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bcl 2 interacting domain  (Novus Biologicals)


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    Novus Biologicals bcl 2 interacting domain
    Bcl 2 Interacting Domain, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/bcl+2+interacting+domain/pmc08301907-39-0-7?v=Novus+Biologicals
    Average 91 stars, based on 11 article reviews
    bcl 2 interacting domain - by Bioz Stars, 2026-07
    91/100 stars

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    Apoptosis sensitivity was partially restored in Chk2 , p53 , and p21 -deficient Fah -/- hepatocytes. ( A–E ) Eight-week-old Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC treatment or 14 days after NTBC withdrawal were challenged with the anti-Fas antibody Jo2. ( A ) Representative macroscopic images of Fas-challenged animals, as well as H&E and TUNEL staining. Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice show morphologic signs of aggravated liver damage and increased numbers of TUNEL-positive hepatocytes. ( B ) Plasma levels of aspartate aminotransferase (AST) as a surrogate marker for liver injury are increased in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice compared with Fah -/- mice off NTBC after Jo2 treatment, but do not reach the levels observed in Fah -/- mice on full NTBC supplementation (n = 3–5 per group, means ± SEM). Control: wild-type (WT) mice. ( C and D ) Jo2 treatment leads to increased cleaved caspase-3 expression ( C , immunoblot on whole liver lysates) and ( D ) activity in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- off NTBC compared with Fah -/- controls (n = 3–6). Activity values were normalized against WT. Means ± SEM are shown. ( E ) Immunoblots to detect the levels of several pro-apoptotic and <t>anti-apoptotic</t> proteins in pooled liver lysates from Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC and 14 days after NTBC withdrawal (n = 3–4). ∗ P ≤ .05. BAX, BCL2-associated X protein; BCL-X, B-cell lymphoma-extra large; BID, BH3 interacting domain death agonist; BIM, BCL2-like 11; FLIP, CASP8 and FADD-like apoptosis regulator; MCL-1, myeloid cell leukemia sequence 1.
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    Apoptosis sensitivity was partially restored in Chk2 , p53 , and p21 -deficient Fah -/- hepatocytes. ( A–E ) Eight-week-old Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC treatment or 14 days after NTBC withdrawal were challenged with the anti-Fas antibody Jo2. ( A ) Representative macroscopic images of Fas-challenged animals, as well as H&E and TUNEL staining. Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice show morphologic signs of aggravated liver damage and increased numbers of TUNEL-positive hepatocytes. ( B ) Plasma levels of aspartate aminotransferase (AST) as a surrogate marker for liver injury are increased in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice compared with Fah -/- mice off NTBC after Jo2 treatment, but do not reach the levels observed in Fah -/- mice on full NTBC supplementation (n = 3–5 per group, means ± SEM). Control: wild-type (WT) mice. ( C and D ) Jo2 treatment leads to increased cleaved caspase-3 expression ( C , immunoblot on whole liver lysates) and ( D ) activity in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- off NTBC compared with Fah -/- controls (n = 3–6). Activity values were normalized against WT. Means ± SEM are shown. ( E ) Immunoblots to detect the levels of several pro-apoptotic and anti-apoptotic proteins in pooled liver lysates from Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC and 14 days after NTBC withdrawal (n = 3–4). ∗ P ≤ .05. BAX, BCL2-associated X protein; BCL-X, B-cell lymphoma-extra large; BID, BH3 interacting domain death agonist; BIM, BCL2-like 11; FLIP, CASP8 and FADD-like apoptosis regulator; MCL-1, myeloid cell leukemia sequence 1.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: p53-Independent Induction of p21 Fails to Control Regeneration and Hepatocarcinogenesis in a Murine Liver Injury Model

    doi: 10.1016/j.jcmgh.2021.01.006

    Figure Lengend Snippet: Apoptosis sensitivity was partially restored in Chk2 , p53 , and p21 -deficient Fah -/- hepatocytes. ( A–E ) Eight-week-old Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC treatment or 14 days after NTBC withdrawal were challenged with the anti-Fas antibody Jo2. ( A ) Representative macroscopic images of Fas-challenged animals, as well as H&E and TUNEL staining. Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice show morphologic signs of aggravated liver damage and increased numbers of TUNEL-positive hepatocytes. ( B ) Plasma levels of aspartate aminotransferase (AST) as a surrogate marker for liver injury are increased in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice compared with Fah -/- mice off NTBC after Jo2 treatment, but do not reach the levels observed in Fah -/- mice on full NTBC supplementation (n = 3–5 per group, means ± SEM). Control: wild-type (WT) mice. ( C and D ) Jo2 treatment leads to increased cleaved caspase-3 expression ( C , immunoblot on whole liver lysates) and ( D ) activity in Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- off NTBC compared with Fah -/- controls (n = 3–6). Activity values were normalized against WT. Means ± SEM are shown. ( E ) Immunoblots to detect the levels of several pro-apoptotic and anti-apoptotic proteins in pooled liver lysates from Fah -/- , Fah/p21 -/- , Fah/p53 -/- , and Fah/Chk2 -/- mice on 100% NTBC and 14 days after NTBC withdrawal (n = 3–4). ∗ P ≤ .05. BAX, BCL2-associated X protein; BCL-X, B-cell lymphoma-extra large; BID, BH3 interacting domain death agonist; BIM, BCL2-like 11; FLIP, CASP8 and FADD-like apoptosis regulator; MCL-1, myeloid cell leukemia sequence 1.

    Article Snippet: BCL2-like 1 (610211; BD Biosciences), Bcl-2 homology 3 interacting domain death agonist at 1:2000 (AF860; Bio-Techne GmbH, formerly R&D Systems, Wiesbaden-Nordenstadt, Germany), BCL2-like 11 (apoptosis facilitator) (B7929; Sigma-Aldrich Chemie GmbH, Taufkirchen, Germany), CASP8 and FADD-like apoptosis regulator (AAP-440; Stressgen), heme oxygenase 1 (ADI-SPA-896F, 1:500; Enzo Life Sciences GmbH, Lörrach, Germany), and myeloid cell leukemia sequence 1 (Mcl-1) (600-401-394; Rockland Immunochemicals Inc, Limerick, PA) also were used.

    Techniques: TUNEL Assay, Staining, Marker, Expressing, Western Blot, Activity Assay, Sequencing