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antibody against ipla2β  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology antibody against ipla2β
    Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of <t>iPLA2β</t> protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.
    Antibody Against Ipla2β, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibody against ipla2β/product/Santa Cruz Biotechnology
    Average 94 stars, based on 24 article reviews
    antibody against ipla2β - by Bioz Stars, 2026-03
    94/100 stars

    Images

    1) Product Images from "Myeloid- and hepatocyte-specific deletion of group VIA calcium-independent phospholipase A2 leads to dichotomous opposing phenotypes during MCD diet-induced NASH."

    Article Title: Myeloid- and hepatocyte-specific deletion of group VIA calcium-independent phospholipase A2 leads to dichotomous opposing phenotypes during MCD diet-induced NASH.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    doi: 10.1016/j.bbadis.2022.166590

    Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.
    Figure Legend Snippet: Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.

    Techniques Used: Homologous Recombination, Plasmid Preparation, Generated, Expressing, Control, MANN-WHITNEY

    Fig. 5. LPla2g6−/−mice show attenuation of liver enzymes, plasma cytokines, and blood monocytes after MCDD feeding. Female control (con) and LPla2g6−/−mice were fed with chow or MCDD for 3.5 weeks. (A) Western blot analysis of hepatic iPLA2β protein (left) and quantification (right). (B) RT-qPCR analysis of hepatic Pla2g6, Pla2g4a, and Pnpla8 (left), as well as Pnpla2 and Pnpla3 (right). (C) Body and liver weights in g as well as liver weights per body weights. (D) Plasma activities of ALT (U/L) and blood glucose levels (mg/dl). (E) Plasma levels (mg/dl) of triglycerides and NEFA. (F) Plasma levels (pg/ml) of TNFα, IL6, and CCL2. (G) The levels (103/μl) of lymphocytes, granulocytes, and monocytes. (H) The levels of lipoxin A4 in plasma (mg/dl) and liver (pg/mg liver). Data are mean ± SEM, N = 4–7 (A–C), N = 3–15 (D–F), N = 5–20 (G), and N = 7–11 (H). ***, p < 0.001, **, p < 0.01, and *, p < 0.05 with Mann-Whitney U tests.
    Figure Legend Snippet: Fig. 5. LPla2g6−/−mice show attenuation of liver enzymes, plasma cytokines, and blood monocytes after MCDD feeding. Female control (con) and LPla2g6−/−mice were fed with chow or MCDD for 3.5 weeks. (A) Western blot analysis of hepatic iPLA2β protein (left) and quantification (right). (B) RT-qPCR analysis of hepatic Pla2g6, Pla2g4a, and Pnpla8 (left), as well as Pnpla2 and Pnpla3 (right). (C) Body and liver weights in g as well as liver weights per body weights. (D) Plasma activities of ALT (U/L) and blood glucose levels (mg/dl). (E) Plasma levels (mg/dl) of triglycerides and NEFA. (F) Plasma levels (pg/ml) of TNFα, IL6, and CCL2. (G) The levels (103/μl) of lymphocytes, granulocytes, and monocytes. (H) The levels of lipoxin A4 in plasma (mg/dl) and liver (pg/mg liver). Data are mean ± SEM, N = 4–7 (A–C), N = 3–15 (D–F), N = 5–20 (G), and N = 7–11 (H). ***, p < 0.001, **, p < 0.01, and *, p < 0.05 with Mann-Whitney U tests.

    Techniques Used: Clinical Proteomics, Control, Western Blot, Quantitative RT-PCR, MANN-WHITNEY



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    Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of <t>iPLA2β</t> protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.
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    Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of <t>iPLA2β</t> protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.
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    Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    Article Title: Myeloid- and hepatocyte-specific deletion of group VIA calcium-independent phospholipase A2 leads to dichotomous opposing phenotypes during MCD diet-induced NASH.

    doi: 10.1016/j.bbadis.2022.166590

    Figure Lengend Snippet: Fig. 1. Generation and verification of conditional Pla2g6 KO mouse lines. (A) PLA2G6 locus before (Pla2g6wt) and after (Pla2g6neoflox) homologous recombination with the targeting vector insert, LoxP, and FRT sites. FLPe recombinase converts the allele Pla2g6neoflox into the allele Pla2g6floxflox (Flox) which lacks the neomycin resistance cassette. Cre recombinase converts the allele Pla2g6floxflox into the null allele Pla2g6Δex6–8, which lacks exon 6–8. (B) Upon breeding Pla2g6floxflox (Flox) with LysM-Cre mouse line, Mφ-specific Pla2g6 KO (MPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein and Pla2g6 mRNA in BMDMs of MPla2g6−/−mice when compared with Flox. Expression of Pla2g4a and PnPla8 mRNA was not altered in MPla2g6−/−BMDMs. (C) Upon breeding Pla2g6floxflox (Flox) with Alb-Cre mouse line, liver-specific Pla2g6 KO (LPla2g6−/−) mice were generated. The deletion was verified by an absence of iPLA2β protein in livers, but not in brain and BMDMs of LPla2g6−/−mice. Control mice were Flox and C57BL6/N WT mice. Data are mean ± SEM, N = 5–7 (B). *, p < 0.05, with Mann-Whitney U tests.

