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tap73  (Novus Biologicals)


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    Structured Review

    Novus Biologicals tap73
    Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. <t>TAp73</t> was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).
    Tap73, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nbp2+24737/pmc13000482-354-30-31?v=Novus+Biologicals
    Average 93 stars, based on 7 article reviews
    tap73 - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "Targeting of Itch by clomipramine or gene therapy improves cognitive defects related to Alzheimer’s disease"

    Article Title: Targeting of Itch by clomipramine or gene therapy improves cognitive defects related to Alzheimer’s disease

    Journal: iScience

    doi: 10.1016/j.isci.2026.115181

    Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. TAp73 was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).
    Figure Legend Snippet: Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. TAp73 was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).

    Techniques Used: Immunoprecipitation, Western Blot, Ubiquitin Proteomics



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    Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. <t>TAp73</t> was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).
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    Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. <t>TAp73</t> was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).
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    Image Search Results


    Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. TAp73 was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).

    Journal: iScience

    Article Title: Targeting of Itch by clomipramine or gene therapy improves cognitive defects related to Alzheimer’s disease

    doi: 10.1016/j.isci.2026.115181

    Figure Lengend Snippet: Clomipramine inhibits Itch and prevents neuronal apoptosis and cell cycle re-entry in neurons from TgAD mice (A) Chemical structure of clomipramine. The chloride moiety is proposed to interact with catalytic cysteine in the HECT domain of Itch. (B) Rat cortical neurons were treated with Aβ 42 and/or clomipramine (75 nM) for 48 h followed by 12 h treatment with the proteasome inhibitor MG132. TAp73 was immunoprecipitated, and western blotting was performed on TAp73-IP with anti-ubiquitin and anti-Itch antibodies. Total protein lysates were also used for western blotting with indicated antibodies. Ubiquitinated TAp73 levels were quantified by densitometry of ubiquitin immunoblot, normalized with respect to the input TAp73, which was also normalized with respect to actin (mean ± SEM, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (C) Rat cortical neurons were treated with Aβ 42 and/or 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. The levels of TAp73, PCNA, and cl_caspase3 were quantified by densitometry, and fold change with respect to untreated (ctrl) neurons was determined (mean ± SEM, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, one-way ANOVA, Tukey’s test, N = 3). (D) Cortical neurons from WT or TgAD mice were treated with 75 nM clomipramine for 48 h followed by western blotting for indicated proteins. TAp73, PCNA, and cl_caspase3 levels were quantified by densitometry, and fold change with respect to untreated WT neurons is provided (mean ± SEM, ∗ p < 0.05, ∗∗ p < 0.01, one-way ANOVA, Tukey’s test, N = 2).

    Article Snippet: PCNA (Santa cruz, cat. no. sc-56; 1:500 for WB, 1:50 for IHC), cleaved caspase 3 (CST, cat. no. 966l; 1:1000 for WB), Itch (CST, cat. no. 12117; 1:1000 for WB), TAp73 (Novus, cat. no. NBP2-24737, 1:1000 for WB, 1:50 for IP), myc-tag (9B11) (CST, cat. no. 2276; 1:2000 for WB, 1:100 for IHC), NeuN (Novus, cat. no. NBP2-67314; 1:100 for IHC), Ubiquitin (Santa cruz, cat. no. sc-8017; 1:1000 for WB) and β-Actin (Santa cruz, cat. no. sc-47778, 1:2000 for WB).

    Techniques: Immunoprecipitation, Western Blot, Ubiquitin Proteomics

    List of antibodies.

    Journal: Cell Death Discovery

    Article Title: SMG6 regulates DNA damage and cell survival in Hippo pathway kinase LATS2-inactivated malignant mesothelioma

    doi: 10.1038/s41420-022-01232-w

    Figure Lengend Snippet: List of antibodies.

    Article Snippet: p73(5B429) , Novus Biologicals , NBP2-24737 , no.

    Techniques: