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Familial apolipoprotein E deficiency.
Open accessAbstract
A unique kindred with premature cardiovascular disease, tubo-eruptive xanthomas, and type III hyperlipoproteinemia (HLP) associated with familial apolipoprotein (apo) E deficiency was examined. Homozygotes (n = 4) had marked increases in cholesterol-rich very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL), which could be effectively lowered with diet and medication (niacin, clofibrate). Homozygotes had only trace amounts of plasma apoE, and accumulations of apoB-48 and apoA-IV in VLDL, IDL, and low density lipoproteins. Radioiodinated VLDL apoB and apoE kinetic studies revealed that the homozygous proband had markedly retarded fractional catabolism of VLDL apoB-100, apoB-48 and plasma apoE, as well as an extremely low apoE synthesis rate as compared to normals. Obligate heterozygotes (n = 10) generally had normal plasma lipids and mean plasma apoE concentrations that were 42% of normal. The data indicate that homozygous familial apoE deficiency is a cause of type III HLP, is associated with markedly decreased apoE production, and that apoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.
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TL;DR
This paper characterizes the first reported kindred with familial apolipoprotein E deficiency, showing that homozygotes develop type III hyperlipoproteinemia with xanthomas and premature cardiovascular disease. It concludes that apoE deficiency is an autosomal recessive condition with markedly decreased apoE production and that apoE is essential for normal catabolism of triglyceride-rich lipoprotein remnants.
Key findings
- Four homozygotes had severe type III hyperlipoproteinemia: mean plasma cholesterol 529±74 mg/dl, triglyceride 221±62 mg/dl, VLDL cholesterol 243±97 mg/dl, LDL cholesterol 230±41 mg/dl, HDL cholesterol 51±16 mg/dl, and VLDL cholesterol/plasma triglyceride ratio 1.09±0.18, all significantly different from normal (P < 0.01).
- Homozygotes had only trace plasma apoE (mean 0.016±0.003 mg/dl, 0.3% of normal), while obligate heterozygotes (n = 10) had mean apoE concentrations 42.1% of normal (P < 0.01).
- In the proband, VLDL apoB-100 residence time was 7.8 times greater than normal and VLDL apoB-48 residence time was 44 times greater than normal; calculated apoE synthesis rate was only 0.15% of that observed in normal females.
- Lipid-lowering therapy was effective: clofibrate produced mean reductions in VLDL cholesterol of 53% of baseline and increases in HDL cholesterol of 75% of baseline (P < 0.01).
Methods
- Clinical, genetic, biochemical, and metabolic characterization of a single kindred with familial apoE deficiency, including four homozygotes, ten obligate heterozygotes, and normal controls.
- Lipoprotein analysis used ultracentrifugation, paper and agarose electrophoresis, analytical ultracentrifugation, electron microscopy, gradient gel electrophoresis, and apolipoprotein quantitation by radial immunodiffusion, radioimmunoassay, enzyme-linked immunoassay, and electroimmunoassay.
- Metabolic studies in the proband and normal subjects used radioiodinated apoE3 and VLDL tracers, with kinetic analysis by SAAM to calculate residence times and synthesis rates.
Limitations
- Stated: whether apoE deficiency alone is sufficient to cause type III hyperlipoproteinemia or whether an additional genetic factor is present in this kindred is uncertain; kinetic data are valid only if the proband synthesizes structurally normal apoE; the apolipoprotein control group was Caucasian while study subjects were Black; consanguinity could not be documented but is possible.
- Evident from the text: findings come from a single small kindred (four homozygotes, ten obligate heterozygotes), limiting generalizability; the paper also notes that the precise defect at the gene level remained to be elucidated.
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Claims the paper makes
87 Own result · 22 Sources not found · 20 Own interpretation · 5 No basis given · 2 Own method
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“accumulations of apoB-48 and apoA-IV in VLDL, IDL, and low density lipo- proteins.”
