rabbit polyclonal e2f1 Search Results


anti e2f1  (OriGene)
93
OriGene anti e2f1
ARRB1 controls cell proliferation and apoptosis in granule cell progenitors (GCPs) via <t>E2F1</t> acetylation. (A) Murine cerebellum Western blot. Representative images of endogenous GLI1 and ARRB1 in murine cerebella at different days (2, 5, 7, 15) of cerebellar development. GAPDH: loading control. (B–G) GCPs experiments. Shh was added to cultures of murine cerebellar GCPs that had or had not undergone siRNA-mediated silencing of ARRB1 (siArrb1). After 48 h of Shh stimulation, GCPs were assayed for: (B) Gli1 mRNA and protein levels (as a read-out of Shh signaling activity), and ARRB1 protein level; ACTIN as loading control; (C) proliferation reflected by bromodeoxyuridine (BrdU) uptake; (D) left: p27 mRNA levels ( (D) right and : Overexpression data are consistent); (E) differentiation reflected by β III tubulin mRNA levels; (F) apoptosis evaluated by TUNEL assay, and (G) ARRB1, E2F1, E2F1-ac, cleaved CASPASE-3 protein expression levels. ACTIN and HISTONE H3: loading controls. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.
Anti E2f1, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti e2f1/product/OriGene
Average 93 stars, based on 1 article reviews
anti e2f1 - by Bioz Stars, 2026-02
93/100 stars
  Buy from Supplier
antibody against e2f1  (Wanleibio)
90
Wanleibio antibody against e2f1
ARRB1 controls cell proliferation and apoptosis in granule cell progenitors (GCPs) via <t>E2F1</t> acetylation. (A) Murine cerebellum Western blot. Representative images of endogenous GLI1 and ARRB1 in murine cerebella at different days (2, 5, 7, 15) of cerebellar development. GAPDH: loading control. (B–G) GCPs experiments. Shh was added to cultures of murine cerebellar GCPs that had or had not undergone siRNA-mediated silencing of ARRB1 (siArrb1). After 48 h of Shh stimulation, GCPs were assayed for: (B) Gli1 mRNA and protein levels (as a read-out of Shh signaling activity), and ARRB1 protein level; ACTIN as loading control; (C) proliferation reflected by bromodeoxyuridine (BrdU) uptake; (D) left: p27 mRNA levels ( (D) right and : Overexpression data are consistent); (E) differentiation reflected by β III tubulin mRNA levels; (F) apoptosis evaluated by TUNEL assay, and (G) ARRB1, E2F1, E2F1-ac, cleaved CASPASE-3 protein expression levels. ACTIN and HISTONE H3: loading controls. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.
Antibody Against E2f1, supplied by Wanleibio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibody against e2f1/product/Wanleibio
Average 90 stars, based on 1 article reviews
antibody against e2f1 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier
e2f1 antibody rabbit polyclonal 12171-1-ap  (ImmunoGen Inc)
90
ImmunoGen Inc e2f1 antibody rabbit polyclonal 12171-1-ap
ARRB1 controls cell proliferation and apoptosis in granule cell progenitors (GCPs) via <t>E2F1</t> acetylation. (A) Murine cerebellum Western blot. Representative images of endogenous GLI1 and ARRB1 in murine cerebella at different days (2, 5, 7, 15) of cerebellar development. GAPDH: loading control. (B–G) GCPs experiments. Shh was added to cultures of murine cerebellar GCPs that had or had not undergone siRNA-mediated silencing of ARRB1 (siArrb1). After 48 h of Shh stimulation, GCPs were assayed for: (B) Gli1 mRNA and protein levels (as a read-out of Shh signaling activity), and ARRB1 protein level; ACTIN as loading control; (C) proliferation reflected by bromodeoxyuridine (BrdU) uptake; (D) left: p27 mRNA levels ( (D) right and : Overexpression data are consistent); (E) differentiation reflected by β III tubulin mRNA levels; (F) apoptosis evaluated by TUNEL assay, and (G) ARRB1, E2F1, E2F1-ac, cleaved CASPASE-3 protein expression levels. ACTIN and HISTONE H3: loading controls. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.
E2f1 Antibody Rabbit Polyclonal 12171 1 Ap, supplied by ImmunoGen Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/e2f1 antibody rabbit polyclonal 12171-1-ap/product/ImmunoGen Inc
Average 90 stars, based on 1 article reviews
e2f1 antibody rabbit polyclonal 12171-1-ap - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


