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rabbit anti trf2  (Novus Biologicals)


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    Structured Review

    Novus Biologicals rabbit anti trf2
    Rabbit Anti Trf2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 124 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti trf2/product/Novus Biologicals
    Average 95 stars, based on 124 article reviews
    rabbit anti trf2 - by Bioz Stars, 2026-06
    95/100 stars

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    Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and <t>TRF2)</t> proteins ( vi ).
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    Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and <t>TRF2)</t> proteins ( vi ).
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    Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and <t>TRF2)</t> proteins ( vi ).
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    Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and TRF2) proteins ( vi ).

    Journal: International Journal of Molecular Sciences

    Article Title: Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk

    doi: 10.3390/ijms27041841

    Figure Lengend Snippet: Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and TRF2) proteins ( vi ).

    Article Snippet: 12 , TRF2 (D1Y5D) rabbit mAb , CST , 13136S , 1:1000 , 1:500.

    Techniques: Saline, Immunohistochemistry, Isolation, Expressing, Western Blot, Staining, Control, Binding Assay