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Abnova anti-brap
Anti Brap, supplied by Abnova, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Recombinant:

Article Title: Identification of novel serum autoantibodies against EID3 in non-functional pancreatic neuroendocrine tumors
Article Snippet: To detect GST-tagged recombinant proteins, western blotting was performed using anti-PTEN (Origene Technologies, Rockville, MD, USA), anti-EID3 (Abcam, Cambridge, UK), anti-EHD1 (Abcam), anti-BRAP (Abnova, Taipei, Taiwan), anti-LGALS9 (GeneTex, Los Angeles, CA, USA), and anti-GST (Rockland, Gilbertsville, PA, USA) antibodies ( ).

Article Title: Identification of novel serum autoantibodies against EID3 in non-functional pancreatic neuroendocrine tumors.
Article Snippet: To detect GST-tagged recombinant proteins, western blotting was performed using anti-PTEN (Origene Technologies, Rockville, MD, USA), anti-EID3 (Abcam, Cambridge, UK), anti-EHD1 (Abcam), anti-BRAP (Abnova, Taipei, Taiwan), anti-LGALS9 (GeneTex, Los Angeles, CA, USA), and anti-GST (Rockland, Gilbertsville, PA, USA) antibodies (Supplementary Table 1).

Western Blot:

Article Title: Identification of novel serum autoantibodies against EID3 in non-functional pancreatic neuroendocrine tumors
Article Snippet: To detect GST-tagged recombinant proteins, western blotting was performed using anti-PTEN (Origene Technologies, Rockville, MD, USA), anti-EID3 (Abcam, Cambridge, UK), anti-EHD1 (Abcam), anti-BRAP (Abnova, Taipei, Taiwan), anti-LGALS9 (GeneTex, Los Angeles, CA, USA), and anti-GST (Rockland, Gilbertsville, PA, USA) antibodies ( ).

Article Title: Identification of novel serum autoantibodies against EID3 in non-functional pancreatic neuroendocrine tumors.
Article Snippet: To detect GST-tagged recombinant proteins, western blotting was performed using anti-PTEN (Origene Technologies, Rockville, MD, USA), anti-EID3 (Abcam, Cambridge, UK), anti-EHD1 (Abcam), anti-BRAP (Abnova, Taipei, Taiwan), anti-LGALS9 (GeneTex, Los Angeles, CA, USA), and anti-GST (Rockland, Gilbertsville, PA, USA) antibodies (Supplementary Table 1).