- Also stated in: § Lipoprotein analysis. · hedged
“These data indicate lack ofapoE and accumulation of apoB-48 and apoA-IV in the VLDL, IDL, and LDL density fractions of subjects with homozygous apoE deficiency.”
§ Familial Apolipoprotein E Deficiency > Abstract
plaincorrelationaln = 4- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Lipoprotein analysis. · hedged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mean plasma apoE concentrations that were 42% of normal.”
§ Familial Apolipoprotein E Deficiency > Abstract
plainn = 10- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Obligate heterozygotes (n = 10) generally had normal plasma lipids”
§ Familial Apolipoprotein E Deficiency > Abstract
plainn = 10- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Homozygotes (n = 4) had marked increases in cho- lesterol-rich very low density lipoproteins (VLDL) and inter- mediate density lipoproteins (IDL)”
§ Familial Apolipoprotein E Deficiency > Abstract
plaindirectn = 4- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“as well as an extremely low apoE synthesis rate as com- pared to normals.”
§ Familial Apolipoprotein E Deficiency > Abstract
plainSingle case- Asserted: passes — The authors put it forward as true.
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- The authors state this as an assumption: The metabolic studies were conducted under steady state conditions, so that the synthesis rate could be calculated from plasma concentration, plasma volume, residence time, and body weight.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Homozygotes had only trace amounts of plasma apoE”
§ Familial Apolipoprotein E Deficiency > Abstract
plainn = 4- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“which could be effectively lowered with diet and medication (niacin, clofibrate).”
§ Familial Apolipoprotein E Deficiency > Abstract
hedgeddirectn = 4- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Radioiodinated VLDL apoB and apoE kinetic studies revealed that the homozygous proband had markedly retarded fractional catabolism of VLDL apoB-100, apoB-48, and plasma apoE”
§ Familial Apolipoprotein E Deficiency > Abstract
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite these decreases, her VLDL cholesterol level was still el- evated at 55 mg/dl.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“Routine laboratory data including complete blood count, chemistries, thyroid, liver, and kidney function tests were within normal limits (except for plasma lipids).”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 42
- Probably not a substantial claim. 26
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The four homozygotes sampled had significant hyperlipidemia associated with elevations in both VLDL and LDL cholesterol (includes both IDL and LDL), and a marked elevation in the VLDL cho- lesterol/plasma triglyceride ratio.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A unique kindred with premature cardiovascular disease, tubo- eruptive xanthomas, and type III hyperlipoproteinemia (HLP) associated with familial apolipoprotein (apo) E deficiency was examined.”
§ Familial Apolipoprotein E Deficiency > Abstract
plaincorrelationaln = 4- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“She was a non- smoker and was not hypertensive.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“She was noted to have significant hypercholesterolemia at age 58 yr, and was placed on a cholesterol-low- ering diet, which caused a decrease in the size of her xanthomas.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One sister (sibling 2) of the proband had a history of tubo-eruptive xanthomas since her 30s.She was noted to be hypercholesterolemic at age 42 yr”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“Nine offspring were healthy and free of xanthomas.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“With clofibrate administered at a dosage of 1 g p.o. twice daily she had mean reductions of 27, 50, 61, and 17% in her plasma cholesterol, triglyceride, VLDL cholesterol, and LDL cholesterol, while her HDL cholesterol increased by 59%.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“She has not as yet been treated with cholesterol-lowering medication.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A 3-wk course of ethinyl estradiol 0.1 rmg p.o. daily caused increases in plasma triglyceride and HDL cholesterol of 148 and 25% and decreases in total cholesterol, VLDL cholesterol, and LDL cholesterol of 11, 13, and 18%, respectively.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Physical examination was unremarkable except for small tubo-eruptive xanthomas on the el- bows and knees, and arcus senilis.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A younger brother (sibling 1) was first noted to have xanthomas in his 20s, was documented to have type III HLP at age 34 yr, and was subsequently placed on a low saturated fat, low cholesterol diet, as well as clofibrate 500 mg p.o., twice daily.