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rabbit anti timp1 monoclonal antibody  (Boster Bio)


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    Structured Review

    Boster Bio rabbit anti timp1 monoclonal antibody
    Rabbit Anti Timp1 Monoclonal Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 128 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti timp1 monoclonal antibody/product/Boster Bio
    Average 94 stars, based on 128 article reviews
    rabbit anti timp1 monoclonal antibody - by Bioz Stars, 2026-02
    94/100 stars

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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and <t>TIMP1</t> downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.
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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and <t>TIMP1</t> downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.
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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and <t>TIMP1</t> downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.
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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and <t>TIMP1</t> downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.
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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and <t>TIMP1</t> downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.
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    The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and TIMP1 downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: The anti-TC effects of HHT are associated with FAK/PI3K/AKT signaling pathway and TIMP1 downregulation (A) The volcano plot showed the 787 differentially expressed proteins in TPC-1 cells between HHT-treated (20 nM, 48 h) and control groups (fold change ≥1.5 or ≤ −1.5 and p values <0.05). (B) The heatmap showed the top 100 differentially expressed proteins. (C) KEGG analysis of the differentially expressed proteins. (D–F) GO analysis of the differentially expressed proteins. (G) Western blotting analysis of the protein expression of TIMP1, FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. (H) RT-qPCR analysis of the mRNA expression of TIMP1 in TPC-1 and 8505C cells after HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Western Blot, Expressing, Quantitative RT-PCR

    TIMP1 overexpression reserves the anti-TC effects of HHT (A) TPC-1 and 8505C cells were transfected with vector or TIMP1 overexpression (oeTIMP1) and then treated with HHT treatment for 48 h. RT-qPCR was performed to analyze the mRNA level of TIMP1. GAPDH was used as the control. (B) Western blotting analysis of the expression of TIMP1, Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. GAPDH was used as the control. (C) and (D) CCK-8 assay was performed to detect cell viability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 24, 48, and 72 h. (E) Colony formation assay was used to detect the colony formation ability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 14 days. (F) Flow cytometry was performed to measure the effect of HHT on the apoptosis of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. (G) and (H) Wound healing assay was performed to detect the cell migration rate. (I) Transwell assay was conducted to measure the cell invasion ability. (J) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: TIMP1 overexpression reserves the anti-TC effects of HHT (A) TPC-1 and 8505C cells were transfected with vector or TIMP1 overexpression (oeTIMP1) and then treated with HHT treatment for 48 h. RT-qPCR was performed to analyze the mRNA level of TIMP1. GAPDH was used as the control. (B) Western blotting analysis of the expression of TIMP1, Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. GAPDH was used as the control. (C) and (D) CCK-8 assay was performed to detect cell viability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 24, 48, and 72 h. (E) Colony formation assay was used to detect the colony formation ability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 14 days. (F) Flow cytometry was performed to measure the effect of HHT on the apoptosis of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. (G) and (H) Wound healing assay was performed to detect the cell migration rate. (I) Transwell assay was conducted to measure the cell invasion ability. (J) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells with HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Over Expression, Transfection, Plasmid Preparation, Quantitative RT-PCR, Western Blot, Expressing, CCK-8 Assay, Colony Assay, Flow Cytometry, Wound Healing Assay, Migration, Transwell Assay