    Article Snippet: Membranes were incubated with a primary antibody against iPLA2β (D-4, sc-376,563 or T-14, sc-14,463, Santa Cruz Biotechnology, Heidelberg, Germany), CD36 (H-300, sc9154, Santa Cruz), PPARα (H-2, sc-398,394, Santa Cruz), CHOP (B-3, sc-7351, Santa Cruz), ELOVL6 (ab69857, Abcam), SCD1 (ab19862, Abcam), αSMA (ab32575, Abcam), VIMENTIN (ab9254, Abcam), SERPINE1 (#3917-1, Epitomics), ACC (#3662, Cell Signaling), PPARγ (#2435, Cell Signaling), CEBPα (clone EP709Y, cat#1704-1, Epitomics), p-JNK (81E11, #4668, Cell Signaling), FASN (C20G5, #3180, Cell Signaling), βACTIN (AC-5, #5441, Sigma), and GAPDH (#2118, Cell Signaling).

    Techniques: Homologous Recombination, Plasmid Preparation, Generated, Expressing, Control, MANN-WHITNEY

    Fig. 5. LPla2g6−/−mice show attenuation of liver enzymes, plasma cytokines, and blood monocytes after MCDD feeding. Female control (con) and LPla2g6−/−mice were fed with chow or MCDD for 3.5 weeks. (A) Western blot analysis of hepatic iPLA2β protein (left) and quantification (right). (B) RT-qPCR analysis of hepatic Pla2g6, Pla2g4a, and Pnpla8 (left), as well as Pnpla2 and Pnpla3 (right). (C) Body and liver weights in g as well as liver weights per body weights. (D) Plasma activities of ALT (U/L) and blood glucose levels (mg/dl). (E) Plasma levels (mg/dl) of triglycerides and NEFA. (F) Plasma levels (pg/ml) of TNFα, IL6, and CCL2. (G) The levels (103/μl) of lymphocytes, granulocytes, and monocytes. (H) The levels of lipoxin A4 in plasma (mg/dl) and liver (pg/mg liver). Data are mean ± SEM, N = 4–7 (A–C), N = 3–15 (D–F), N = 5–20 (G), and N = 7–11 (H). ***, p < 0.001, **, p < 0.01, and *, p < 0.05 with Mann-Whitney U tests.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    Article Title: Myeloid- and hepatocyte-specific deletion of group VIA calcium-independent phospholipase A2 leads to dichotomous opposing phenotypes during MCD diet-induced NASH.

    doi: 10.1016/j.bbadis.2022.166590

    Figure Lengend Snippet: Fig. 5. LPla2g6−/−mice show attenuation of liver enzymes, plasma cytokines, and blood monocytes after MCDD feeding. Female control (con) and LPla2g6−/−mice were fed with chow or MCDD for 3.5 weeks. (A) Western blot analysis of hepatic iPLA2β protein (left) and quantification (right). (B) RT-qPCR analysis of hepatic Pla2g6, Pla2g4a, and Pnpla8 (left), as well as Pnpla2 and Pnpla3 (right). (C) Body and liver weights in g as well as liver weights per body weights. (D) Plasma activities of ALT (U/L) and blood glucose levels (mg/dl). (E) Plasma levels (mg/dl) of triglycerides and NEFA. (F) Plasma levels (pg/ml) of TNFα, IL6, and CCL2. (G) The levels (103/μl) of lymphocytes, granulocytes, and monocytes. (H) The levels of lipoxin A4 in plasma (mg/dl) and liver (pg/mg liver). Data are mean ± SEM, N = 4–7 (A–C), N = 3–15 (D–F), N = 5–20 (G), and N = 7–11 (H). ***, p < 0.001, **, p < 0.01, and *, p < 0.05 with Mann-Whitney U tests.

    Article Snippet: Membranes were incubated with a primary antibody against iPLA2β (D-4, sc-376,563 or T-14, sc-14,463, Santa Cruz Biotechnology, Heidelberg, Germany), CD36 (H-300, sc9154, Santa Cruz), PPARα (H-2, sc-398,394, Santa Cruz), CHOP (B-3, sc-7351, Santa Cruz), ELOVL6 (ab69857, Abcam), SCD1 (ab19862, Abcam), αSMA (ab32575, Abcam), VIMENTIN (ab9254, Abcam), SERPINE1 (#3917-1, Epitomics), ACC (#3662, Cell Signaling), PPARγ (#2435, Cell Signaling), CEBPα (clone EP709Y, cat#1704-1, Epitomics), p-JNK (81E11, #4668, Cell Signaling), FASN (C20G5, #3180, Cell Signaling), βACTIN (AC-5, #5441, Sigma), and GAPDH (#2118, Cell Signaling).

    Techniques: Clinical Proteomics, Control, Western Blot, Quantitative RT-PCR, MANN-WHITNEY