ARRB1 controls cell proliferation and apoptosis in granule cell progenitors (GCPs) via E2F1 acetylation. (A) Murine cerebellum Western blot. Representative images of endogenous GLI1 and ARRB1 in murine cerebella at different days (2, 5, 7, 15) of cerebellar development. GAPDH: loading control. (B–G) GCPs experiments. Shh was added to cultures of murine cerebellar GCPs that had or had not undergone siRNA-mediated silencing of ARRB1 (siArrb1). After 48 h of Shh stimulation, GCPs were assayed for: (B) Gli1 mRNA and protein levels (as a read-out of Shh signaling activity), and ARRB1 protein level; ACTIN as loading control; (C) proliferation reflected by bromodeoxyuridine (BrdU) uptake; (D) left: p27 mRNA levels ( (D) right and : Overexpression data are consistent); (E) differentiation reflected by β III tubulin mRNA levels; (F) apoptosis evaluated by TUNEL assay, and (G) ARRB1, E2F1, E2F1-ac, cleaved CASPASE-3 protein expression levels. ACTIN and HISTONE H3: loading controls. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Cell and Developmental Biology

Article Title: β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum

doi: 10.3389/fcell.2023.990711

Figure Lengend Snippet: ARRB1 controls cell proliferation and apoptosis in granule cell progenitors (GCPs) via E2F1 acetylation. (A) Murine cerebellum Western blot. Representative images of endogenous GLI1 and ARRB1 in murine cerebella at different days (2, 5, 7, 15) of cerebellar development. GAPDH: loading control. (B–G) GCPs experiments. Shh was added to cultures of murine cerebellar GCPs that had or had not undergone siRNA-mediated silencing of ARRB1 (siArrb1). After 48 h of Shh stimulation, GCPs were assayed for: (B) Gli1 mRNA and protein levels (as a read-out of Shh signaling activity), and ARRB1 protein level; ACTIN as loading control; (C) proliferation reflected by bromodeoxyuridine (BrdU) uptake; (D) left: p27 mRNA levels ( (D) right and : Overexpression data are consistent); (E) differentiation reflected by β III tubulin mRNA levels; (F) apoptosis evaluated by TUNEL assay, and (G) ARRB1, E2F1, E2F1-ac, cleaved CASPASE-3 protein expression levels. ACTIN and HISTONE H3: loading controls. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The following antibodies were used: anti-GLI1 (L42B10, Cell Signaling), anti-CASPASE-3 (D3R6Y, Cell Signaling), anti-β-ARRESTIN1 K-16 (sc-8182; Santa Cruz Biotechnology), anti-ACTIN I-19 (sc-1616; Santa Cruz Biotechnology), anti-E2F1 C-20 (sc-193; Santa Cruz Biotechnology), anti-E2F1 (acetyl K120/K125) (AP10555SU-N, Acris Antibodies); anti-ZIC1 (ab72694; Abcam); anti-PARP p85 Fragment (G7342; Promega), anti-SP1 1C6 (sc-420X; Santa Cruz Biotechnology), anti-PCNA (2586; Cell signaling), anti-H3 (ab 1971, Abcam), and anti-GAPDH (ab8245; Abcam).

