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polyclonal rabbit anti-human timp3 antibody  (Millipore)

 
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    Structured Review

    Millipore polyclonal rabbit anti-human timp3 antibody
    <t>TIMP3</t> is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)
    Polyclonal Rabbit Anti Human Timp3 Antibody, supplied by Millipore, 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/polyclonal rabbit anti-human timp3 antibody/product/Millipore
    Average 90 stars, based on 1 article reviews
    polyclonal rabbit anti-human timp3 antibody - by Bioz Stars, 2026-02
    90/100 stars

    Images

    1) Product Images from "TIMP3 Is Reduced in Atherosclerotic Plaques From Subjects With Type 2 Diabetes and Increased by SirT1"

    Article Title: TIMP3 Is Reduced in Atherosclerotic Plaques From Subjects With Type 2 Diabetes and Increased by SirT1

    Journal: Diabetes

    doi: 10.2337/db09-0280

    TIMP3 is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)
    Figure Legend Snippet: TIMP3 is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)

    Techniques Used: Expressing, Western Blot, Immunohistochemistry, Activity Assay, Fluorimetry Assay

    Effects of diabetes on TIMP3 expression in vascular cells. A : TIMP3 expression in CASMC treated with various metabolic stimuli: high glucose (HG) 20 mmol/l; mannitol (Man) 20 mmol/l; insulin (Ins) 10 −7 M; LDL 100 μg/ml; oxidized LDL (oxLDL) 100 μg/ml; glycated LDL (glyLDL) 100 μg/ml; LXR agonists (T0901317 [T090] 5 μmol/l; GW3965 [GW] 3 μmol/l; R-hydroxycholesterol [RH] 10 μmol/l; 22-S-hydroxycholesterol [SH] 10 μmol/l); SirT1 inhibitor (Sirtinol) 50 μmol/l. n = 4 for all experiments; * P < 0.05 by Student's t test versus control (CT). B : Sirtinol increased ADAM17 activity in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : TIMP3 expression in HUVEC and THP1 treated with Sirtinol and high glucose (20 mmol/l). n = 4 for all experiments; * P < 0.05 by Student's t test versus control. D : SirT1 expression is reduced in CASMC, HUVEC, and THP1 treated with high glucose (20 mmol/l) compared with control. n = 4 for all experiments; * P < 0.05 by Student's t test. E : SirT1 levels are decreased in type 2 diabetic compared with NGT subjects. * P < 0.05 by Student's t test. F : SirT1 correlates with TIMP3 in atherosclerotic plaques from NGT ( n = 37) and type 2 diabetic (DM2) ( n = 23) subjects.
    Figure Legend Snippet: Effects of diabetes on TIMP3 expression in vascular cells. A : TIMP3 expression in CASMC treated with various metabolic stimuli: high glucose (HG) 20 mmol/l; mannitol (Man) 20 mmol/l; insulin (Ins) 10 −7 M; LDL 100 μg/ml; oxidized LDL (oxLDL) 100 μg/ml; glycated LDL (glyLDL) 100 μg/ml; LXR agonists (T0901317 [T090] 5 μmol/l; GW3965 [GW] 3 μmol/l; R-hydroxycholesterol [RH] 10 μmol/l; 22-S-hydroxycholesterol [SH] 10 μmol/l); SirT1 inhibitor (Sirtinol) 50 μmol/l. n = 4 for all experiments; * P < 0.05 by Student's t test versus control (CT). B : Sirtinol increased ADAM17 activity in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : TIMP3 expression in HUVEC and THP1 treated with Sirtinol and high glucose (20 mmol/l). n = 4 for all experiments; * P < 0.05 by Student's t test versus control. D : SirT1 expression is reduced in CASMC, HUVEC, and THP1 treated with high glucose (20 mmol/l) compared with control. n = 4 for all experiments; * P < 0.05 by Student's t test. E : SirT1 levels are decreased in type 2 diabetic compared with NGT subjects. * P < 0.05 by Student's t test. F : SirT1 correlates with TIMP3 in atherosclerotic plaques from NGT ( n = 37) and type 2 diabetic (DM2) ( n = 23) subjects.

