scholarly journals Multidimensional profiling of plasma lipoproteins by size exclusion chromatography followed by reverse-phase protein arrays

2011 ◽  
Vol 52 (12) ◽  
pp. 2323-2331 ◽  
Author(s):  
Gregor Dernick ◽  
Stefan Obermüller ◽  
Cyrill Mangold ◽  
Christine Magg ◽  
Hugues Matile ◽  
...  
Keyword(s):  
Size Exclusion Chromatography ◽  
Size Exclusion ◽  
Plasma Lipoproteins ◽  
Reverse Phase ◽  
Protein Arrays ◽  
Phase Protein ◽  
Exclusion Chromatography

scholarly journals Purification of bacteriocins using size-exclusion chromatography

2016 ◽  
Vol 11 (2) ◽  
pp. 281 ◽  
Author(s):  
Vivek K. Bajpai ◽  
Irfan A. Rather ◽  
Alshammari Fanar Hamad
Keyword(s):  
Mass Spectrometry ◽  
Ammonium Sulfate ◽  
Size Exclusion Chromatography ◽  
Size Exclusion ◽  
Ammonium Sulfate Precipitation ◽  
Reverse Phase Hplc ◽  
Reverse Phase ◽  
Cell Free Supernatant ◽  
Video Clips ◽  
Exclusion Chromatography

<p>The bacteriocin purification involves following main steps. a). Extraction of cell-free-supernatant of bacteria. b). Ammonium sulfate precipitation. c). Dialysis. d). Diafiltration using PVP and e). Size-exclusion chromatography. However, depending on the nature of work, the compound could be further analyzed by reverse-phase HPLC, NMR, mass spectrometry and sequencing.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/u1BmWfOTS9w">Part 1</a>: 4 min 52 sec</p><p><a href="https://youtube.com/v/aF45JFnwErc">Part 2</a>: 1 min 47 sec</p>

Size exclusion chromatography of polysaccharides with reverse phase liquid chromatography

2014 ◽  
Vol 1323 ◽  
pp. 97-103 ◽  
Author(s):  
Yan He ◽  
Weiying Hou ◽  
Melissa Thompson ◽  
Heidi Holovics ◽  
Tracy Hobson ◽  
...  
Keyword(s):  
Liquid Chromatography ◽  
Size Exclusion Chromatography ◽  
Size Exclusion ◽  
Reverse Phase ◽  
Reverse Phase Liquid Chromatography ◽  
Exclusion Chromatography ◽  
Phase Liquid

Contribution à l'étude du polymorphisme de quelques métallothionéines par chromatographie liquide de haute performance

1994 ◽  
Vol 72 (5) ◽  
pp. 1238-1245 ◽  
Author(s):  
Guy Bordin ◽  
Fernando Cordeiro Raposo ◽  
Adela-Rosa Rodriguez
Keyword(s):  
Size Exclusion Chromatography ◽  
Rabbit Liver ◽  
Size Exclusion ◽  
Reverse Phase ◽  
Reverse Phase Chromatography ◽  
Exclusion Chromatography

Four commercially available metallothioneins from rabbit liver (RL, RL I, RL II) and from horse kidney (HK) have been studied by size exclusion chromatography and by reverse-phase chromatography, to characterize their polymorphism. The isoforms are detected by UV at 250 nm. Separations by size exclusion show that the metallothioneins are partially dimerized, with molar rates of dimer ranging from 5% for HK to 15% for RL II. The four chromatograms obtained by reverse phase exhibit a different morphology: RL separates in four main isoforms, RL I into two, RL II into three, and HK into two. An attribution of the various peaks for the RL, RL I, and RL II series is proposed. The comparable results obtained by the two methods allow us to estimate that RL is composed of 20–30% RL I and 70–80% of RL II.

CHARACTERIZATION OF A NEW LCAT MUTATION CAUSING FAMILIAL LCAT DEFICIENCY (FLD) AND THE ROLE OF APOE AS A MODIFIER GENE OF THE FLD PHENOTYPE

2009 ◽  
Vol 32 (6S) ◽  
pp. 3
Author(s):  
A Baass ◽  
H Wassef ◽  
M Tremblay ◽  
L Bernier ◽  
R Dufour ◽  
...  
Keyword(s):  
Modifier Gene ◽  
Size Exclusion ◽  
Plasma Lipoproteins ◽  
Lipoprotein Profile ◽  
Exclusion Chromatography ◽  
Low Hdl ◽  
Lcat Deficiency ◽  
Apoe Genotypes

Introduction: LCAT (lecithin:cholesterol acyltransferase ) is an enzyme which plays an essential role in cholesterol esterification and reverse cholesterol transport. Familial LCAT deficiency (FLD) is a disease characterized by a defect in LCAT resulting in extremely low HDL-C, premature corneal opacities, anemia as well as proteinuria and renal failure. Method: We have identified two brothers presenting characteristics of familial LCAT deficiency. We sequenced the LCAT gene, measured the lipid profile as well as the LCAT activity in 15 members of this kindred. We also characterized the plasma lipoproteins by agarose gel electrophoresis and size exclusion chromatography and sequenced several candidate genes related to dysbetalipoproteinemia in this family. Results: We have identified the first French Canadian kindred with familial LCAT deficiency. Two brothers affected by FLD, were homozygous for a novel LCAT mutation. This c.102delG mutation occurs at the codon for His35 causing a frameshift that stops transcription at codon 61 abolishing LCAT enzymatic activity both in vivo and in vitro. It has a dramatic effect on the lipoprotein profile, with an important reduction of HDL-C in both heterozygotes (22%) and homozygotes (88%) and a significant decrease in LDL-C in heterozygotes (35%) as well as homozygotes (58%). Furthermore, the lipoprotein profile differed markedly between the two affected brothers who had different APOE genotypes. We propose that APOE could be an important modifier gene explaining heterogeneity in lipoprotein profiles observed among FLD patients. Our results suggest that a LCAT-/- genotype associated with an APOE ?2 allele could be a novel mechanism leading to dysbetalipoproteinemia.

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