio gene ( elav > htrio , trio 1/s137203 , n = 16). Overexpression of the htrio gene in flies ( elav > htrio , n = 17) increased bouton number, branch length and branch number compared with elav > + control flies. Data are mean ± SEM, **** p < 0.0001, n.s., no significance. One-way ANOVA test with Tukey’s post hoc test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Staining, Muscles, Over Expression, Mutagenesis, Control

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: e2f1 , miR-33 and trio mutant flies exhibit aberrant locomotor behaviors. Locomotor behaviors of L3 larvae of indicated genotypes were assayed by measuring numbers of 0.5 cm 2 grids crossed in 30 s ( A , C and E ), and numbers of full-body peristaltic contractions in 1 min ( B , D and F ). Data were acquired from 30 samples. A Numbers of grids crossed were reduced of e2f1 07172/i2 mutant flies compared with w 1118 flies, and elav ts > e2f1 flies compared with elav ts > + control flies, and overexpression of e2f1 by elav ts -Gal4 rescued motor deficitsin e2f1 07172/i2 mutant flies ( elav ts > e2f1 , e2f1 07172/i2 ). B Numbers of full-body peristaltic contractions were reduced of e2f1 07172/i2 mutant flies compared with w 1118 flies, and elav ts > e2f1 flies compared with ela ts > + control flies, and overexpression of e2f1 by elav ts -Gal4 rescued motor deficits in e2f 07172/i2 mutant flies ( elav ts > e2f1 , e2f1 07172/i2 ). C Numbers of grids crossed were reduced of miR-33 KO flies compared with w 1118 flies, and elav > miR-33 flies compared with elav > + control flies, and overexpression of miR-33 by elav-Gal4 rescued motor deficits in miR-33 KO flies ( elav > miR-33 , miR-33 KO ). D Numbers of full-body peristaltic contractions were reduced of miR-33 KO flies compared with w 1118 flies, and elav > miR-33 flies compared with elav > + control flies, and overexpression of miR-33 by elav-Gal4 rescued motor deficits in miR-33 KO flies ( elav > miR-33 , miR-33 KO ). E Numbers of grids crossed were reduced of trio 1/s137203 mutant flies compared with w 1118 flies, and elav > trio flies compared with elav > + control flies, and overexpression of trio by elav-Gal4 rescued motor deficits in trio 1/s137203 mutant flies ( elav > trio , trio 1/s137203 ). F Numbers of full-body peristaltic peristaltic contractions were reduced of trio 1/s137203 mutant flies compared with w 1118 flies, and elav > trio flies compared with elav > + control flies, and overexpression of trio by elav-Gal4 rescued motor deficits in trio 1/s137203 mutant flies ( elav > trio , trio 1/s137203 ). Data are mean ± SEM. **** p < 0.0001, n.s., no significance. One-way ANOVA test with Tukey’s post hoc test

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Mutagenesis, Control, Over Expression

Journal: Cell Communication and Signaling : CCS

Article Title: E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio

doi: 10.1186/s12964-025-02612-2

Figure Lengend Snippet: A model. The E2f1/miR-33/Trio signaling is critical for neurodevelopment and conserved between Drosophila and human. Loss or dysregulated expression of any member in the signaling disrupts axon patterning, causes abnormal synaptic growth at neuromuscular junctions (NMJs), and eventually leads to aberrant locomotor behaviors. Keeping the activity and well-balanced dosage of the E2f1/miR-33/Trio signaling is essential for neuron development and synaptic plasticity

Article Snippet: Soluble chromatin from HEK-293T cells was immunoprecipitated using the human anti-E2F1 antibody (Cell Signaling, #3742).

Techniques: Expressing, Activity Assay