    Techniques Used: Expressing, Control, Activity Assay

    Regulation of TIMP3 expression in CASMC. A : SirT1 knockdown decreased TIMP3 expression but not TIMP1 , TIMP2 , TIMP4 , ADAM10 , ADAM17 , or MMP9 in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test versus control. B : SirT1 knockdown decreased TIMP3 expression in HUVEC and THP1. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : SirT1 cDNA overexpression increased Timp3 promoter activity. n = 4 for all experiments; ** P < 0.01 by one-way ANOVA. D : SirT1 overexpression increased and prevented loss of TIMP3 expression caused by high glucose (HG; 20 mmol/l) in CASMC, HUVEC, and THP1. n = 4 for all experiments; * P < 0.05 by Student's t test.
    Figure Legend Snippet: Regulation of TIMP3 expression in CASMC. A : SirT1 knockdown decreased TIMP3 expression but not TIMP1 , TIMP2 , TIMP4 , ADAM10 , ADAM17 , or MMP9 in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test versus control. B : SirT1 knockdown decreased TIMP3 expression in HUVEC and THP1. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : SirT1 cDNA overexpression increased Timp3 promoter activity. n = 4 for all experiments; ** P < 0.01 by one-way ANOVA. D : SirT1 overexpression increased and prevented loss of TIMP3 expression caused by high glucose (HG; 20 mmol/l) in CASMC, HUVEC, and THP1. n = 4 for all experiments; * P < 0.05 by Student's t test.

    Techniques Used: Expressing, Knockdown, Control, Over Expression, Activity Assay



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    polyclonal rabbit anti-human timp3 antibody  (Millipore)
    90
    Millipore polyclonal rabbit anti-human timp3 antibody
    <t>TIMP3</t> is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)
    Polyclonal Rabbit Anti Human Timp3 Antibody, supplied by Millipore, 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/polyclonal rabbit anti-human timp3 antibody/product/Millipore
    Average 90 stars, based on 1 article reviews
    polyclonal rabbit anti-human timp3 antibody - by Bioz Stars, 2026-02
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    TIMP3 is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)

    Journal: Diabetes

    Article Title: TIMP3 Is Reduced in Atherosclerotic Plaques From Subjects With Type 2 Diabetes and Increased by SirT1

    doi: 10.2337/db09-0280

    Figure Lengend Snippet: TIMP3 is reduced in atherosclerotic plaques of subjects with type 2 diabetes (DM2). ADAM10 , ADAM17 , and MMP9 ( A ) as well as TIMPs ( B ) expression in NGT ( n = 37) and type 2 diabetes ( n = 23) subjects; *** P < 0.001 by one-way ANOVA. C : Western blot using extracellular matrix extracts from representative NGT ( n = 2) and type 2 diabetic ( n = 4) subjects. * P < 0.05 NGT vs. type 2 diabetes by Student's t test. D–J : Immunohistochemistry confirmed that TIMP3 is reduced in type 2 diabetic ( n = 8) versus NGT ( n = 8) subjects; one representative image is shown for TIMP3, anti–α smooth muscle actin, and CD68 for NGT ( D–F ; 4× magnification) and type 2 diabetic ( G–J ; 4× magnification) subjects. K and I : ADAM17 activity measured by a fluorimetric assay ( K ) and MMP9 activity measured by a fluorimetric assay ( I ) are increased in type 2 diabetic ( n = 23) compared with NGT ( n = 37) subjects; *** P < 0.001 by Student's t test for both. (A high-quality digital representation of this figure is available in the online issue.)

    Article Snippet: Immunohistochemistry was performed on serial 3-μm thick sections cut from paraffin blocks of carotid plaques using the following antibodies: 1 ) polyclonal rabbit anti-human TIMP3 antibody (Calbiochem, San Diego, CA), 2 ) monoclonal anti-CD68 (human macrophage) antibody (DAKO, Glostrup, Denmark), and 3 ) monoclonal anti-α smooth muscle actin antibody (Europa Ventana Medical System, Illkirch, France).

    Techniques: Expressing, Western Blot, Immunohistochemistry, Activity Assay, Fluorimetry Assay

    Effects of diabetes on TIMP3 expression in vascular cells. A : TIMP3 expression in CASMC treated with various metabolic stimuli: high glucose (HG) 20 mmol/l; mannitol (Man) 20 mmol/l; insulin (Ins) 10 −7 M; LDL 100 μg/ml; oxidized LDL (oxLDL) 100 μg/ml; glycated LDL (glyLDL) 100 μg/ml; LXR agonists (T0901317 [T090] 5 μmol/l; GW3965 [GW] 3 μmol/l; R-hydroxycholesterol [RH] 10 μmol/l; 22-S-hydroxycholesterol [SH] 10 μmol/l); SirT1 inhibitor (Sirtinol) 50 μmol/l. n = 4 for all experiments; * P < 0.05 by Student's t test versus control (CT). B : Sirtinol increased ADAM17 activity in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : TIMP3 expression in HUVEC and THP1 treated with Sirtinol and high glucose (20 mmol/l). n = 4 for all experiments; * P < 0.05 by Student's t test versus control. D : SirT1 expression is reduced in CASMC, HUVEC, and THP1 treated with high glucose (20 mmol/l) compared with control. n = 4 for all experiments; * P < 0.05 by Student's t test. E : SirT1 levels are decreased in type 2 diabetic compared with NGT subjects. * P < 0.05 by Student's t test. F : SirT1 correlates with TIMP3 in atherosclerotic plaques from NGT ( n = 37) and type 2 diabetic (DM2) ( n = 23) subjects.