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Obligate heterozygotes (offspring of homozy- gotes) had mean plasma lipid and lipoprotein cholesterol values within the 5th-95th percentile of the normal non-White pop-”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plainSingle case- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one. The quote only partly states this claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The proband's father died at age 62 yr of a myocardial infarction and coronary artery disease documented at autopsy.He had a history of angina for the previous 12 yr, a history of cigarette smoking, and a long history of xanthomas on his ears, scalp, elbows, and knees.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite these dramatic reductions, his VLDL cho- lesterol was still elevated above the 95th percentile of normal at 83 mg/ dl.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Clofibrate administration (1 g p.o., three times daily) resulted in decreases in total cholesterol, triglyceride, and VLDL cholesterol of 7, 34, and 29%, and increases in HDL cholesterol of 66% as compared with values on diet only.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite these effects her VLDL cholesterol remained elevated at 76 mg/dl.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Coronary an- giography at age 60 yr revealed an 80% narrowing of the first diagonal branch of the left anterior descending coronary artery; other coronary arteries had no detectable narrowing.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The proband for the apoE-deficient kindred was a 60- year-old Black female of 161 cm height, 69.8 kg, with a 10-year history of small tubo-eruptive xanthomas on her elbows and knees, a 5-yr history of hypertension, a history of intermittent cigarette smoking, and a 3-yr history of chest pain consistent with angina pectoris.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This therapy resulted in a further decrease in VLDL cholesterol of 27%, with no change in HDL cholesterol.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The proband's oldest sister (sibling 7) was 68 yr of age with a history ofmild exertional chest pain for the past several years, and a long history of tubo-eruptive xanthomas on her elbows and knees.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“Plasma concentra- tions of vitamins A and E as measured by high pressure liquid chro- matography, and plasma fatty acid composition as determined by gas liquid chromatography were within normal limits.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“The addition of nicotinic acid 1 g p.o., three times daily to this regimen resulted in further decreases in total cholesterol, VLDL cholesterol and LDL cholesterol of 23, 35, and 26%, respectively, with an increase in HDL cholesterol of 10%, and little effect on triglyc- erides.”
§ Familial Apolipoprotein E Deficiency > Methods
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“The proband's mother was alive and well, except for arthritis, at age 87 yr.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, the proband's mother and a paternal uncle both had hyperlipidemia.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“No corneal opacification, lymphad- enopathy, or hepatosplenomegaly was noted.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At age 46 yr he suffered a mild stroke resulting in temporary right hemiparesis.”
§ Familial Apolipoprotein E Deficiency > Methods
plainSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Analytical ultracentrifugation ofthe proband's plasma in- dicated a significant increase in VLDL and IDL and no clear LDL peak”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
hedgedSingle case- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“VLDL particles were extremely heterogeneous in size as indicated by the large standard deviation; this heterogeneity was confirmed by scanning of gra- dient gels that demonstrated the presence of at least four com- ponents.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
boostedSingle case- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mean particle diameters (nm±SD) based on electron microscopy were: VLDL, 36.5±11.5;IDL, 3 1.0±3.9;LDL, 26.9±4.2;HDL2b, 10.5±1.3; and HDL2a+3, 8.3±1.7.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plainSingle case- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“About 50% of the offspring of the proband's parents were homozygotes, and no homozygotes have been found among the offspring ofthe proband or any ofher homozygous siblings.”
§ Familial Apolipoprotein E Deficiency > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Premature CAD and stroke events were evident among homozygotes, but were not strikingly premature.”
§ Familial Apolipoprotein E Deficiency > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No increases in LDL (d, 1.019- 1.063 g/ml) constituents were noted.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Consistent results were obtained in all three homo- zygotes tested.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Gradient gel electrophoresis and electron microscopy data on lipoproteins isolated from the proband indicate the presence of small, dense VLDL, and heterogeneous populations within IDL and LDL.”
