scholarly journals Erratum: Statin-induced expression change of INSIG1 in lymphoblastoid cell lines correlates with plasma triglyceride statin response in a sex-specific manner

2016 ◽  
Vol 16 (3) ◽  
pp. 301-301 ◽  
Author(s):  
E Theusch ◽  
K Kim ◽  
K Stevens ◽  
J D Smith ◽  
Y-DI Chen ◽  
...  
Keyword(s):  
Cell Lines ◽  
Plasma Triglyceride ◽  
Lymphoblastoid Cell Lines ◽  
Expression Change ◽  
Induced Expression ◽  
Specific Manner ◽  
Statin Response

scholarly journals Identifying genetic modulators of statin response using subject-derived lymphoblastoid cell lines

2021 ◽  
Author(s):  
Yu-Lin Kuang ◽  
Elizabeth Theusch ◽  
Ronald M Krauss ◽  
Marisa W Medina
Keyword(s):  
Adverse Effects ◽  
Cell Lines ◽  
Significant Risk ◽  
Density Lipoprotein ◽  
Statin Treatment ◽  
Interindividual Variation ◽  
Lipid Lowering ◽  
Lymphoblastoid Cell Lines ◽  
Increased Risk ◽  
Statin Response

Although statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) have proven effective in reducing plasma low-density lipoprotein levels and risk of cardiovascular disease, their lipid lowering efficacy is highly variable among individuals. Furthermore, statin treatment carries a small but significant risk of adverse effects, most notably myopathy and new onset diabetes. Hence, identification of biomarkers for predicting patients who would most likely benefit from statin treatment without incurring increased risk of adverse effects can have a significant public health impact. In this review, we discuss the rationale for the use of subject-derived lymphoblastoid cell lines in studies of statin pharmacogenomics and describe a variety of approaches we have employed to identify novel genetic markers associated with interindividual variation in statin response.

scholarly journals Genetic variants modulate gene expression statin response in human lymphoblastoid cell lines

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Elizabeth Theusch ◽  
Yii-Der I. Chen ◽  
Jerome I. Rotter ◽  
Ronald M. Krauss ◽  
Marisa W. Medina
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Genetic Variants ◽  
Lymphoblastoid Cell Lines ◽  
Human Lymphoblastoid Cell ◽  
Human Lymphoblastoid Cell Lines ◽  
Statin Response

MicroRNAs in Human Lymphoblastoid Cell Lines

2012 ◽  
Vol 22 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Sung-Mi Shim ◽  
Hye-Young Nam ◽  
Jae-Eun Lee ◽  
Jun-Woo Kim ◽  
Bok-Ghee Han ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
Human Lymphoblastoid Cell ◽  
Human Lymphoblastoid Cell Lines

scholarly journals No defect in G1/S cell cycle arrest in irradiated Li-Fraumeni lymphoblastoid cell lines

1996 ◽  
Vol 74 (5) ◽  
pp. 698-703 ◽  
Author(s):  
KJ Williams ◽  
J Heighway ◽  
JM Birch ◽  
JD Norton ◽  
D Scott
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
Cycle Arrest ◽  
Li Fraumeni

scholarly journals Focal segmental glomerulosclerosis is associated with a PDSS2 haplotype and, independently, with a decreased content of coenzyme Q10

2013 ◽  
Vol 305 (8) ◽  
pp. F1228-F1238 ◽  
Author(s):  
David L. Gasser ◽  
Cheryl A. Winkler ◽  
Min Peng ◽  
Ping An ◽  
Louise M. McKenzie ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Cell Lines ◽  
Coenzyme Q ◽  
Lymphoblastoid Cell Lines ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Collapsing Glomerulopathy ◽  
Segmental Glomerulosclerosis ◽  
Increased Risk ◽  
Common Causes

Focal segmental glomerulosclerosis (FSGS) and collapsing glomerulopathy are common causes of nephrotic syndrome. Variants in >20 genes, including genes critical for mitochondrial function, have been associated with these podocyte diseases. One such gene, PDSS2, is required for synthesis of the decaprenyl tail of coenzyme Q10 (Q10) in humans. The mouse gene Pdss2 is mutated in the kd/kd mouse model of collapsing glomerulopathy. We examined the hypothesis that human PDSS2 polymorphisms are associated with podocyte diseases. We genotyped 377 patients with primary FSGS or collapsing glomerulopathy, together with 900 controls, for 9 single-nucleotide polymorphisms in the PDSS2 gene in a case-control study. Subjects included 247 African American (AA) and 130 European American (EA) patients and 641 AA and 259 EA controls. Among EAs, a pair of proxy SNPs was significantly associated with podocyte disease, and patients homozygous for one PDSS2 haplotype had a strongly increased risk for podocyte disease. By contrast, the distribution of PDSS2 genotypes and haplotypes was similar in AA patients and controls. Thus a PDSS2 haplotype, which has a frequency of 13% in the EA control population and a homozygote frequency of 1.2%, is associated with a significantly increased risk for FSGS and collapsing glomerulopathy in EAs. Lymphoblastoid cell lines from FSGS patients had significantly less Q10 than cell lines from controls; contrary to expectation, this finding was independent of PDSS2 haplotype. These results suggest that FSGS patients have Q10 deficiency and that this deficiency is manifested in patient-derived lymphoblastoid cell lines.

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