    Journal: Diabetes

    Article Title: TIMP3 Is Reduced in Atherosclerotic Plaques From Subjects With Type 2 Diabetes and Increased by SirT1

    doi: 10.2337/db09-0280

    Figure Lengend Snippet: Effects of diabetes on TIMP3 expression in vascular cells. A : TIMP3 expression in CASMC treated with various metabolic stimuli: high glucose (HG) 20 mmol/l; mannitol (Man) 20 mmol/l; insulin (Ins) 10 −7 M; LDL 100 μg/ml; oxidized LDL (oxLDL) 100 μg/ml; glycated LDL (glyLDL) 100 μg/ml; LXR agonists (T0901317 [T090] 5 μmol/l; GW3965 [GW] 3 μmol/l; R-hydroxycholesterol [RH] 10 μmol/l; 22-S-hydroxycholesterol [SH] 10 μmol/l); SirT1 inhibitor (Sirtinol) 50 μmol/l. n = 4 for all experiments; * P < 0.05 by Student's t test versus control (CT). B : Sirtinol increased ADAM17 activity in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : TIMP3 expression in HUVEC and THP1 treated with Sirtinol and high glucose (20 mmol/l). n = 4 for all experiments; * P < 0.05 by Student's t test versus control. D : SirT1 expression is reduced in CASMC, HUVEC, and THP1 treated with high glucose (20 mmol/l) compared with control. n = 4 for all experiments; * P < 0.05 by Student's t test. E : SirT1 levels are decreased in type 2 diabetic compared with NGT subjects. * P < 0.05 by Student's t test. F : SirT1 correlates with TIMP3 in atherosclerotic plaques from NGT ( n = 37) and type 2 diabetic (DM2) ( n = 23) subjects.

    Article Snippet: Immunohistochemistry was performed on serial 3-μm thick sections cut from paraffin blocks of carotid plaques using the following antibodies: 1 ) polyclonal rabbit anti-human TIMP3 antibody (Calbiochem, San Diego, CA), 2 ) monoclonal anti-CD68 (human macrophage) antibody (DAKO, Glostrup, Denmark), and 3 ) monoclonal anti-α smooth muscle actin antibody (Europa Ventana Medical System, Illkirch, France).

    Techniques: Expressing, Control, Activity Assay

    Regulation of TIMP3 expression in CASMC. A : SirT1 knockdown decreased TIMP3 expression but not TIMP1 , TIMP2 , TIMP4 , ADAM10 , ADAM17 , or MMP9 in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test versus control. B : SirT1 knockdown decreased TIMP3 expression in HUVEC and THP1. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : SirT1 cDNA overexpression increased Timp3 promoter activity. n = 4 for all experiments; ** P < 0.01 by one-way ANOVA. D : SirT1 overexpression increased and prevented loss of TIMP3 expression caused by high glucose (HG; 20 mmol/l) in CASMC, HUVEC, and THP1. n = 4 for all experiments; * P < 0.05 by Student's t test.

    Journal: Diabetes

    Article Title: TIMP3 Is Reduced in Atherosclerotic Plaques From Subjects With Type 2 Diabetes and Increased by SirT1

    doi: 10.2337/db09-0280

    Figure Lengend Snippet: Regulation of TIMP3 expression in CASMC. A : SirT1 knockdown decreased TIMP3 expression but not TIMP1 , TIMP2 , TIMP4 , ADAM10 , ADAM17 , or MMP9 in CASMC. n = 4 for all experiments; *** P < 0.001 by Student's t test versus control. B : SirT1 knockdown decreased TIMP3 expression in HUVEC and THP1. n = 4 for all experiments; *** P < 0.001 by Student's t test. C : SirT1 cDNA overexpression increased Timp3 promoter activity. n = 4 for all experiments; ** P < 0.01 by one-way ANOVA. D : SirT1 overexpression increased and prevented loss of TIMP3 expression caused by high glucose (HG; 20 mmol/l) in CASMC, HUVEC, and THP1. n = 4 for all experiments; * P < 0.05 by Student's t test.

    Article Snippet: Immunohistochemistry was performed on serial 3-μm thick sections cut from paraffin blocks of carotid plaques using the following antibodies: 1 ) polyclonal rabbit anti-human TIMP3 antibody (Calbiochem, San Diego, CA), 2 ) monoclonal anti-CD68 (human macrophage) antibody (DAKO, Glostrup, Denmark), and 3 ) monoclonal anti-α smooth muscle actin antibody (Europa Ventana Medical System, Illkirch, France).

    Techniques: Expressing, Knockdown, Control, Over Expression, Activity Assay