§ Familial Apolipoprotein E Deficiency > Discussion
hedgedSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
In the paper
“Type III HLP has been associated with abnormalities of apolipoprotein (apo) E (5)(6)(7)(8)(9)(10)(11)(12).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites (5)(6)(7)(8)(9)(10)(11)(12)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Type III HLP patients generally present in adulthood, often develop premature coronary artery disease and peripheral vascular disease, and may have palmar and tubo- eruptive xanthomas (1-3).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [1]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [2]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [3]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“These lipoproteins in type III HLP are cholesterol rich, and migrate to an abnormal beta position on electrophoresis (4).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [4]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“ApoE is a glycoprotein of 34,000 kD, which serves as a con- stituent ofplasma triglyceride-rich lipoproteins and high density lipoproteins (HDL) (7).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Human apoE is a polymorphic protein having three major isoforms separated by isoelectric focusing (apoE2, E3, and E4) (5,6).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Type III hyperlipoproteinemia (HLP)' is an uncommon lipid disorder characterized by elevations of both plasma cholesterol and triglyceride due to an increase in chylomicron remnants, very low density lipoproteins (VLDL), and intermediate density lipoproteins (IDL) (1)(2)(3).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites (1)(2)(3)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“More recently, the apoE4 allele has been associated with elevated LDL choles- terol levels in plasma (14)(15)(16).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites (14)(15)(16)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Type III HLP has been associated with apoE2 homozygosity, various rare mutations of apoE, and apoE deficiency (5)(6)(7)(8)(9)(10)(11)(12).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites (5)(6)(7)(8)(9)(10)(11)(12)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“ApoE3 is the most common isoform present in the general population, may be associated with normal plasma lipids, and has been proposed to be the normal allele (5,6).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“Each of the known polymorphic forms of apoE is coded by a separate allele, and those alleles are inherited in a codominant fashion at a single genetic locus (6).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“An increased prevalence ofthe apoE4 phenotype has been observed in patients with type V hyperlipoproteinemia (13).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [13]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These subjects are probably also heterozygotes.”
§ Familial Apolipoprotein E Deficiency > Lipoprotein analysis.
hedgedSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All blood samples were obtained while subjects had been off lipid lowering medication for at least 3 wk and while on an ad lib.diet, except for homozygous siblings 1, 2, and 7, whose blood samples were examined while on an outpatient low saturated fat, low cholesterol diet.”
§ Familial Apolipoprotein E Deficiency > Methods
plainn = 3- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The primary amino acid sequence of apoE has been reported, and it has been shown that apoE4 differs from apoE3 by an arginine for cysteine substitution at residue 112, while apoE2 differs from apoE3 by a cysteine for arginine substitution at residue 158 (7,8).”
§ Familial Apolipoprotein E Deficiency > Introduction
What the sources say
- Not matchedcites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is most likely that the proband's father was a homozygote since he had xanthomas”
§ Familial Apolipoprotein E Deficiency > Discussion
hedgeddirectSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The aging process and/or menopause may affect the expression of the hyperlipidemia in heterozygotes and ho- mozygotes.”
§ Familial Apolipoprotein E Deficiency > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The apoE gene was present in homozygotes, and no restriction fragment length polymorphism was noted (45, 46).”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
What the sources say
- Not matchedcites [45]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [46]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“Recent data examining apoE messenger (m)RNA levels in macrophages from homo- zygotes indicate only trace amounts of mRNA to be present as compared with normal macrophages, and an additional abnormal apoE mRNA band was also observed (45).”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
What the sources say
- Not matchedcites [45]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data suggest that remnant lipoprotein particles containing apo- lipoproteins such as apoB-48 and apoA-IV, found in the pro- band's plasma but lacking in normal fasting plasma, may en- hance the uptake of apoE.”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
hedgedconditionalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The combined data are consistent with the concepts that familial apoE deficiency is a rare autosomal recessive condition associated with type III hyperlipoproteinemia and markedly de- creased apoE production”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
hedgedcorrelationalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, apoB-48 and/or apoA-IV may also play a role in the uptake of triglyceride-rich lipoproteins, since apoE was catabolized at a significantly greater fractional catabolic rate on lipoproteins isolated from the proband than on normal li- poproteins when studied in normal subjects.”