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The expression of <t>BRAP</t> and its mouse homolog in skin tissues and the skin injury induced by IMQ in both BC004004 -/- mice and their wild type control mice. (A) The expression of BRAP in both normal human skin and the skin of patient with psoriasis by immunohistochemistry analysis of tissue samples with anti-BRAP antibody. BRAP is expressed in the epidermis of both normal skin tissue and skin tissue with psoriasis (magnification: 100×(scale bar = 200 μm) and 400×(scale bar = 50 μm)). (B) BRAP homologous protein was present in skin tissues as revealed by Western blotting in wild-type control mice BC004004 +/+ with imiquimod (IMQ) treatment for 7 day. The total protein extract from one wild type mice skin representing each day of IMQ treatment was loaded in one well. The expression of β-actin from the same sample was used as a loading control. (C) Representative photographs of psoriasis-like lesions on back skin of BC004004 +/+ mice and BC004004 -/- mice after 7 days of IMQ treatment. Vaseline treatment was applied on control groups as a vehicle control. (D) Daily body weights throughout the 7-day IMQ treatment were shown in the upper left panel. The characteristics of skin lesion were depicted as redness, scaling scores and thickness of back skin and scored according to a murine Psoriasis Area and Severity Index (PASI) score table. Data are presented as mean ± SD; n = 9 in each group. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001.
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The expression of <t>BRAP</t> and its mouse homolog in skin tissues and the skin injury induced by IMQ in both BC004004 -/- mice and their wild type control mice. (A) The expression of BRAP in both normal human skin and the skin of patient with psoriasis by immunohistochemistry analysis of tissue samples with anti-BRAP antibody. BRAP is expressed in the epidermis of both normal skin tissue and skin tissue with psoriasis (magnification: 100×(scale bar = 200 μm) and 400×(scale bar = 50 μm)). (B) BRAP homologous protein was present in skin tissues as revealed by Western blotting in wild-type control mice BC004004 +/+ with imiquimod (IMQ) treatment for 7 day. The total protein extract from one wild type mice skin representing each day of IMQ treatment was loaded in one well. The expression of β-actin from the same sample was used as a loading control. (C) Representative photographs of psoriasis-like lesions on back skin of BC004004 +/+ mice and BC004004 -/- mice after 7 days of IMQ treatment. Vaseline treatment was applied on control groups as a vehicle control. (D) Daily body weights throughout the 7-day IMQ treatment were shown in the upper left panel. The characteristics of skin lesion were depicted as redness, scaling scores and thickness of back skin and scored according to a murine Psoriasis Area and Severity Index (PASI) score table. Data are presented as mean ± SD; n = 9 in each group. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001.
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Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of <t>BRAP</t> homologous protein in mice detected by western blot <t>with</t> <t>anti-BRAP</t> antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.
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Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of <t>BRAP</t> homologous protein in mice detected by western blot <t>with</t> <t>anti-BRAP</t> antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.
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Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of <t>BRAP</t> homologous protein in mice detected by western blot <t>with</t> <t>anti-BRAP</t> antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.
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Relation of phenotypes induced by <t>BRAP</t> and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP <t>,</t> <t>neurofibromin,</t> as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .
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Relation of phenotypes induced by <t>BRAP</t> and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP <t>,</t> <t>neurofibromin,</t> as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .
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Relation of phenotypes induced by <t>BRAP</t> and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP <t>,</t> <t>neurofibromin,</t> as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .
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Relation of phenotypes induced by <t>BRAP</t> and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP <t>,</t> <t>neurofibromin,</t> as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .
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The expression of BRAP and its mouse homolog in skin tissues and the skin injury induced by IMQ in both BC004004 -/- mice and their wild type control mice. (A) The expression of BRAP in both normal human skin and the skin of patient with psoriasis by immunohistochemistry analysis of tissue samples with anti-BRAP antibody. BRAP is expressed in the epidermis of both normal skin tissue and skin tissue with psoriasis (magnification: 100×(scale bar = 200 μm) and 400×(scale bar = 50 μm)). (B) BRAP homologous protein was present in skin tissues as revealed by Western blotting in wild-type control mice BC004004 +/+ with imiquimod (IMQ) treatment for 7 day. The total protein extract from one wild type mice skin representing each day of IMQ treatment was loaded in one well. The expression of β-actin from the same sample was used as a loading control. (C) Representative photographs of psoriasis-like lesions on back skin of BC004004 +/+ mice and BC004004 -/- mice after 7 days of IMQ treatment. Vaseline treatment was applied on control groups as a vehicle control. (D) Daily body weights throughout the 7-day IMQ treatment were shown in the upper left panel. The characteristics of skin lesion were depicted as redness, scaling scores and thickness of back skin and scored according to a murine Psoriasis Area and Severity Index (PASI) score table. Data are presented as mean ± SD; n = 9 in each group. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001.

Journal: International Journal of Medical Sciences

Article Title: Bombesin receptor-activated protein homolog deficiency altered the pattern of pathological changes of psoriasis - like skin lesion in mice

doi: 10.7150/ijms.89492

Figure Lengend Snippet: The expression of BRAP and its mouse homolog in skin tissues and the skin injury induced by IMQ in both BC004004 -/- mice and their wild type control mice. (A) The expression of BRAP in both normal human skin and the skin of patient with psoriasis by immunohistochemistry analysis of tissue samples with anti-BRAP antibody. BRAP is expressed in the epidermis of both normal skin tissue and skin tissue with psoriasis (magnification: 100×(scale bar = 200 μm) and 400×(scale bar = 50 μm)). (B) BRAP homologous protein was present in skin tissues as revealed by Western blotting in wild-type control mice BC004004 +/+ with imiquimod (IMQ) treatment for 7 day. The total protein extract from one wild type mice skin representing each day of IMQ treatment was loaded in one well. The expression of β-actin from the same sample was used as a loading control. (C) Representative photographs of psoriasis-like lesions on back skin of BC004004 +/+ mice and BC004004 -/- mice after 7 days of IMQ treatment. Vaseline treatment was applied on control groups as a vehicle control. (D) Daily body weights throughout the 7-day IMQ treatment were shown in the upper left panel. The characteristics of skin lesion were depicted as redness, scaling scores and thickness of back skin and scored according to a murine Psoriasis Area and Severity Index (PASI) score table. Data are presented as mean ± SD; n = 9 in each group. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001.

