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primary rabbit polyclonal antibodies against abca1  (Danaher Inc)


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    Danaher Inc primary rabbit polyclonal antibodies against abca1
    Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) <t>ABCA1</t> and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)
    Primary Rabbit Polyclonal Antibodies Against Abca1, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+rabbit+polyclonal+antibodies+against+abca1/pmc10770909-33-0-21
    Average 86 stars, based on 1 article reviews
    primary rabbit polyclonal antibodies against abca1 - by Bioz Stars, 2026-08
    86/100 stars

    Images

    1) Product Images from "Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis"

    Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis

    Journal: Chinese Medicine

    doi: 10.1186/s13020-023-00876-9

    Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) ABCA1 and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)
    Figure Legend Snippet: Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) ABCA1 and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)

    Techniques Used: Expressing, Staining, Cell Culture, Western Blot

    Model for the function of combined treatment of T0 and MGF in the AS related dyslipidemia targeting autophagy in cholesterol efflux from macrophage foam cells. On the one hand, T0 alone or T0 and MGF promote macrophage cholesterol efflux by activating LXRα to augment the expression of ABCA1 and ABCG1 and also enhance lipophagy in atherosclerotic lesion. Of note, in mammalian macrophage foam cells, lipid droplets are tagged for autophagic fusion, possibly beginning with mTOR-AMPK signaling to initiate lipid droplet degradation for further cholesterol depletion. On the other hand, T0-induced hepatic lipid abnormal accumulation is attenuated by MGF. In this scenario, MGF may activate AMPK signaling to suppress lipid synthesis and accelerate lipolysis for β-oxidation of free fatty acid. Alternatively, hepatic lipid droplets may be degraded through autophagy mechanism mediated by AMPK, and relative classical factors LC3, ATGs and p38 to facilitate hepatic lipophagy
    Figure Legend Snippet: Model for the function of combined treatment of T0 and MGF in the AS related dyslipidemia targeting autophagy in cholesterol efflux from macrophage foam cells. On the one hand, T0 alone or T0 and MGF promote macrophage cholesterol efflux by activating LXRα to augment the expression of ABCA1 and ABCG1 and also enhance lipophagy in atherosclerotic lesion. Of note, in mammalian macrophage foam cells, lipid droplets are tagged for autophagic fusion, possibly beginning with mTOR-AMPK signaling to initiate lipid droplet degradation for further cholesterol depletion. On the other hand, T0-induced hepatic lipid abnormal accumulation is attenuated by MGF. In this scenario, MGF may activate AMPK signaling to suppress lipid synthesis and accelerate lipolysis for β-oxidation of free fatty acid. Alternatively, hepatic lipid droplets may be degraded through autophagy mechanism mediated by AMPK, and relative classical factors LC3, ATGs and p38 to facilitate hepatic lipophagy

    Techniques Used: Expressing



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    primary rabbit polyclonal antibodies against abca1  (Danaher Inc)
    86
    Danaher Inc primary rabbit polyclonal antibodies against abca1
    Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) <t>ABCA1</t> and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)
    Primary Rabbit Polyclonal Antibodies Against Abca1, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+rabbit+polyclonal+antibodies+against+abca1/pmc10770909-33-0-21
    Average 86 stars, based on 1 article reviews
    primary rabbit polyclonal antibodies against abca1 - by Bioz Stars, 2026-08
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) ABCA1 and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)

    Journal: Chinese Medicine

    Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis

    doi: 10.1186/s13020-023-00876-9

    Figure Lengend Snippet: Treatment of T0 and MGF activates expression of LXR target molecules in macrophage and inhibits foam cell formation. A Peritoneal macrophages collected from mice were stained with Oil Red O or anti-bodipy antibody (green) to evaluate formation of foam cells (> 10 lipid droplets per cell, > 10 fields per sample), scale bar, 20 μm; and cholesterol contents were measured. *** p < 0.001, n = 3. Expression of ( B ) ABCA1 and ( C ) ABCG1 (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections from Apoe −/− mice and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. ** p < 0.01, n = 3. Expression of ABCA1, ABCG1, LXRα and CD36 in cultured peritoneal macrophages ( D ) and RAW264.7 cells ( E ) was determined by western blot with total proteins extracted from cell samples. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)

    Article Snippet: Primary rabbit polyclonal antibodies against ABCA1 (ab18180), ABCG1 (ab218528), LC3 (ab192890), SREBP-1c (ab28481), FAS (ab133619), and β-actin (ab8227) were purchased from Abcam (Cambridge, MA, USA).

    Techniques: Expressing, Staining, Cell Culture, Western Blot

    Model for the function of combined treatment of T0 and MGF in the AS related dyslipidemia targeting autophagy in cholesterol efflux from macrophage foam cells. On the one hand, T0 alone or T0 and MGF promote macrophage cholesterol efflux by activating LXRα to augment the expression of ABCA1 and ABCG1 and also enhance lipophagy in atherosclerotic lesion. Of note, in mammalian macrophage foam cells, lipid droplets are tagged for autophagic fusion, possibly beginning with mTOR-AMPK signaling to initiate lipid droplet degradation for further cholesterol depletion. On the other hand, T0-induced hepatic lipid abnormal accumulation is attenuated by MGF. In this scenario, MGF may activate AMPK signaling to suppress lipid synthesis and accelerate lipolysis for β-oxidation of free fatty acid. Alternatively, hepatic lipid droplets may be degraded through autophagy mechanism mediated by AMPK, and relative classical factors LC3, ATGs and p38 to facilitate hepatic lipophagy

    Journal: Chinese Medicine

    Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis

    doi: 10.1186/s13020-023-00876-9

    Figure Lengend Snippet: Model for the function of combined treatment of T0 and MGF in the AS related dyslipidemia targeting autophagy in cholesterol efflux from macrophage foam cells. On the one hand, T0 alone or T0 and MGF promote macrophage cholesterol efflux by activating LXRα to augment the expression of ABCA1 and ABCG1 and also enhance lipophagy in atherosclerotic lesion. Of note, in mammalian macrophage foam cells, lipid droplets are tagged for autophagic fusion, possibly beginning with mTOR-AMPK signaling to initiate lipid droplet degradation for further cholesterol depletion. On the other hand, T0-induced hepatic lipid abnormal accumulation is attenuated by MGF. In this scenario, MGF may activate AMPK signaling to suppress lipid synthesis and accelerate lipolysis for β-oxidation of free fatty acid. Alternatively, hepatic lipid droplets may be degraded through autophagy mechanism mediated by AMPK, and relative classical factors LC3, ATGs and p38 to facilitate hepatic lipophagy

    Article Snippet: Primary rabbit polyclonal antibodies against ABCA1 (ab18180), ABCG1 (ab218528), LC3 (ab192890), SREBP-1c (ab28481), FAS (ab133619), and β-actin (ab8227) were purchased from Abcam (Cambridge, MA, USA).

    Techniques: Expressing