§ Familial Apolipoprotein E Deficiency > Apolipoprotein quantitation indicated elevations of apoli- poproteins A-I, A-II, and C-II in plasma, and a threefold increase
hedgedconditionalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
The metabolic studies were conducted under steady state conditions, so that the synthesis rate could be calculated from plasma concentration, plasma volume, residence time, and body weight.
“Under steady state conditions: synthesis rate (mg/kg d) = [(plasma concentration, mg/dl) (plasma volume, dl)] + [(residence time, days) (body wt, kg)].”
The authors state this as an assumption.
The proband synthesizes apoE that is structurally normal.
“The kinetic data therefore are valid only if the proband syn- thesizes apoE that is structurally normal.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Interestingly, insufficient levels of apoE also lead to hypertriglyceridemia, because less apoE protein is present to serve as ligands for the LDL receptor and LRP, clinically illustrated by familial apoE deficiency [9,26,27].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [26]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Of the 11 cases of APOE deficiency with reported mutation sites, four were homozygotes and seven were compound heterozygotes or heterozygotes27, 29-40).”
From Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features (2025) · cites this paper as [32]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Two cases with no reported mutation site and homozygotes for APOE deficiency due to variant in the intron 3 acceptor site (c.237-2A>G)32, 33) and APOE deficiency (Glu79fsTer98)34) with almost no detectable apoE have been reported to cause severe type III HLP, including various xanthomas as well as palmar linear xanthomas (Table 1).”
From Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features (2025) · cites this paper as [32]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In vivo and in vitro studies have shown that mutations in apoE that diminish binding of apoE-containing lipoproteins to the LDL receptor are associated with high plasma cholesterol levels and cause premature atherosclerosis in humans and experimental animals ( 1-3, 7, 8 ).”
From Molecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4 (2011) · cites this paper as [2]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The characteristics of the APOE polymorphism thus suggest a qualitative importance of apoE, whereas studies of familial absolute apoE deficiency suggest a quantitative importance of plasma apoE levels in lipid metabolism [26,27].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [26]
The cited source says what the claim attributes to it.
In the citing paper
“Type III hyperlipoproteinemia is characterized by elevations of both plasma cholesterol and triglycerides due to an increase in chylomicron remnants, VLDL and IDL [9,26,52].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [26]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“LDL Homozygotes 79.2± 12.1 (27.8) 63.0±5.1 (22.1) 93±5 (32.6) 31±11 (10.9)”
§ Familial Apolipoprotein E Deficiency > Methods
Reported 100 · recomputed 93.4
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“Family 4 Sibling 4 59 F 237 217 28 156 53 0.24 E3”
§ Familial Apolipoprotein E Deficiency > Methods
Reported 0.24 · recomputed 0.129032
Citations
Cites
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Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders
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Identification of multiple subclasses of plasma low density lipoproteins in normal humans.
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Boyles, J. K., Pitas, R. E., Wilson, E., Mahley, R. W., & Taylor, J. M. (1985) · Journal of Clinical Investigation · doi:10.1172/jci112130 · Cited by 829
Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders
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Human apolipoprotein E. The complete amino acid sequence
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Characterization of human high-density lipoproteins by gradient gel electrophoresis
Blanche, P. J., Gong, E. L., Forte, T. M., & Nichols, A. V. (1981) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(81)90253-8 · Cited by 614
Self-citationZannis, V. I., & Breslow, J. L. (1981) · Biochemistry · doi:10.1021/bi00507a059 · Cited by 563
Mahley, R. W., Hui, D. Y., Innerarity, T. L., & Weisgraber, K. H. (1981) · Journal of Clinical Investigation · doi:10.1172/jci110365 · Cited by 373
Rall, S. C., Weisgraber, K. H., Innerarity, T. L., & Mahley, R. W. (1982) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.79.15.4696 · Cited by 345
Research works printed but not linked: 2
- Gregg, R. E., D. Wilson, E. Rubalcaba, R. Ronan, and H. B. Brewer, Jr. Immunoquantitation of apolipoprotein E. In Proceedings of the Workshop on Apolipoprotein Quantitation. K. Lippel, editor. DHHS, NIH Publ. No. 83-1266: 383-401.
