Human Lipoprotein Lipase Complementary DNA Sequence

Wion, Karen L.; Kirchgessner, Todd G.; Lusis, Aldons J.; Schotz, Michael C.; Lawn, Richard M.

doi:10.1126/science.3823907

Cited by 477 publications

(237 citation statements)

References 14 publications

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“…The LPL preparation was characterized by 15% SDS-PAGE, as described previously (11). A complementary DNA encoding the human LPL sequence of 448 amino acids has previously been isolated (12); the calculated molecular weight for the mature protein is 50,394, and with 3 glycosylation sites, a total molecular weight of 60,000 is expected. A 15% SDS gel revealed 2 bands of 60 kd and 55 kd, respectively.…”

Section: Methodsmentioning

confidence: 99%

Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus

Reichlin

Fesmire

Quintero-Del-Rio

et al. 2002

Arthritis & Rheumatism

116

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Objective. To demonstrate the binding of bovine lipoprotein lipase (LPL) by IgG from sera obtained from patients with systemic lupus erythematosus (SLE) and other rheumatic diseases, and the relationship of anti-LPL to triglyceride levels in SLE.Method. Binding of LPL by IgG from sera obtained from patients with SLE and other rheumatic diseases was measured by an enzyme-linked immunosorbent assay technique. Lipid profiles for fasting blood samples obtained from SLE patients and control subjects were determined.Results. Sera obtained from 105 patients with SLE were assessed for reactivity with LPL, and 49 (47%) of the results were positive. Sera obtained from patients with rheumatoid arthritis (RA) (n ‫؍‬ 80), Sjögren's syndrome (n ‫؍‬ 30), polymyositis and dermatomyositis (n ‫؍‬ 30), and progressive systemic sclerosis (n ‫؍‬ 31) were also studied, and 10 (13%), 3 (10%), 12 (40%), and 13 (42%), respectively, were positive for reactivity with LPL. It was determined that all affinity-purified antidouble-stranded DNA (dsDNA) antibodies and 4 of 5 monoclonal anti-dsDNA antibodies bound to LPL. The binding of IgG depleted of anti-dsDNA to LPL indicates a second anti-LPL activity in SLE. Measurements of fasting lipid levels in SLE patients with anti-LPL revealed a strong positive correlation of antibody levels and total serum triglycerides, apolipoprotein B, and apolipoprotein E concentrations.Conclusion. Antibodies to LPL occurred in 47% of SLE patients and in a similar percentage of patients with polymyositis or systemic sclerosis. The prevalence of these antibodies was less in patients with RA or Sjögren's syndrome. It is hypothesized that the elevated triglyceride levels in SLE patients are in part attributable to anti-LPL, and this lipid abnormality could contribute to the premature atherosclerosis known to be present in patients with SLE.

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Section: Methodsmentioning

confidence: 99%

Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus

Reichlin

Fesmire

Quintero-Del-Rio

et al. 2002

Arthritis & Rheumatism

116

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“…4) H RAM TQ TLAHDH TI SRAQEH PVS VKNVIKLSLE SQ IRIVGA AN RWGAQ Q IRWGA R TRLVGK AGYTKLVGQD 117 128 129 129 120 Published sequences of other human lipases [28][29][30][31][32] are compared with our sequence. The alignment starts with the leader peptide and the cleavage sites are indicated by slashes (/ /).…”

Section: Expression Of Nmd Is Restricted To a Few Human Organs Andmentioning

confidence: 99%

nmd, a novel gene differentially expressed in human melanoma cell lines, encodes a new atypical member of the enzyme family of lipases

et al. 1997

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nmd, a novel gene, was isolated by applying the differential mRNA display method to human melanoma cell lines with different metastatic capacity. In a panel of 17 other human tumor cell lines, nmd RNA expression could only be detected at low levels in T24 (bladder carcinoma) and Caco-2 (colon adenocarcinoma). Furthermore, it was found in placenta and liver, but not in skin, colon, spleen, lung, muscle, prostate and kidney. Sequence analysis classified the nmd gene product as a new member of the enzyme family of lipases (almost 30% identity in amino acid sequence with other human lipases). Active site residues of lipases were conserved in NMD, but NMD lacks the regulatory lid domain, which controls entry to the active site in classical lipases. A similar deletion was earlier reported by others in the guinea pig pancreatic (phospho)lipase GPLRP2 and the phospholipase Al from hornet venom (Dolml).

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“…The human GRL genomic DNA was provided by R Evans 21 and the human LPL cDNA clone by R Lawn. 22 Five micrograms of genomic DNA were digested for 18 -20 h with 30 U of the DraI for a2-ADR, BanI for b2-ADR and BclI for GRL according Gene interactions and obesity phenotypes O Ukkola et al to conditions recommended by the manufacturer. Southern blot analysis was performed as described earlier.…”

Section: Dna Analysesmentioning

confidence: 99%

Interactions among the glucocorticoid receptor, lipoprotein lipase and adrenergic receptor genes and abdominal fat in the Québec Family Study

et al. 2001

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OBJECTIVE:To investigate whether interactions between glucocorticoid receptor (GRL), lipoprotein lipase (LPL) and adrenergic receptor (ADR) gene markers contribute to individual differences in indicators of adiposity and abdominal obesity, including visceral fat level. DESIGN AND SUBJECTS: Cross-sectional study; 742 individuals from the phase 2 of the Québec Family Study cohort. MEASUREMENTS: Total body fat assessed by hydrodensitometry and the sum of six skinfolds. Abdominal fat areas measured by computed tomography and adjusted for age, sex and total fat mass in all analyses. GRL Bcl I, a2A-ADR Dra I and b2-ADR Ban I markers were typed by Southern blot, and other markers by polymerase chain reaction technique. RESULTS: It is confirmed that the 4.5 kb allele of the GRL BclI polymorphism is associated with a higher amount of abdominal visceral fat (AVF) depot (P for trend < 0.001) independent of the level of total body fat. Furthermore, the a2-ADR Dra I variant is associated with lower cross-sectional areas of abdominal total (P ¼ 0.003) and subcutaneous (P ¼ 0.012) adipose tissue. Genegene interactions between GRL and a2-ADR genes affecting overall adiposity (P ¼ 0.016) as well as between GRL and b2-ADR genes (P ¼ 0.049) having influence on total abdominal fat levels were observed. When the three genes were considered together in the same analysis, significant interactions having influence on overall adiposity (P ¼ 0.017), abdominal total (P ¼ 0.032) and visceral fat (P ¼ 0.002) were observed. About 1 -2% of the total variation in total fatness and abdominal fat was explained by these gene -gene interactions. CONCLUSION: There is an association between the GRL BclI polymorphism and increased AVF levels independent of the level of total body fat. The a2-ADR DraI variant is associated with a lower cross-sectional area of abdominal total fat. Numerous interactions between GRL and ADR markers on overall adiposity and total abdominal fat as well as between GRL, LPL and ADR genes on overall adiposity, abdominal total and visceral fat suggest that the genetic architecture of body fat content and adipose tissue distribution is complex although some genes, like GRL, may have ubiquitous effects.

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Human Lipoprotein Lipase Complementary DNA Sequence

Cited by 477 publications

References 14 publications

Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus

Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus

nmd, a novel gene differentially expressed in human melanoma cell lines, encodes a new atypical member of the enzyme family of lipases

Interactions among the glucocorticoid receptor, lipoprotein lipase and adrenergic receptor genes and abdominal fat in the Québec Family Study

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