    TIMP1 downregulation enhances the anti-TC effects of HHT (A) TPC-1 and 8505C cells were transfected with negative control (siNC) or TIMP1-targeting siRNA (siTIMP1) and then treated with HHT for 48 h. RT-qPCR was performed to analyze the mRNA level of TIMP1. GAPDH was used as the control. (B) Western blotting analysis of the expression of TIMP1, Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/siTIMP1 and 8505C/siTIMP1 with HHT treatment for 48 h. GAPDH was used as the control. (C) and (D) CCK-8 assay was performed to detect cell viability of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 24, 48, and 72 h. (E) Colony formation assay was used to detect the colony formation ability of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 14 days. (F) Flow cytometry was performed to measure the effect of HHT on the apoptosis of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 48 h. (G) and (H) Wound healing assay was performed to detect the cell migration rate. (I) Transwell assay was conducted to measure the cell invasion ability. (J) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/siTIMP1 and 8505C/siTIMP1 with HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: TIMP1 downregulation enhances the anti-TC effects of HHT (A) TPC-1 and 8505C cells were transfected with negative control (siNC) or TIMP1-targeting siRNA (siTIMP1) and then treated with HHT for 48 h. RT-qPCR was performed to analyze the mRNA level of TIMP1. GAPDH was used as the control. (B) Western blotting analysis of the expression of TIMP1, Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/siTIMP1 and 8505C/siTIMP1 with HHT treatment for 48 h. GAPDH was used as the control. (C) and (D) CCK-8 assay was performed to detect cell viability of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 24, 48, and 72 h. (E) Colony formation assay was used to detect the colony formation ability of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 14 days. (F) Flow cytometry was performed to measure the effect of HHT on the apoptosis of TPC-1/siTIMP1 and 8505C/siTIMP1 cells with HHT treatment for 48 h. (G) and (H) Wound healing assay was performed to detect the cell migration rate. (I) Transwell assay was conducted to measure the cell invasion ability. (J) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/siTIMP1 and 8505C/siTIMP1 with HHT treatment for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Transfection, Negative Control, Quantitative RT-PCR, Western Blot, Expressing, CCK-8 Assay, Colony Assay, Flow Cytometry, Wound Healing Assay, Migration, Transwell Assay

    Re-expression of TIMP1 attenuates the enhancement of anti-TC effects of HHT induced by TIMP1 knockdown (A) TIMP1 expression in TPC-1 and 8505C cells was downregulated by transfecting with stable TIMP1 knockdown (shTIMP1) and re-expressed by transfecting with oeTIMP1. Colony formation assay was performed to detect the colony formation ability of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 14 days. (B) Wound healing assay was performed to detect the migration rate of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT. (C) Flow cytometry detected the effect of HHT on the apoptosis of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 48 h. (D) Western blotting analysis of the expression of TIMP1, AKT, and p-AKT in TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: Re-expression of TIMP1 attenuates the enhancement of anti-TC effects of HHT induced by TIMP1 knockdown (A) TIMP1 expression in TPC-1 and 8505C cells was downregulated by transfecting with stable TIMP1 knockdown (shTIMP1) and re-expressed by transfecting with oeTIMP1. Colony formation assay was performed to detect the colony formation ability of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 14 days. (B) Wound healing assay was performed to detect the migration rate of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT. (C) Flow cytometry detected the effect of HHT on the apoptosis of TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 48 h. (D) Western blotting analysis of the expression of TIMP1, AKT, and p-AKT in TPC-1 and 8505C cells transfected with shTIMP1 and/or oeTIMP1 and treated with HHT for 48 h. GAPDH was used as the control. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Expressing, Colony Assay, Transfection, Wound Healing Assay, Migration, Flow Cytometry, Western Blot

    HHT restrains TC growth in vivo (A) The establishment of xenografts tumor model. (B) Images of tumor xenografts obtained at the end of the animal experiment. (C) The change of the tumor volume throughout the study. (D) The tumor weight at the end of the experiment. (E) Representative IHC staining images of TIMP1 and Ki-67 in xenograft tumors. (F) Representative TUNEL staining images of tumor tissues. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: HHT restrains TC growth in vivo (A) The establishment of xenografts tumor model. (B) Images of tumor xenografts obtained at the end of the animal experiment. (C) The change of the tumor volume throughout the study. (D) The tumor weight at the end of the experiment. (E) Representative IHC staining images of TIMP1 and Ki-67 in xenograft tumors. (F) Representative TUNEL staining images of tumor tissues. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: In Vivo, Immunohistochemistry, TUNEL Assay, Staining