Techniques: Western Blot, Control, Activity Assay, Over Expression, TUNEL Assay, Expressing

E2F1-ac targets’ transcripts after ARRB1 modulation. (A,B) Expression of pro-apoptotic E2F1-ac target genes ( Trp73, Casp3 and Casp7 ) in GCPs that had or had not undergone siArrb1 (black) or over-expression of Arrb1 (Arrb1-HA) (orange). (C,D) Expression of proliferative (grey) and epithelial mesenchymal transition (violet) E2f1-ac target genes ( Cdc25a, Birc5, Tyms, Zeb1, Zeb2, Vim and Fn1 ) in GCPs that had or had not undergone siArrb1. Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001. (E) IHC staining for ARRB1 and P27 in representative mouse cerebellum sections at several differentiation stages (p2, p4, p7, p10, p15) (upper panels). Magnification ×10; insets ×40. Scale bar, 250 µm. CASPASE-3 and CDC25A indexes (expressed as percentage) calculated as DAB positive cells of total number of cells (bottom panels). Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.001 vs. p10. # p < 0.05; ## p < 0.01 vs. p15.

Journal: Frontiers in Cell and Developmental Biology

Article Title: β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum

doi: 10.3389/fcell.2023.990711

Figure Lengend Snippet: E2F1-ac targets’ transcripts after ARRB1 modulation. (A,B) Expression of pro-apoptotic E2F1-ac target genes ( Trp73, Casp3 and Casp7 ) in GCPs that had or had not undergone siArrb1 (black) or over-expression of Arrb1 (Arrb1-HA) (orange). (C,D) Expression of proliferative (grey) and epithelial mesenchymal transition (violet) E2f1-ac target genes ( Cdc25a, Birc5, Tyms, Zeb1, Zeb2, Vim and Fn1 ) in GCPs that had or had not undergone siArrb1. Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001. (E) IHC staining for ARRB1 and P27 in representative mouse cerebellum sections at several differentiation stages (p2, p4, p7, p10, p15) (upper panels). Magnification ×10; insets ×40. Scale bar, 250 µm. CASPASE-3 and CDC25A indexes (expressed as percentage) calculated as DAB positive cells of total number of cells (bottom panels). Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.001 vs. p10. # p < 0.05; ## p < 0.01 vs. p15.

Article Snippet: The following antibodies were used: anti-GLI1 (L42B10, Cell Signaling), anti-CASPASE-3 (D3R6Y, Cell Signaling), anti-β-ARRESTIN1 K-16 (sc-8182; Santa Cruz Biotechnology), anti-ACTIN I-19 (sc-1616; Santa Cruz Biotechnology), anti-E2F1 C-20 (sc-193; Santa Cruz Biotechnology), anti-E2F1 (acetyl K120/K125) (AP10555SU-N, Acris Antibodies); anti-ZIC1 (ab72694; Abcam); anti-PARP p85 Fragment (G7342; Promega), anti-SP1 1C6 (sc-420X; Santa Cruz Biotechnology), anti-PCNA (2586; Cell signaling), anti-H3 (ab 1971, Abcam), and anti-GAPDH (ab8245; Abcam).

Techniques: Expressing, Over Expression, Immunohistochemistry

ARRB1-E2F1 complex direct regulates the expression of E2F1-ac pro-apoptotic targets. (A,B) qPCR-ChIP assay of ARRB1 in GCPs stimulated or not with Shh. Immunoprecipitation with IgG was performed as control. Eluted DNA was amplified by qPCR using primers specific for the regulatory region of the indicated genes. Actin and Gapdh (not shown) were used as endogenous non-enriched regions. qPCR data are presented as percentage of ChIP input controls. Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Cell and Developmental Biology

Article Title: β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum

doi: 10.3389/fcell.2023.990711

Figure Lengend Snippet: ARRB1-E2F1 complex direct regulates the expression of E2F1-ac pro-apoptotic targets. (A,B) qPCR-ChIP assay of ARRB1 in GCPs stimulated or not with Shh. Immunoprecipitation with IgG was performed as control. Eluted DNA was amplified by qPCR using primers specific for the regulatory region of the indicated genes. Actin and Gapdh (not shown) were used as endogenous non-enriched regions. qPCR data are presented as percentage of ChIP input controls. Data represent means ± S.D., from at least three independent experiments; * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The following antibodies were used: anti-GLI1 (L42B10, Cell Signaling), anti-CASPASE-3 (D3R6Y, Cell Signaling), anti-β-ARRESTIN1 K-16 (sc-8182; Santa Cruz Biotechnology), anti-ACTIN I-19 (sc-1616; Santa Cruz Biotechnology), anti-E2F1 C-20 (sc-193; Santa Cruz Biotechnology), anti-E2F1 (acetyl K120/K125) (AP10555SU-N, Acris Antibodies); anti-ZIC1 (ab72694; Abcam); anti-PARP p85 Fragment (G7342; Promega), anti-SP1 1C6 (sc-420X; Santa Cruz Biotechnology), anti-PCNA (2586; Cell signaling), anti-H3 (ab 1971, Abcam), and anti-GAPDH (ab8245; Abcam).

