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lpl sirna mm_lpl_5  (Qiagen)


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    Structured Review

    Qiagen lpl sirna mm_lpl_5
    Chylomicron-mediated GLP-1 release in GLUTag cells is dependent on LPL. ( a ) Lpl expression was examined by RNA sequencing FACS-sorted primary L cells (GLU-Venus-positive, L+) and negative cells (GLU-Venus-negative, L−) collected in parallel from murine duodenum and GLUTag cells. FPKM, fragments per kilobase per million reads. ( b ) GLP-1 secretion from GLUTag cells treated with chylomicrons (CM; 10 μg/ml) in the presence or absence of orlistat (1 μg/ml, following 30 min pre-treatment). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, *** p < 0.001. ( c ) GLUTag cells were transfected with <t>30</t> <t>nmol/l</t> Lpl <t>siRNA</t> or negative control (Ctrl) siRNA, and knockdown was validated by qRT-PCR. Data are presented as means ± SEM, n = 5–6 from three independent experiments; unpaired t test, ** p < 0.01. ( d ) GLP-1 secretion from negative control (white bars) or Lpl siRNA (grey bars) transfected GLUTag cells treated with chylomicrons (CM; 10 μg/ml) or forskolin/IBMX (F/I; 10 μmol/l each) in the presence of glucose (10 mmol/l). Data represent means ± SEM, n = 8–9 wells from three independent experiments; one-way ANOVA, * p < 0.05, *** p < 0.001
    Lpl Sirna Mm Lpl 5, supplied by Qiagen, 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/lpl sirna mm_lpl_5/product/Qiagen
    Average 90 stars, based on 1 article reviews
    lpl sirna mm_lpl_5 - by Bioz Stars, 2026-04
    90/100 stars

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    1) Product Images from "Chylomicrons stimulate incretin secretion in mouse and human cells"

    Article Title: Chylomicrons stimulate incretin secretion in mouse and human cells

    Journal: Diabetologia

    doi: 10.1007/s00125-017-4420-2

    Chylomicron-mediated GLP-1 release in GLUTag cells is dependent on LPL. ( a ) Lpl expression was examined by RNA sequencing FACS-sorted primary L cells (GLU-Venus-positive, L+) and negative cells (GLU-Venus-negative, L−) collected in parallel from murine duodenum and GLUTag cells. FPKM, fragments per kilobase per million reads. ( b ) GLP-1 secretion from GLUTag cells treated with chylomicrons (CM; 10 μg/ml) in the presence or absence of orlistat (1 μg/ml, following 30 min pre-treatment). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, *** p < 0.001. ( c ) GLUTag cells were transfected with 30 nmol/l Lpl siRNA or negative control (Ctrl) siRNA, and knockdown was validated by qRT-PCR. Data are presented as means ± SEM, n = 5–6 from three independent experiments; unpaired t test, ** p < 0.01. ( d ) GLP-1 secretion from negative control (white bars) or Lpl siRNA (grey bars) transfected GLUTag cells treated with chylomicrons (CM; 10 μg/ml) or forskolin/IBMX (F/I; 10 μmol/l each) in the presence of glucose (10 mmol/l). Data represent means ± SEM, n = 8–9 wells from three independent experiments; one-way ANOVA, * p < 0.05, *** p < 0.001
    Figure Legend Snippet: Chylomicron-mediated GLP-1 release in GLUTag cells is dependent on LPL. ( a ) Lpl expression was examined by RNA sequencing FACS-sorted primary L cells (GLU-Venus-positive, L+) and negative cells (GLU-Venus-negative, L−) collected in parallel from murine duodenum and GLUTag cells. FPKM, fragments per kilobase per million reads. ( b ) GLP-1 secretion from GLUTag cells treated with chylomicrons (CM; 10 μg/ml) in the presence or absence of orlistat (1 μg/ml, following 30 min pre-treatment). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, *** p < 0.001. ( c ) GLUTag cells were transfected with 30 nmol/l Lpl siRNA or negative control (Ctrl) siRNA, and knockdown was validated by qRT-PCR. Data are presented as means ± SEM, n = 5–6 from three independent experiments; unpaired t test, ** p < 0.01. ( d ) GLP-1 secretion from negative control (white bars) or Lpl siRNA (grey bars) transfected GLUTag cells treated with chylomicrons (CM; 10 μg/ml) or forskolin/IBMX (F/I; 10 μmol/l each) in the presence of glucose (10 mmol/l). Data represent means ± SEM, n = 8–9 wells from three independent experiments; one-way ANOVA, * p < 0.05, *** p < 0.001

    Techniques Used: Expressing, RNA Sequencing, Transfection, Negative Control, Knockdown, Quantitative RT-PCR

    Chylomicrons stimulate GLP-1 release via FFA1 in GLUTag cells. ( a ) FFA1 ( Ffar1 ) expression was examined by RNA sequencing FACS-sorted primary L cells (GLU-Venus-positive, L+) and negative cells (GLU-Venus-negative, L−) collected in parallel from murine duodenum and GLUTag cells. FPKM, fragments per kilobase per million reads. ( b ) GLP-1 secretion from GLUTag cells treated with chylomicrons (CM; 10 μg/ml) or the selective FFA1 agonist AM-1638 (1 μmol/l) in the presence or absence of the FFA1 antagonist GW1100 (1 μmol/l, with 30 min pre-treatment). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, *** p < 0.001. ( c ) GLUTag cells were transfected with 30 nmol/l Ffar1 siRNA or negative control (Ctrl) siRNA, and knockdown was validated by qRT-PCR. Data are presented as means ± SEM, n = 7 from three independent experiments; unpaired t test, * p < 0.05. ( d ) GLP-1 secretion from negative control (white bars) or Ffar1 siRNA (grey bars) transfected GLUTag cells treated with chylomicrons (CM; 10 μg/ml), AM-1638 (1 μmol/l) or forskolin/IBMX (F/I; 10 μmol/l each) in the presence of glucose (10 mmol/l). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: Chylomicrons stimulate GLP-1 release via FFA1 in GLUTag cells. ( a ) FFA1 ( Ffar1 ) expression was examined by RNA sequencing FACS-sorted primary L cells (GLU-Venus-positive, L+) and negative cells (GLU-Venus-negative, L−) collected in parallel from murine duodenum and GLUTag cells. FPKM, fragments per kilobase per million reads. ( b ) GLP-1 secretion from GLUTag cells treated with chylomicrons (CM; 10 μg/ml) or the selective FFA1 agonist AM-1638 (1 μmol/l) in the presence or absence of the FFA1 antagonist GW1100 (1 μmol/l, with 30 min pre-treatment). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, *** p < 0.001. ( c ) GLUTag cells were transfected with 30 nmol/l Ffar1 siRNA or negative control (Ctrl) siRNA, and knockdown was validated by qRT-PCR. Data are presented as means ± SEM, n = 7 from three independent experiments; unpaired t test, * p < 0.05. ( d ) GLP-1 secretion from negative control (white bars) or Ffar1 siRNA (grey bars) transfected GLUTag cells treated with chylomicrons (CM; 10 μg/ml), AM-1638 (1 μmol/l) or forskolin/IBMX (F/I; 10 μmol/l each) in the presence of glucose (10 mmol/l). Data represent means ± SEM, n = 9 wells from three independent experiments; one-way ANOVA, ** p < 0.01, *** p < 0.001

    Techniques Used: Expressing, RNA Sequencing, Transfection, Negative Control, Knockdown, Quantitative RT-PCR



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