Article Snippet: The following antibodies and their corresponding dilutions were used: BRAP (Abcam, cat: ab181073; 1:2,000), IL-23 (Santa Cruz, cat: sc-271279,1:1,000;), IL-1β (Santa Cruz, cat: 12742,1:1,000), IL-10 (Santa Cruz, cat: 8438, 1:1,000), IL-17 (Affinity, cat: DF6127, 1:2,000), IL-17 (Santa Cruz, cat: sc-374218, 1:1,000), TNF-α (Santa Cruz, cat: sc-52746, 1:1,000), CK5 (Affinity, cat: AF5479, 1:2,000), β-Actin (Santa Cruz, cat: sc-47778, 1:5,000), CK14 (Santa Cruz, cat: sc-53253, 1:1,000), TGF-β1 (Abcam, cat: ab64715, 1:2,000), HRP-conjugated goat anti-Mouse IgG (H+L) (Proteintech, cat: SA00001-1, 1:5,000), HRP-conjugated goat anti-rabbit IgG(H+L) (SouthernBiotech, cat: 4050-05; 1: 5,000).

Techniques: Expressing, Immunohistochemistry, Western Blot

TSLP expression was increased by down-regulation of BRAP or its mouse homolog. (A) Double immunofluorescence staining by IL-23 and CD11c in skin tissue sections from IMQ treated mice (magnification: 200×); scale bar = 100 μm. Immunostaining with IL-23 antibody was shown as red fluorescence. Immunostaining using antibodies against CD11c was shown as green fluorescence. Nuclei of the cells were localized by DAPI (blue). The orange signals in the merged picture, some of which were shown by red arrows, indicate the co-distribution of IL-23 and CD11c in the cytoplasm of cells. (B) Immunohistochemistry analysis of skin tissue sections using TSLP antibody. Day 0 indicates that the samples were made before the first IMQ application. (C) Daily serum levels of TSLP during the 7-day IMQ treatment as determined by ELISA. (D) Western blot analysis of BRAP expression in HaCaT cells transfected with siRNA to silence C6orf89 expression. (E) ELISA analysis of TSLP content in the culture media of HaCaT cells with C6orf89 expression silenced by siRNA transfection.

Journal: International Journal of Medical Sciences

Article Title: Bombesin receptor-activated protein homolog deficiency altered the pattern of pathological changes of psoriasis - like skin lesion in mice

doi: 10.7150/ijms.89492

Figure Lengend Snippet: TSLP expression was increased by down-regulation of BRAP or its mouse homolog. (A) Double immunofluorescence staining by IL-23 and CD11c in skin tissue sections from IMQ treated mice (magnification: 200×); scale bar = 100 μm. Immunostaining with IL-23 antibody was shown as red fluorescence. Immunostaining using antibodies against CD11c was shown as green fluorescence. Nuclei of the cells were localized by DAPI (blue). The orange signals in the merged picture, some of which were shown by red arrows, indicate the co-distribution of IL-23 and CD11c in the cytoplasm of cells. (B) Immunohistochemistry analysis of skin tissue sections using TSLP antibody. Day 0 indicates that the samples were made before the first IMQ application. (C) Daily serum levels of TSLP during the 7-day IMQ treatment as determined by ELISA. (D) Western blot analysis of BRAP expression in HaCaT cells transfected with siRNA to silence C6orf89 expression. (E) ELISA analysis of TSLP content in the culture media of HaCaT cells with C6orf89 expression silenced by siRNA transfection.

Article Snippet: The following antibodies and their corresponding dilutions were used: BRAP (Abcam, cat: ab181073; 1:2,000), IL-23 (Santa Cruz, cat: sc-271279,1:1,000;), IL-1β (Santa Cruz, cat: 12742,1:1,000), IL-10 (Santa Cruz, cat: 8438, 1:1,000), IL-17 (Affinity, cat: DF6127, 1:2,000), IL-17 (Santa Cruz, cat: sc-374218, 1:1,000), TNF-α (Santa Cruz, cat: sc-52746, 1:1,000), CK5 (Affinity, cat: AF5479, 1:2,000), β-Actin (Santa Cruz, cat: sc-47778, 1:5,000), CK14 (Santa Cruz, cat: sc-53253, 1:1,000), TGF-β1 (Abcam, cat: ab64715, 1:2,000), HRP-conjugated goat anti-Mouse IgG (H+L) (Proteintech, cat: SA00001-1, 1:5,000), HRP-conjugated goat anti-rabbit IgG(H+L) (SouthernBiotech, cat: 4050-05; 1: 5,000).

Techniques: Expressing, Double Immunofluorescence Staining, Immunostaining, Fluorescence, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Western Blot, Transfection

Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of BRAP homologous protein in mice detected by western blot with anti-BRAP antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.

Journal: Stress (Amsterdam, Netherlands)

Article Title: Lack of bombesin receptor-activated protein homologous protein impairs hippocampal synaptic plasticity and promotes chronic unpredictable mild stress induced behavioral changes in mice.

doi: 10.1080/10253890.2022.2155513

Figure Lengend Snippet: Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of BRAP homologous protein in mice detected by western blot with anti-BRAP antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.