Techniques: Expressing, Immunoprecipitation, Control, Amplification

ARRB1 controls NSCs apoptosis via E2F1 acetylation. (A) Effects of Arrb1-HA overexpression and mock transfection (control) of NSCs on ARRB1 and E2F1-ac protein levels (Western blot assay-left) and Trp73 and Cdc25a mRNA levels (right). * p < 0.05 vs. mock transfected cells (Mock). GAPDH: loading control for Western blot. (B) Western Blot analysis of endogenous ARRB1, E2F1, and E2F1-ac expression in NSCs cultured in SCM (0 h) and after 8–24 h culture in DFM. GAPDH: loading control. Effects of si-Arrb1 or scrambled control (siCtr) on (C) Trp73 and Cdc25a mRNA levels (left) and ARRB1 protein levels (Western blot assay-right) in NSCs cultured in SCM (0 h) and after 18 h culture in DFM. ACTIN: loading control for Western blot. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . * p < 0.05 vs. scrambled control (siCtr).

Journal: Frontiers in Cell and Developmental Biology

Article Title: β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum

doi: 10.3389/fcell.2023.990711

Figure Lengend Snippet: ARRB1 controls NSCs apoptosis via E2F1 acetylation. (A) Effects of Arrb1-HA overexpression and mock transfection (control) of NSCs on ARRB1 and E2F1-ac protein levels (Western blot assay-left) and Trp73 and Cdc25a mRNA levels (right). * p < 0.05 vs. mock transfected cells (Mock). GAPDH: loading control for Western blot. (B) Western Blot analysis of endogenous ARRB1, E2F1, and E2F1-ac expression in NSCs cultured in SCM (0 h) and after 8–24 h culture in DFM. GAPDH: loading control. Effects of si-Arrb1 or scrambled control (siCtr) on (C) Trp73 and Cdc25a mRNA levels (left) and ARRB1 protein levels (Western blot assay-right) in NSCs cultured in SCM (0 h) and after 18 h culture in DFM. ACTIN: loading control for Western blot. For Western blot, densitometry values are shown below the blots and densitometric graphs are presented in . * p < 0.05 vs. scrambled control (siCtr).

Article Snippet: The following antibodies were used: anti-GLI1 (L42B10, Cell Signaling), anti-CASPASE-3 (D3R6Y, Cell Signaling), anti-β-ARRESTIN1 K-16 (sc-8182; Santa Cruz Biotechnology), anti-ACTIN I-19 (sc-1616; Santa Cruz Biotechnology), anti-E2F1 C-20 (sc-193; Santa Cruz Biotechnology), anti-E2F1 (acetyl K120/K125) (AP10555SU-N, Acris Antibodies); anti-ZIC1 (ab72694; Abcam); anti-PARP p85 Fragment (G7342; Promega), anti-SP1 1C6 (sc-420X; Santa Cruz Biotechnology), anti-PCNA (2586; Cell signaling), anti-H3 (ab 1971, Abcam), and anti-GAPDH (ab8245; Abcam).

