Human/Mouse Lipoprotein Lipase/LPL Antibody

Lipoprotein Lipase/LPL in SH‑SY5Y Human Cell Line.

Lipoprotein Lipase/LPL was detected in immersion fixed SH-SY5Y human neuroblastoma cell line using Goat Anti-Human Lipoprotein Lipase/LPL Antigen Affinity-purified Polyclonal Antibody (Catalog # AF7197) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Goat IgG Secondary Antibody (red, upper panel; Catalog # NL001) and counterstained with DAPI (blue, lower panel). Specific staining was localized to cell surfaces and cytoplasm. View our protocol for Fluorescent ICC Staining of Cells on Coverslips. This application has not been tested in mouse samples.

Lipoprotein Lipase/LPL in Human Heart.

Lipoprotein Lipase/LPL was detected in immersion fixed paraffin-embedded sections of human heart using Goat Anti-Human/Mouse Lipoprotein Lipase/LPL Antigen Affinity-purified Polyclonal Antibody (Catalog # AF7197) at 3 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Goat IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC004). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to cardiomyocytes. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

Detection of Lipoprotein Lipase/LPL by Western Blot

Obesity in Par-4-/- mice is rescued by deletion of C3. (A) Par-4 and C3 double knockout (DKO) mice are not obese. Weight of age-matched DKO (n=13, 10, 8 and 4 for each time point respectively) and Par-4+/+ (n=27, 16, 9, 5 for each time point respectively) male mice was determined over the course of 7 months; representative images of Par-4+/+ and DKO at 5-6 months are shown. (B) DKO mice do not show increased fat accumulation. Six-month-old DKO (n=8) and Par-4+/+ (n=7) male mice were examined for fat mass by Echo-MRI and adipocyte hypertrophy. (C) Triglyceride absorption is similar in DKO, C3KO and Par-4+/+ mice. DKO (n=5-6), C3-/- (n=4) and Par-4+/+ (n=11) male mice were fasted overnight and injected intraperitoneally with tyloxapol, 30 min before oral gavage of olive oil. Plasma was collected at the indicated time intervals after fat load, and triglycerides were quantified. Plasma was also subjected to western blot analysis for ApoB48. ApoB48 levels in the plasma were normalized to albumin in corresponding Coomassie blue gels, and fold change at each time point is shown (n=4). (D) LPL is upregulated in the adipose tissue of AKO and Par-4-/- mice. LPL protein levels were determined by western blot analysis in visceral adipose tissue and heart from AKO, Par-4-/- and Par-4+/+ mice (n=3). (E) LPL is not increased in the adipose tissue of DKO mice. LPL protein levels were determined by western blot analysis in visceral adipose tissue and heart from Par-4+/+ (n=4) and DKO (n= 4) male mice. LPL levels were normalized to beta -tubulin levels and fold change was calculated. Mean ± SEM, *P < 0.05, **P < 0.01, by the Student’s t-test. Also see Figures S6, S13. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/35425699), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Lipoprotein Lipase/LPL by Western Blot

Obesity in Par-4-/- mice is rescued by deletion of C3. (A) Par-4 and C3 double knockout (DKO) mice are not obese. Weight of age-matched DKO (n=13, 10, 8 and 4 for each time point respectively) and Par-4+/+ (n=27, 16, 9, 5 for each time point respectively) male mice was determined over the course of 7 months; representative images of Par-4+/+ and DKO at 5-6 months are shown. (B) DKO mice do not show increased fat accumulation. Six-month-old DKO (n=8) and Par-4+/+ (n=7) male mice were examined for fat mass by Echo-MRI and adipocyte hypertrophy. (C) Triglyceride absorption is similar in DKO, C3KO and Par-4+/+ mice. DKO (n=5-6), C3-/- (n=4) and Par-4+/+ (n=11) male mice were fasted overnight and injected intraperitoneally with tyloxapol, 30 min before oral gavage of olive oil. Plasma was collected at the indicated time intervals after fat load, and triglycerides were quantified. Plasma was also subjected to western blot analysis for ApoB48. ApoB48 levels in the plasma were normalized to albumin in corresponding Coomassie blue gels, and fold change at each time point is shown (n=4). (D) LPL is upregulated in the adipose tissue of AKO and Par-4-/- mice. LPL protein levels were determined by western blot analysis in visceral adipose tissue and heart from AKO, Par-4-/- and Par-4+/+ mice (n=3). (E) LPL is not increased in the adipose tissue of DKO mice. LPL protein levels were determined by western blot analysis in visceral adipose tissue and heart from Par-4+/+ (n=4) and DKO (n= 4) male mice. LPL levels were normalized to beta -tubulin levels and fold change was calculated. Mean ± SEM, *P < 0.05, **P < 0.01, by the Student’s t-test. Also see Figures S6, S13. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/35425699), licensed under a CC-BY license. Not internally tested by R&D Systems.