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rabbit anti p erk  (Boster Bio)


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    Boster Bio rabbit anti p erk
    Rabbit Anti P Erk, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+erk/EPHB1%2F2%2F3%2F4+Colorimetric+Cell-Based+ELISA+Kit/10__1096_slash_fj__202504963rr-87-9-14
    Average 94 stars, based on 1 article reviews
    rabbit anti p erk - by Bioz Stars, 2026-09
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    Related Articles

    Incubation:

    Article Title: PM 2 .5 exposure-induced ferroptosis in neuronal cells via inhibiting ERK/CREB pathway.
    Article Snippet: Funding information The Young Talents Project of Hubei Provincial Health Commission (NO.WJ2021Q053); Jianghan University Abstract PM2.5 exposure has been demonstrated to correlate with neurological disorders recently.. Ferroptosis is recognized as a newly found programmed form of cell death associated with neurodegenerative diseases, while glutathione peroxidase 4 (GPX4) is a key regulator of ferroptosis.. However, the relationship between PM2.5-induced neurotoxicity and ferroptosis is still unclear.

    Concentration Assay:

    Article Title: PM 2 .5 exposure-induced ferroptosis in neuronal cells via inhibiting ERK/CREB pathway.
    Article Snippet: Funding information The Young Talents Project of Hubei Provincial Health Commission (NO.WJ2021Q053); Jianghan University Abstract PM2.5 exposure has been demonstrated to correlate with neurological disorders recently.. Ferroptosis is recognized as a newly found programmed form of cell death associated with neurodegenerative diseases, while glutathione peroxidase 4 (GPX4) is a key regulator of ferroptosis.. However, the relationship between PM2.5-induced neurotoxicity and ferroptosis is still unclear.



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    JD-02 inhibits HSV-1 replication by suppressing the <t>Raf/MEK/ERK</t> signaling pathway. (A) Western blot analysis was conducted to assess the effects of HSV-1 (MOI=0.1) infection on the protein levels <t>of</t> <t>BRAF,</t> MEK and ERK, with and without treatment using JD-02. (B) Treatment with JD-02 at the specified concentration influences the protein levels of BRAF, MEK and ERK in HaCaT cells over a 12-h period. (C and D) HaCaT cells were subjected to transfection with either N.C. siRNA or ERK siRNA for a period of 48 h. Subsequently, the cells were infected with HSV-1 (MOI=0.1) for an additional 24 h. The DNA copy number of the viral gene UL54, as well as the viral protein expression of gB, ICP0, ICP27, ERK and p-ERK were evaluated. (E) The DNA copy numbers of the viral genes UL30 , UL52 and UL54 in HaCaT cells infected with HSV-1 (MOI=0.1) and subsequently treated with either JD-02 (1 μ M) or U0126 (10 μ M) for 24 h, were quantified using reverse transcription-quantitative PCR. (F) Western blot analysis of viral proteins (gB, ICP0 and ICP27), ERK and p-ERK expression in HaCaT cell infected with HSV-1 (MOI=0.1) and treated with U0126 for indicated concentration. (G) Western blot analysis of UL30 overexpression in HaCaT cells treated with U0126. Data are presented as the mean ± SD (n=3). * P<0.05, ** P<0.01, *** P<0.01 and **** P<0.0001 compared with the HSV-1 group. HSV, Herpes Simplex Virus; MOI, multiplicity of infection; N.C., negative control; siRNA, small interfering RNA; p-, phosphorylated.
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    JD-02 inhibits HSV-1 replication by suppressing the <t>Raf/MEK/ERK</t> signaling pathway. (A) Western blot analysis was conducted to assess the effects of HSV-1 (MOI=0.1) infection on the protein levels <t>of</t> <t>BRAF,</t> MEK and ERK, with and without treatment using JD-02. (B) Treatment with JD-02 at the specified concentration influences the protein levels of BRAF, MEK and ERK in HaCaT cells over a 12-h period. (C and D) HaCaT cells were subjected to transfection with either N.C. siRNA or ERK siRNA for a period of 48 h. Subsequently, the cells were infected with HSV-1 (MOI=0.1) for an additional 24 h. The DNA copy number of the viral gene UL54, as well as the viral protein expression of gB, ICP0, ICP27, ERK and p-ERK were evaluated. (E) The DNA copy numbers of the viral genes UL30 , UL52 and UL54 in HaCaT cells infected with HSV-1 (MOI=0.1) and subsequently treated with either JD-02 (1 μ M) or U0126 (10 μ M) for 24 h, were quantified using reverse transcription-quantitative PCR. (F) Western blot analysis of viral proteins (gB, ICP0 and ICP27), ERK and p-ERK expression in HaCaT cell infected with HSV-1 (MOI=0.1) and treated with U0126 for indicated concentration. (G) Western blot analysis of UL30 overexpression in HaCaT cells treated with U0126. Data are presented as the mean ± SD (n=3). * P<0.05, ** P<0.01, *** P<0.01 and **** P<0.0001 compared with the HSV-1 group. HSV, Herpes Simplex Virus; MOI, multiplicity of infection; N.C., negative control; siRNA, small interfering RNA; p-, phosphorylated.
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    Image Search Results


