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Your search keyword '"YANG, Chaojie"' showing total 9 results
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9 results on '"YANG, Chaojie"'

1. Lymphocyte activation gene-3-associated protein networks are associated with HDL-cholesterol and mortality in the Trans-omics for Precision Medicine program

Author

Manichaikul, Ani, Lin, Honghuang, Kang, Chansuk, Yang, Chaojie, Rich, Stephen S, Taylor, Kent D, Guo, Xiuqing, Rotter, Jerome I, Craig Johnson, W, Cornell, Elaine, Tracy, Russell P, Peter Durda, J, Liu, Yongmei, Vasan, Ramachandran S, Adrienne Cupples, L, Gerszten, Robert E, Clish, Clary B, Jain, Deepti, Conomos, Matthew P, Blackwell, Thomas, Papanicolaou, George J, and Rodriguez, Annabelle

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Heart Disease, Biotechnology, Human Genome, Heart Disease - Coronary Heart Disease, Clinical Research, Cardiovascular, Atherosclerosis, Aging, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Cholesterol, HDL, Chromatin, Humans, Lymphocyte Activation, Membrane Proteins, Precision Medicine, Biological sciences, Biomedical and clinical sciences
Abstract

Deficiency of the immune checkpoint lymphocyte activation gene-3 (LAG3) protein is significantly associated with both elevated HDL-cholesterol (HDL-C) and myocardial infarction risk. We determined the association of genetic variants within ±500 kb of LAG3 with plasma LAG3 and defined LAG3-associated plasma proteins with HDL-C and clinical outcomes. Whole genome sequencing and plasma proteomics were obtained from the Multi-Ethnic Study of Atherosclerosis (MESA) and the Framingham Heart Study (FHS) cohorts as part of the Trans-Omics for Precision Medicine program. In situ Hi-C chromatin capture was performed in EBV-transformed cell lines isolated from four MESA participants. Genetic association analyses were performed in MESA using multivariate regression models, with validation in FHS. A LAG3-associated protein network was tested for association with HDL-C, coronary heart disease, and all-cause mortality. We identify an association between the LAG3 rs3782735 variant and plasma LAG3 protein. Proteomics analysis reveals 183 proteins significantly associated with LAG3 with four proteins associated with HDL-C. Four proteins discovered for association with all-cause mortality in FHS shows nominal associations in MESA. Chromatin capture analysis reveals significant cis interactions between LAG3 and C1S, LRIG3, TNFRSF1A, and trans interactions between LAG3 and B2M. A LAG3-associated protein network has significant associations with HDL-C and mortality.

Published
2022

2. Whole genome sequence analysis of pulmonary function and COPD in 19,996 multi-ethnic participants.

Author

Zhao, Xutong, Qiao, Dandi, Yang, Chaojie, Kasela, Silva, Kim, Wonji, Ma, Yanlin, Shrine, Nick, Batini, Chiara, Sofer, Tamar, Taliun, Sarah A Gagliano, Sakornsakolpat, Phuwanat, Balte, Pallavi P, Prokopenko, Dmitry, Yu, Bing, Lange, Leslie A, Dupuis, Josée, Cade, Brian E, Lee, Jiwon, Gharib, Sina A, Daya, Michelle, Laurie, Cecelia A, Ruczinski, Ingo, Cupples, L Adrienne, Loehr, Laura R, Bartz, Traci M, Morrison, Alanna C, Psaty, Bruce M, Vasan, Ramachandran S, Wilson, James G, Taylor, Kent D, Durda, Peter, Johnson, W Craig, Cornell, Elaine, Guo, Xiuqing, Liu, Yongmei, Tracy, Russell P, Ardlie, Kristin G, Aguet, François, VanDenBerg, David J, Papanicolaou, George J, Rotter, Jerome I, Barnes, Kathleen C, Jain, Deepti, Nickerson, Deborah A, Muzny, Donna M, Metcalf, Ginger A, Doddapaneni, Harshavardhan, Dugan-Perez, Shannon, Gupta, Namrata, Gabriel, Stacey, Rich, Stephen S, O'Connor, George T, Redline, Susan, Reed, Robert M, Laurie, Cathy C, Daviglus, Martha L, Preudhomme, Liana K, Burkart, Kristin M, Kaplan, Robert C, Wain, Louise V, Tobin, Martin D, London, Stephanie J, Lappalainen, Tuuli, Oelsner, Elizabeth C, Abecasis, Goncalo R, Silverman, Edwin K, Barr, R Graham, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Cho, Michael H, and Manichaikul, Ani