Techniques: Over Expression, Transfection, Control, Western Blot, Expressing, Cell Culture

Schematic model of ARRB1/E2F1-ac functions in GCPs and NSCs. Overview of roles played by ARRB1/E2F1-ac in normal cerebellar development. (A) : Committed neuronal precursors (i.e., NSCs grown in DFM, GCPs). In our previous works, we identified miR-326 as a miRNA necessary for maturation of granule cell progenitors (GCPs) into mature granule cells . Moreover, this miRNA is integrated into the first intron of the Arrb1 gene and shares the same regulatory regions as its host gene. miR-326 also contributes to ARRB1 functions by blunting proliferative signals mediated by E2F1, Hedgehog, and Notch, and by promoting cell differentiation ( ; ; ; ). Committed neuronal precursors express ARRB1 and mir-326, which regulate their development at multiple levels. Shh signaling upregulates ARRB1 levels and promotes its translocation to the nucleus. There ARRB1, in complex with P300, induces acetylation of E2F1 (E2F1-ac), redirecting the transcription factors activity from survival/proliferative gene targets towards those that promote apoptosis ( Trp73, Caspases 3 and 7 ). Interacting with CREB and P300, ARRB1 upregulates the expression and nuclear accumulation of P27, which eventually blocks cell cycle progression. miR-326 favors neuronal cell differentiations by inhibiting multiple survival/proliferative signaling: E2F1, Hedgehog (Hh) and Notch via direct binding of the 3′-UTRs of E2f1, Smo, Gli2, Notch1 and Notch2 . (B) : In NSCs, non-expression of ARRB1 and miR-326 promotes cell proliferation, survival, and stemness by favoring non-acetylated E2F1 activity and active Hedgehog (Hh) and Notch signaling.

Journal: Frontiers in Cell and Developmental Biology

Article Title: β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum

doi: 10.3389/fcell.2023.990711

Figure Lengend Snippet: Schematic model of ARRB1/E2F1-ac functions in GCPs and NSCs. Overview of roles played by ARRB1/E2F1-ac in normal cerebellar development. (A) : Committed neuronal precursors (i.e., NSCs grown in DFM, GCPs). In our previous works, we identified miR-326 as a miRNA necessary for maturation of granule cell progenitors (GCPs) into mature granule cells . Moreover, this miRNA is integrated into the first intron of the Arrb1 gene and shares the same regulatory regions as its host gene. miR-326 also contributes to ARRB1 functions by blunting proliferative signals mediated by E2F1, Hedgehog, and Notch, and by promoting cell differentiation ( ; ; ; ). Committed neuronal precursors express ARRB1 and mir-326, which regulate their development at multiple levels. Shh signaling upregulates ARRB1 levels and promotes its translocation to the nucleus. There ARRB1, in complex with P300, induces acetylation of E2F1 (E2F1-ac), redirecting the transcription factors activity from survival/proliferative gene targets towards those that promote apoptosis ( Trp73, Caspases 3 and 7 ). Interacting with CREB and P300, ARRB1 upregulates the expression and nuclear accumulation of P27, which eventually blocks cell cycle progression. miR-326 favors neuronal cell differentiations by inhibiting multiple survival/proliferative signaling: E2F1, Hedgehog (Hh) and Notch via direct binding of the 3′-UTRs of E2f1, Smo, Gli2, Notch1 and Notch2 . (B) : In NSCs, non-expression of ARRB1 and miR-326 promotes cell proliferation, survival, and stemness by favoring non-acetylated E2F1 activity and active Hedgehog (Hh) and Notch signaling.

Article Snippet: The following antibodies were used: anti-GLI1 (L42B10, Cell Signaling), anti-CASPASE-3 (D3R6Y, Cell Signaling), anti-β-ARRESTIN1 K-16 (sc-8182; Santa Cruz Biotechnology), anti-ACTIN I-19 (sc-1616; Santa Cruz Biotechnology), anti-E2F1 C-20 (sc-193; Santa Cruz Biotechnology), anti-E2F1 (acetyl K120/K125) (AP10555SU-N, Acris Antibodies); anti-ZIC1 (ab72694; Abcam); anti-PARP p85 Fragment (G7342; Promega), anti-SP1 1C6 (sc-420X; Santa Cruz Biotechnology), anti-PCNA (2586; Cell signaling), anti-H3 (ab 1971, Abcam), and anti-GAPDH (ab8245; Abcam).

Techniques: Cell Differentiation, Translocation Assay, Activity Assay, Expressing, Binding Assay