Article Snippet: The transferred PVDF membranes were incubated with the following primary antibodies with dilutions indicated respectively: b-actin (Sigma, cat: A5441, 1:10,000), BDNF (Abcam, cat: ab108319, 1:1000), Trk-B (Boster, cat: BA0623, 1:1000), BRAP (Abcam, cat: ab181073, 1:1000), GluN2A (CUSABIO, cat: CSB-PA14129A0Rb, 1:500), PSD95 (Sangon Biotech, cat: D261092, 1:500), synaptophysin (ABclonal, cat: A6344, 1:1000).

Techniques: Suspension, Western Blot, Expressing

Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of BRAP homologous protein in mice detected by western blot with anti-BRAP antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.

Journal: Stress (Amsterdam, Netherlands)

Article Title: Lack of bombesin receptor-activated protein homologous protein impairs hippocampal synaptic plasticity and promotes chronic unpredictable mild stress induced behavioral changes in mice.

doi: 10.1080/10253890.2022.2155513

Figure Lengend Snippet: Figure 2. The analysis of behavioral tests after exposure to chronic unpredictable mild stress (CUMS). (A) Body weight changes throughout the CUMS procedure. (B) Immobility time of bc004004þ/þ and bc004004 / mice in the forced swimming test with treatment of CUMS. (C) Analysis of sucrose preference tests during the CUMS procedure. (D) Immobility time of bc004004þ/þ and bc004004 / mice in the tail suspension test after 21-day CUMS exposure. (E) Total distance traveled in the different regions in the open field test after 21-day CUMS exposure. Two-way ANOVA was performed followed by Tukey’s multiple comparisons. (F) The expres sion of BRAP homologous protein in mice detected by western blot with anti-BRAP antibody. The protein extracts of hippocampus tissues of the mice was used in western blot after 21-day of CUMS treatment. The expression of b-actin from the same sample was used as loading controls. Data are presented as mean ± SD. p <.05, p <.01, p <.001,p <.0001, n ¼ 8.

Article Snippet: The transferred PVDF membranes were incubated with the following primary antibodies with dilutions indicated respectively: b-actin (Sigma, cat: A5441, 1:10,000), BDNF (Abcam, cat: ab108319, 1:1000), Trk-B (Boster, cat: BA0623, 1:1000), BRAP (Abcam, cat: ab181073, 1:1000), GluN2A (CUSABIO, cat: CSB-PA14129A0Rb, 1:500), PSD95 (Sangon Biotech, cat: D261092, 1:500), synaptophysin (ABclonal, cat: A6344, 1:1000).

Techniques: Suspension, Western Blot, Expressing

Relation of phenotypes induced by BRAP and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP , neurofibromin, as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .

Journal: Cancers

Article Title: Mutation of PTPN11 (Encoding SHP-2) Promotes MEK Activation and Malignant Progression in Neurofibromin-Deficient Cells in a Manner Sensitive to BRAP Mutation

doi: 10.3390/cancers14102377

Figure Lengend Snippet: Relation of phenotypes induced by BRAP and PTPN11 missense mutations to NF1 inactivation. Immunoblot analysis was performed for SHP-2, BRAP , neurofibromin, as well as phosphorylated and total forms of Akt, ERK, and MEK in parental HeLa cells as well as HeLa cells transiently expressing SHP-2 (G503V) or BRAP (G370A). The uncropped western blot figures are shown in . ( A ) or in the corresponding stably infected cells transfected with control or NF1 siRNAs for 48 h ( B ). sNF96.2-GFP cells expressing SHP-2 (G503V) and BRAP (G370A) are shown for comparison to indicate the cleavage product of SHP-2 (arrowhead). The uncropped western blot figures are shown in .

Article Snippet: Immunoblot analysis was performed as previously described [ ] with primary antibodies to phosphorylated Akt (#4060), to Akt (#9272), to phosphorylated ERK1/2 (#4370), to ERK1/2 (#9102), to phosphorylated MEK (#9121), to MEK (#9122), to phosphorylated S6 (#4858), to S6 (#2217), to phosphorylated STAT3 (#9131), to STAT3 (#4904), and to SHP-2 (#3752), all of which were obtained from Cell Signaling Technology, as well as with those to BRAP (sc-166012), to neurofibromin (sc-376886), and to α-tubulin (sc-32293) from Santa Cruz Biotechnology.

Techniques: Western Blot, Expressing, Stable Transfection, Infection, Transfection, Control, Comparison