- McConathy, W. J., P. Alaupovic, and J. D. Fesmire. 1982. Various applications of electroimmunoassay for plasma apolipoproteins. In Pro- ceedings of the Workshop in Apolipoprotein Quantification. K. Lippel, editor. NIH Publication No. 83-1266: 276-282.
Cited by
Sorted by citations
Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology
Mahley, R. W. (1988) · Science · doi:10.1126/science.3283935 · Cited by 4,028
Plump, A. S., Smith, J. D., Hayek, T., Aalto-Setälä, K., Walsh, A., Verstuyft, J. G., Rubin, E. M., & Breslow, J. L. (1992) · Cell · doi:10.1016/0092-8674(92)90362-g · Cited by 2,263
Apolipoprotein E polymorphism and atherosclerosis.
Davignon, J., Gregg, R. E., & Sing, C. F. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.1.1 · Cited by 1,981
Self-citationIshibashi, S., Brown, M. S., Goldstein, J. L., Gerard, R. D., Hammer, R. E., & Herz, J. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116663 · Cited by 1,354
Miyata, M., & Smith, J. D. (1996) · Nature Genetics · doi:10.1038/ng0996-55 · Cited by 735
Apolipoprotein E: Structure-Function Relationships
Weisgraber, K. H. (1994) · Advances in Protein Chemistry · doi:10.1016/s0065-3233(08)60642-7 · Cited by 830
Herz, J., Clouthier, D. E., & Hammer, R. E. (1992) · Cell · doi:10.1016/0092-8674(92)90511-a · Cited by 497
Rosenson, R. S., Brewer, H. B., Chapman, M. J., Fazio, S., Hussain, M. M., Kontush, A., Krauss, R. M., Otvos, J. D., Remaley, A. T., & Schaefer, E. J. (2011) · Clinical Chemistry · doi:10.1373/clinchem.2010.155333 · Cited by 523
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Metadata
- Authors
- Schaefer, E. J., Gregg, R. E., Ghiselli, G., Forte, T. M., Ordovas, J. M., Zech, L. A., & Brewer, H. B.
- Affiliations
- Tufts University (US)
- Houston Methodist (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1986-11-01
- Volume
- 78
- Issue
- 5
- Pages
- 1206-1219
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC423806
- OpenAlex
- W2169149496
- Cited by
- 313
- References
- 48
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 3 · 2023: 5 · 2021: 3 · 2020: 6 · 2019: 5 · 2018: 8 · 2017: 3 · 2016: 5 · 2015: 6 · 2014: 13 · 2013: 2 · 2012: 9
- FWCI
- 6.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Oklahoma Medical Research Foundation
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Keywords
- apolipoprotein E deficiency, type III hyperlipoproteinemia, familial hypertriglyceridemia, premature cardiovascular disease, VLDL, intermediate density lipoprotein, apolipoprotein B-48, apolipoprotein A-IV, nicotinic acid, clofibrate, triglyceride-rich lipoproteins, heterozygotes, homozygotes
- MeSH terms
- Adolescent, Adult, Aged, Apolipoproteins E, Child, Cholesterol, Female, Homozygote, Humans, Hyperlipoproteinemia Type III, Lipoproteins, Male, Middle Aged, Pedigree, Phospholipids, Reference Values, Skin Diseases, Triglycerides, Xanthomatosis
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