    JD-02 inhibits HSV-1 replication by suppressing the Raf/MEK/ERK signaling pathway. (A) Western blot analysis was conducted to assess the effects of HSV-1 (MOI=0.1) infection on the protein levels of BRAF, MEK and ERK, with and without treatment using JD-02. (B) Treatment with JD-02 at the specified concentration influences the protein levels of BRAF, MEK and ERK in HaCaT cells over a 12-h period. (C and D) HaCaT cells were subjected to transfection with either N.C. siRNA or ERK siRNA for a period of 48 h. Subsequently, the cells were infected with HSV-1 (MOI=0.1) for an additional 24 h. The DNA copy number of the viral gene UL54, as well as the viral protein expression of gB, ICP0, ICP27, ERK and p-ERK were evaluated. (E) The DNA copy numbers of the viral genes UL30 , UL52 and UL54 in HaCaT cells infected with HSV-1 (MOI=0.1) and subsequently treated with either JD-02 (1 μ M) or U0126 (10 μ M) for 24 h, were quantified using reverse transcription-quantitative PCR. (F) Western blot analysis of viral proteins (gB, ICP0 and ICP27), ERK and p-ERK expression in HaCaT cell infected with HSV-1 (MOI=0.1) and treated with U0126 for indicated concentration. (G) Western blot analysis of UL30 overexpression in HaCaT cells treated with U0126. Data are presented as the mean ± SD (n=3). * P<0.05, ** P<0.01, *** P<0.01 and **** P<0.0001 compared with the HSV-1 group. HSV, Herpes Simplex Virus; MOI, multiplicity of infection; N.C., negative control; siRNA, small interfering RNA; p-, phosphorylated.

    Journal: International Journal of Molecular Medicine

    Article Title: Novel Hsp90 inhibitor JD-02 inhibits HSV-1 infection via the Raf/MEK/ERK signaling pathway

    doi: 10.3892/ijmm.2026.5810

    Figure Lengend Snippet: JD-02 inhibits HSV-1 replication by suppressing the Raf/MEK/ERK signaling pathway. (A) Western blot analysis was conducted to assess the effects of HSV-1 (MOI=0.1) infection on the protein levels of BRAF, MEK and ERK, with and without treatment using JD-02. (B) Treatment with JD-02 at the specified concentration influences the protein levels of BRAF, MEK and ERK in HaCaT cells over a 12-h period. (C and D) HaCaT cells were subjected to transfection with either N.C. siRNA or ERK siRNA for a period of 48 h. Subsequently, the cells were infected with HSV-1 (MOI=0.1) for an additional 24 h. The DNA copy number of the viral gene UL54, as well as the viral protein expression of gB, ICP0, ICP27, ERK and p-ERK were evaluated. (E) The DNA copy numbers of the viral genes UL30 , UL52 and UL54 in HaCaT cells infected with HSV-1 (MOI=0.1) and subsequently treated with either JD-02 (1 μ M) or U0126 (10 μ M) for 24 h, were quantified using reverse transcription-quantitative PCR. (F) Western blot analysis of viral proteins (gB, ICP0 and ICP27), ERK and p-ERK expression in HaCaT cell infected with HSV-1 (MOI=0.1) and treated with U0126 for indicated concentration. (G) Western blot analysis of UL30 overexpression in HaCaT cells treated with U0126. Data are presented as the mean ± SD (n=3). * P<0.05, ** P<0.01, *** P<0.01 and **** P<0.0001 compared with the HSV-1 group. HSV, Herpes Simplex Virus; MOI, multiplicity of infection; N.C., negative control; siRNA, small interfering RNA; p-, phosphorylated.

    Article Snippet: These primary antibodies included ICP0 (1:1,000; cat. no. ab6513; Abcam), ICP27 (1:1,000; cat. no. ab53480; Abcam), gD (1:1,000; cat. no. ab6507; Abcam), gB (1:500; cat. no. sc-56987; Santa Cruz Biotechnology, Inc.), Raf-B (1:500; cat. no. sc-166; Santa Cruz Biotechnology, Inc.), p-BRAF (1:1,000; cat. no. 2696T; Cell Signaling Technology, Inc.), ERK (1:1,000; cat. no. 4695S; Cell Signaling Technology, Inc.), p-ERK (1:1,000; cat. no. 4370S; Cell Signaling Technology, Inc.), MEK1/2 (1:1,000; cat. no. AF6385; Affinity Biosciences), p-MEK1/2 (1:1,000; cat. no. 9154T; Cell Signaling Technology, Inc.), Flag (1:1,000; cat. no. 14793S; Cell Signaling Technology, Inc.), HA (1:1,000; cat. no. 3724S; Cell Signaling Technology, Inc.).

    Techniques: Western Blot, Infection, Concentration Assay, Transfection, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Over Expression, Virus, Negative Control, Small Interfering RNA