Subjects
NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Lung, Humans, Pulmonary Disease, Chronic Obstructive, Genetic Predisposition to Disease, Intracellular Signaling Peptides and Proteins, Calcium-Binding Proteins, Small Ubiquitin-Related Modifier Proteins, Follow-Up Studies, Feasibility Studies, Polymorphism, Single Nucleotide, Adult, Aged, Aged, 80 and over, Middle Aged, African Americans, Female, Male, Protein Inhibitors of Activated STAT, Respiratory Physiological Phenomena, Genome-Wide Association Study, Genetic Loci, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Whole Genome Sequencing, and over, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive
Abstract

Chronic obstructive pulmonary disease (COPD), diagnosed by reduced lung function, is a leading cause of morbidity and mortality. We performed whole genome sequence (WGS) analysis of lung function and COPD in a multi-ethnic sample of 11,497 participants from population- and family-based studies, and 8499 individuals from COPD-enriched studies in the NHLBI Trans-Omics for Precision Medicine (TOPMed) Program. We identify at genome-wide significance 10 known GWAS loci and 22 distinct, previously unreported loci, including two common variant signals from stratified analysis of African Americans. Four novel common variants within the regions of PIAS1, RGN (two variants) and FTO show evidence of replication in the UK Biobank (European ancestry n ~ 320,000), while colocalization analyses leveraging multi-omic data from GTEx and TOPMed identify potential molecular mechanisms underlying four of the 22 novel loci. Our study demonstrates the value of performing WGS analyses and multi-omic follow-up in cohorts of diverse ancestry.

Published
2020

3. Publisher Correction: Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

4. Publisher Correction: Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

5. Whole genome sequence analysis of pulmonary function and COPD in 19,996 multi-ethnic participants

Author

Zhao, Xutong, Qiao, Dandi, Yang, Chaojie, Kasela, Silva, Kim, Wonji, Ma, Yanlin, Shrine, Nick, Batini, Chiara, Sofer, Tamar, Taliun, Sarah A Gagliano, Sakornsakolpat, Phuwanat, Balte, Pallavi P, Prokopenko, Dmitry, Yu, Bing, Lange, Leslie A, Dupuis, Josée, Cade, Brian E, Lee, Jiwon, Gharib, Sina A, Daya, Michelle, Laurie, Cecelia A, Ruczinski, Ingo, Cupples, L Adrienne, Loehr, Laura R, Bartz, Traci M, Morrison, Alanna C, Psaty, Bruce M, Vasan, Ramachandran S, Wilson, James G, Taylor, Kent D, Durda, Peter, Johnson, W Craig, Cornell, Elaine, Guo, Xiuqing, Liu, Yongmei, Tracy, Russell P, Ardlie, Kristin G, Aguet, François, VanDenBerg, David J, Papanicolaou, George J, Rotter, Jerome I, Barnes, Kathleen C, Jain, Deepti, Nickerson, Deborah A, Muzny, Donna M, Metcalf, Ginger A, Doddapaneni, Harshavardhan, Dugan-Perez, Shannon, Gupta, Namrata, Gabriel, Stacey, Rich, Stephen S, O’Connor, George T, Redline, Susan, Reed, Robert M, Laurie, Cathy C, Daviglus, Martha L, Preudhomme, Liana K, Burkart, Kristin M, Kaplan, Robert C, Wain, Louise V, Tobin, Martin D, London, Stephanie J, Lappalainen, Tuuli, Oelsner, Elizabeth C, Abecasis, Goncalo R, Silverman, Edwin K, Barr, R Graham, Cho, Michael H, and Manichaikul, Ani

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Human Genome, Biotechnology, Lung, Chronic Obstructive Pulmonary Disease, 2.1 Biological and endogenous factors, 2.4 Surveillance and distribution, Aetiology, Respiratory, Good Health and Well Being, Adult, Black or African American, Aged, Aged, 80 and over, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Calcium-Binding Proteins, Feasibility Studies, Female, Follow-Up Studies, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Intracellular Signaling Peptides and Proteins, Male, Middle Aged, Polymorphism, Single Nucleotide, Protein Inhibitors of Activated STAT, Pulmonary Disease, Chronic Obstructive, Respiratory Physiological Phenomena, Small Ubiquitin-Related Modifier Proteins, Whole Genome Sequencing, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group
Abstract

Chronic obstructive pulmonary disease (COPD), diagnosed by reduced lung function, is a leading cause of morbidity and mortality. We performed whole genome sequence (WGS) analysis of lung function and COPD in a multi-ethnic sample of 11,497 participants from population- and family-based studies, and 8499 individuals from COPD-enriched studies in the NHLBI Trans-Omics for Precision Medicine (TOPMed) Program. We identify at genome-wide significance 10 known GWAS loci and 22 distinct, previously unreported loci, including two common variant signals from stratified analysis of African Americans. Four novel common variants within the regions of PIAS1, RGN (two variants) and FTO show evidence of replication in the UK Biobank (European ancestry n ~ 320,000), while colocalization analyses leveraging multi-omic data from GTEx and TOPMed identify potential molecular mechanisms underlying four of the 22 novel loci. Our study demonstrates the value of performing WGS analyses and multi-omic follow-up in cohorts of diverse ancestry.

Published
2020

6. Publisher Correction: Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group
Abstract

The original version of this article contained an error in the name of the author Ramachandran S. Vasan, which was incorrectly given as Vasan S. Ramachandran. This has now been corrected in both the PDF and HTML versions of the article.

Published
2018

7. Publisher Correction: Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group
Abstract

The original version of this article contained an error in the name of the author Ramachandran S. Vasan, which was incorrectly given as Vasan S. Ramachandran. This has now been corrected in both the PDF and HTML versions of the article.

Published
2018

8. Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group, Humans, Cardiovascular Diseases, Lipoprotein(a), Adaptor Proteins, Vesicular Transport, Risk Factors, Gene Expression, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Genome, Human, African Continental Ancestry Group, European Continental Ancestry Group, Cholesterol, LDL, Genome-Wide Association Study, DNA Copy Number Variations, Whole Genome Sequencing, Atherosclerosis, Genetics, Cardiovascular, Prevention, Human Genome, Heart Disease, 2.1 Biological and endogenous factors
Abstract

Lipoprotein(a), Lp(a), is a modified low-density lipoprotein particle that contains apolipoprotein(a), encoded by LPA, and is a highly heritable, causal risk factor for cardiovascular diseases that varies in concentrations across ancestries. Here, we use deep-coverage whole genome sequencing in 8392 individuals of European and African ancestry to discover and interpret both single-nucleotide variants and copy number (CN) variation associated with Lp(a). We observe that genetic determinants between Europeans and Africans have several unique determinants. The common variant rs12740374 associated with Lp(a) cholesterol is an eQTL for SORT1 and independent of LDL cholesterol. Observed associations of aggregates of rare non-coding variants are largely explained by LPA structural variation, namely the LPA kringle IV 2 (KIV2)-CN. Finally, we find that LPA risk genotypes confer greater relative risk for incident atherosclerotic cardiovascular diseases compared to directly measured Lp(a), and are significantly associated with measures of subclinical atherosclerosis in African Americans.

Published
2018

9. Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Author

Zekavat, Seyedeh M, Ruotsalainen, Sanni, Handsaker, Robert E, Alver, Maris, Bloom, Jonathan, Poterba, Timothy, Seed, Cotton, Ernst, Jason, Chaffin, Mark, Engreitz, Jesse, Peloso, Gina M, Manichaikul, Ani, Yang, Chaojie, Ryan, Kathleen A, Fu, Mao, Johnson, W Craig, Tsai, Michael, Budoff, Matthew, Vasan, Ramachandran S, Cupples, L Adrienne, Rotter, Jerome I, Rich, Stephen S, Post, Wendy, Mitchell, Braxton D, Correa, Adolfo, Metspalu, Andres, Wilson, James G, Salomaa, Veikko, Kellis, Manolis, Daly, Mark J, Neale, Benjamin M, McCarroll, Steven, Surakka, Ida, Esko, Tonu, Ganna, Andrea, Ripatti, Samuli, Kathiresan, Sekar, Natarajan, Pradeep, and NHLBI TOPMed Lipids Working Group

Subjects
NHLBI TOPMed Lipids Working Group, Humans, Cardiovascular Diseases, Lipoprotein(a), Adaptor Proteins, Vesicular Transport, Risk Factors, Gene Expression, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Genome, Human, Cholesterol, LDL, Genome-Wide Association Study, DNA Copy Number Variations, Whole Genome Sequencing, White People, Black People, Genetics, Prevention, Heart Disease, Human Genome, Atherosclerosis, Cardiovascular, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being
Abstract

Lipoprotein(a), Lp(a), is a modified low-density lipoprotein particle that contains apolipoprotein(a), encoded by LPA, and is a highly heritable, causal risk factor for cardiovascular diseases that varies in concentrations across ancestries. Here, we use deep-coverage whole genome sequencing in 8392 individuals of European and African ancestry to discover and interpret both single-nucleotide variants and copy number (CN) variation associated with Lp(a). We observe that genetic determinants between Europeans and Africans have several unique determinants. The common variant rs12740374 associated with Lp(a) cholesterol is an eQTL for SORT1 and independent of LDL cholesterol. Observed associations of aggregates of rare non-coding variants are largely explained by LPA structural variation, namely the LPA kringle IV 2 (KIV2)-CN. Finally, we find that LPA risk genotypes confer greater relative risk for incident atherosclerotic cardiovascular diseases compared to directly measured Lp(a), and are significantly associated with measures of subclinical atherosclerosis in African Americans.

Published
2018

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