    The FAK/PI3K/AKT signaling pathway is required for TC progression induced by TIMP1 (A) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK2256098 (GSK) and/or LY294002 (LY) for 48 h. (B) and (C) CCK-8 assay was performed to detect cell viability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 24, 48, and 72 h. (D) Colony formation assay was conducted to determine the clonogenic ability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 14 days. (E) Flow cytometry was used to detect the apoptosis of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 48 h. (F) Western blotting analysis of the expression of Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 48 h. GAPDH was used as the control. (G) Wound healing assay was performed to detect cell migration ability. (H) Transwell assay was performed to detect cell invasion ability. (I) HHT exerts anti-TC effects by inhibiting the TIMP1/FAK/PI3K/AKT signaling pathway. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: The FAK/PI3K/AKT signaling pathway is required for TC progression induced by TIMP1 (A) Western blotting analysis of the expression of FAK, p-FAK, PI3K, p-PI3K, AKT, and p-AKT in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK2256098 (GSK) and/or LY294002 (LY) for 48 h. (B) and (C) CCK-8 assay was performed to detect cell viability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 24, 48, and 72 h. (D) Colony formation assay was conducted to determine the clonogenic ability of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 14 days. (E) Flow cytometry was used to detect the apoptosis of TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 48 h. (F) Western blotting analysis of the expression of Bax, Bcl2, cleaved caspase-3, E-cadherin, and N-cadherin in TPC-1/oeTIMP1 and 8505C/oeTIMP1 cells treated with GSK and/or LY for 48 h. GAPDH was used as the control. (G) Wound healing assay was performed to detect cell migration ability. (H) Transwell assay was performed to detect cell invasion ability. (I) HHT exerts anti-TC effects by inhibiting the TIMP1/FAK/PI3K/AKT signaling pathway. Data are presented as mean ± SD. ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Western Blot, Expressing, CCK-8 Assay, Colony Assay, Flow Cytometry, Wound Healing Assay, Migration, Transwell Assay

    TIMP1 expression is upregulated in TC and associated with invasive clinical features (A) The mRNA expression level of TIMP1 in normal thyroid tissues and TC tissues from the TCGA database. (B) Representative IHC staining images of TIMP1 in TC and normal thyroid tissues. (C) TIMP1 expression in TC was higher than that in normal thyroid tissues based on immunoreactivity score. (D) High TIMP1 expression was correlated to lymph node metastases and higher risk stratification. ns, no significance; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: TIMP1 expression is upregulated in TC and associated with invasive clinical features (A) The mRNA expression level of TIMP1 in normal thyroid tissues and TC tissues from the TCGA database. (B) Representative IHC staining images of TIMP1 in TC and normal thyroid tissues. (C) TIMP1 expression in TC was higher than that in normal thyroid tissues based on immunoreactivity score. (D) High TIMP1 expression was correlated to lymph node metastases and higher risk stratification. ns, no significance; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Expressing, Immunohistochemistry

    The correlation between  TIMP1  expression and clinical features in TC

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet: The correlation between TIMP1 expression and clinical features in TC

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Expressing

    Journal: iScience

    Article Title: Repurposing homoharringtonine for thyroid cancer treatment through TIMP1/FAK/PI3K/AKT signaling pathway

    doi: 10.1016/j.isci.2024.109829

    Figure Lengend Snippet:

    Article Snippet: Rabbit monoclonal anti-TIMP1 , Abcam , Cat# ab211926.

    Techniques: Virus, Plasmid Preparation, Recombinant, CCK-8 Assay, TUNEL Assay, Apoptosis Assay, Mass Spectrometry, Sequencing, shRNA, Software

    Antibodies used in the present study

    Journal: BMC Cancer

    Article Title: Remodeling of extracellular matrix by normal and tumor-associated fibroblasts promotes cervical cancer progression

    doi: 10.1186/s12885-015-1272-3

    Figure Lengend Snippet: Antibodies used in the present study

    Article Snippet: TIMP1 (D10E6) , Rabbit monoclonal IgG , Cell Signaling , 8946 , - , 1:1000.

    Techniques: