Search

Your search keyword '"Chang, Deh-Ming"' showing total 452 results
Start Over Author "Chang, Deh-Ming"
452 results on '"Chang, Deh-Ming"'

2. Genetic associations of leptin-related polymorphisms with systemic lupus erythematosus

Author

Zhao, Jian, Wu, Hui, Langefeld, Carl D, Kaufman, Kenneth M, Kelly, Jennifer A, Bae, Sang-Cheol, networks, Marta E Alarcón-Riquelme for the BIOLUPUS and GENLES, Alarcón, Graciela S, Anaya, Juan-Manuel, Criswell, Lindsey A, Freedman, Barry I, Kamen, Diane L, Gilkeson, Gary S, Jacob, Chaim O, James, Judith A, Merrill, Joan T, Gaffney, Patrick M, Sivils, Kathy Moser, Niewold, Timothy B, Petri, Michelle A, Song, Seung Taek, Jeong, Hye-jin, Ramsey-Goldman, Rosalind, Reveille, John D, Scofield, R Hal, Stevens, Anne M, Boackle, Susan A, Vilá, Luis M, Chang, Deh-Ming, Song, Yeong Wook, Vyse, Timothy J, Harley, John B, Brown, Elizabeth E, Edberg, Jeffrey C, Kimberly, Robert P, Hahn, Bevra H, Grossman, Jennifer M, Tsao, Betty P, and La Cava, Antonio

Subjects
Biomedical and Clinical Sciences, Immunology, Clinical Research, Autoimmune Disease, Genetic Testing, Genetics, Lupus, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Case-Control Studies, Genetic Predisposition to Disease, Genotype, Humans, Leptin, Lupus Erythematosus, Systemic, Polymorphism, Single Nucleotide, Systemic lupus erythematosus, Leptin pathway, Gene polymorphisms, Marta E. Alarcón-Riquelme for the BIOLUPUS and GENLES networks
Abstract

Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE.

Published
2015

5. Fine mapping of Xq28: both MECP2 and IRAK1 contribute to risk for systemic lupus erythematosus in multiple ancestral groups

Author

Kaufman, Kenneth M, Zhao, Jian, Kelly, Jennifer A, Hughes, Travis, Adler, Adam, Sanchez, Elena, Ojwang, Joshua O, Langefeld, Carl D, Ziegler, Julie T, Williams, Adrienne H, Comeau, Mary E, Marion, Miranda C, Glenn, Stuart B, Cantor, Rita M, Grossman, Jennifer M, Hahn, Bevra H, Song, Yeong Wook, Yu, Chack-Yung, James, Judith A, Guthridge, Joel M, Brown, Elizabeth E, Alarcón, Graciela S, Kimberly, Robert P, Edberg, Jeffrey C, Ramsey-Goldman, Rosalind, Petri, Michelle A, Reveille, John D, Vilá, Luis M, Anaya, Juan-Manuel, Boackle, Susan A, Stevens, Anne M, Freedman, Barry I, Criswell, Lindsey A, Group, Bernardo A Pons-Estel on behalf of the Argentine Collaborative, Lee, Joo-Hyun, Lee, Ji-Seon, Chang, Deh-Ming, Scofield, R Hal A, Gilkeson, Gary S, Merrill, Joan T, Niewold, Timothy B, Vyse, Timothy James, Bae, Sang-Cheol, network, Marta E Alarcón-Riquelme on behalf of the BIOLUPUS, Jacob, Chaim O, Sivils, Kathy Moser, Gaffney, Patrick M, Harley, John B, Sawalha, Amr H, and Tsao, Betty P

Subjects
Human Genome, Autoimmune Disease, Lupus, Genetics, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Base Sequence, Chromosome Mapping, Chromosomes, Human, X, Genetic Predisposition to Disease, Genotype, Haplotypes, Humans, Interleukin-1 Receptor-Associated Kinases, Lupus Erythematosus, Systemic, Methyl-CpG-Binding Protein 2, Molecular Sequence Data, Polymorphism, Single Nucleotide, Racial Groups, Real-Time Polymerase Chain Reaction, Risk Factors, Argentine Collaborative Group, BIOLUPUS network, Clinical Sciences, Immunology, Public Health and Health Services, Arthritis & Rheumatology
Abstract

ObjectivesThe Xq28 region containing IRAK1 and MECP2 has been identified as a risk locus for systemic lupus erythematosus (SLE) in previous genetic association studies. However, due to the strong linkage disequilibrium between IRAK1 and MECP2, it remains unclear which gene is affected by the underlying causal variant(s) conferring risk of SLE.MethodsWe fine-mapped ≥136 SNPs in a ∼227 kb region on Xq28, containing IRAK1, MECP2 and seven adjacent genes (L1CAM, AVPR2, ARHGAP4, NAA10, RENBP, HCFC1 and TMEM187), for association with SLE in 15 783 case-control subjects derived from four different ancestral groups.ResultsMultiple SNPs showed strong association with SLE in European Americans, Asians and Hispanics at p

Published
2013

6. Brief Report: Single‐nucleotide polymorphisms in VKORC1 are risk factors for systemic lupus erythematosus in Asians

Author

Kaiser, Rachel, Taylor, Kimberly E, Deng, Yun, Zhao, Jian, Li, Yonghong, Nititham, Joanne, Chang, Monica, Catanese, Joseph, Begovich, Ann B, Brown, Elizabeth E, Edberg, Jeffrey C, McGwin, Gerald, Alarcón, Graciela S, Ramsey‐Goldman, Rosalind, Reveille, John D, Vila, Luis M, Petri, Michelle, Kimberly, Robert P, Feng, Xuebing, Sun, Lingyun, Shen, Nan, Li, Wei, Lu, Jian‐Xin, Wakeland, Edward K, Li, Quan‐Zhen, Yang, Wanling, Lau, Yu‐Lung, Liu, Fei‐Lan, Chang, Deh‐Ming, Yu, Chack‐Yung, Song, Yeong W, Group, Hwee Siew Howe and the Tan Tock Seng Hospital Systemic Lupus Erythematosus Study, Tsao, Betty P, and Criswell, Lindsey A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Health Sciences, Genetics, Autoimmune Disease, Lupus, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Adult, Asian People, Case-Control Studies, Female, Genetic Predisposition to Disease, Genotype, Hemostasis, Humans, Lupus Erythematosus, Systemic, Male, Middle Aged, Mixed Function Oxygenases, Polymorphism, Single Nucleotide, Risk Factors, Venous Thrombosis, Vitamin K Epoxide Reductases, Hwee Siew Howe and the Tan Tock Seng Hospital Systemic Lupus Erythematosus Study Group, Clinical Sciences, Immunology, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectiveThe increased risk of thrombosis in systemic lupus erythematosus (SLE) may be partially explained by interrelated genetic pathways for thrombosis and SLE. The present study was undertaken to investigate whether 33 established and novel single-nucleotide polymorphisms (SNPs) in 20 genes involved in hemostasis pathways that have been associated with deep venous thrombosis (DVT) in the general population are risk factors for SLE among Asian subjects.MethodsPatients in the discovery cohort were enrolled in 1 of 2 North American SLE cohorts. Patients in the replication cohort were enrolled in 1 of 4 Asian or 2 North American cohorts. We first genotyped 263 Asian patients with SLE and 357 healthy Asian control subjects for 33 SNPs in the discovery phase, and then genotyped 5 SNPs in up to an additional 1,496 patients and 993 controls in the replication phase. Patients were compared to controls for bivariate association with minor alleles. Principal components analysis was used to control for intra-Asian ancestry in the replication cohort.ResultsTwo genetic variants in the gene VKORC1 were highly significant in both the discovery and replication cohorts: rs9934438 (in the discovery cohort, odds ratio [OR] 2.45, P=2×10(-9); in the replication cohort, OR 1.54, P=4×10(-6)) and rs9923231 (in the discovery cohort, OR 2.40, P=6×10(-9); in the replication cohort, OR 1.53, P=5×10(-6)). These associations were significant in the replication cohort after adjustment for intra-Asian ancestry: for rs9934438, OR 1.34, P=0.0029; for rs9923231, OR 1.34, P=0.0032.ConclusionGenetic variants in VKORC1, which are involved in vitamin K reduction and associated with DVT, correlate with SLE development in Asian subjects. These results suggest that there may be intersecting genetic pathways for the development of SLE and thrombosis.

Published
2013

7. SUMO-defective c-Maf preferentially transactivates Il21 to exacerbate autoimmune diabetes

Author

Hsu, Chao-Yuan, Yeh, Li-Tzu, Fu, Shin-Huei, Chien, Ming-Wei, Liu, Yu-Wen, Miaw, Shi-Chuen, Chang, Deh-Ming, and Sytwu, Huey- Kang

Subjects
Diabetes mellitus -- Genetic aspects -- Development and progression -- Care and treatment, Cellular proteins -- Health aspects, Interleukin-21 -- Health aspects, Transcription factors -- Health aspects, Gene expression -- Health aspects, Health care industry
Abstract

SUMOylation is involved in the development of several inflammatory diseases, but the physiological significance of SUMOmodulated c-Maf in autoimmune diabetes is not completely understood. Here, we report that an age-dependent attenuation of c-Maf SUMOylation in [CD4.sup.+] T cells is positively correlated with the IL-21-mediated diabetogenesis in NOD mice. Using 2 strains of T cell-specific transgenic NOD mice overexpressing wild-type c-Maf (Tg-WTc) or SUMOylation site-mutated c-Maf (Tg-KRc), we demonstrated that Tg-KRc mice developed diabetes more rapidly than Tg-WTc mice in a [CD4.sup.+] T cell- autonomous manner. Moreover, SUMO-defective c-Maf preferentially transactivated Il21 to promote the development of [CD4.sup.+] T cells with an extrafollicular helper T cell phenotype and expand the numbers of granzyme B- producing effector/memory [CD8.sup.+] T cells. Furthermore, SUMO-defective c-Maf selectively inhibited recruitment of Daxx/HDAC2 to the II21 promoter and enhanced histone acetylation mediated by CREB-binding protein (CBP) and p300. Using pharmacological interference with CBP/p300, we illustrated that CBP30 treatment ameliorated c-Maf-mediated/IL-21-based diabetogenesis. Taken together, our results show that the SUMOylation status of c-Maf has a stronger regulatory effect on IL-21 than the level of c-Maf expression, through an epigenetic mechanism. These findings provide new insights into how SUMOylation modulates the pathogenesis of autoimmune diabetes in a T cell-restricted manner and on the basis of a single transcription factor., Introduction The conjugation of small ubiquitin-like modifier (SUMO) to specific lysine residues of cellular proteins is a dynamic and reversible posttranslational modification (1). Deficiencies in SUMOylation enzymes have been reported [...]

Published
2018
Full Text
View/download PDF

18. Sex-specific association of X-linked Toll-like receptor 7 (TLR7) with male systemic lupus erythematosus

Author

Shen, Nan, Fu, Qiong, Deng, Yun, Qian, Xiaoxia, Zhao, Jian, Kaufman, Kenneth M., Wu, Yee Ling, Yu, C. Yung, Tang, Yuanjia, Chen, Ji-Yih, Yang, Wanling, Wong, Maida, Kawasaki, Aya, Tsuchiya, Naoyuki, Sumida, Takayuki, Kawaguchi, Yasushi, Howe, Hwee Siew, Mok, Mo Yin, Bang, So-Young, Liu, Fei-Lan, Chang, Deh-Ming, Takasaki, Yoshinari, Hashimoto, Hiroshi, Harley, John B., Guthridge, Joel M., Grossman, Jennifer M., Cantor, Rita M., Song, Yeong Wook, Bae, Sang-Cheol, Chen, Shunle, Hahn, Bevra H., Lau, Yu Lung, Tsao, Betty P., and Smith, Kenneth G. C.

Published
2010

19. Association of a Common Complement Receptor 2 Haplotype with Increased Risk of Systemic Lupus Erythematosus

Author

Wu, Hui, Boackle, Susan A., Hanvivadhanakul, Punchong, Ulgiati, Daniela, Grossman, Jennifer M., Lee, Youngho, Shen, Nan, Abraham, Lawrence J., Mercer, Timothy R., Park, Elly, Hebert, Lee A., Rovin, Brad H., Birmingham, Dan J., Chang, Deh-Ming, Chen, Chung Jen, McCurdy, Deborah, Badsha, Humeira M., Thong, Bernard Y. H., Chng, Hiok H., Arnett, Frank C., Wallace, Daniel J., Yu, C. Yung, Hahn, Bevra H., Cantor, Rita M., and Tsao, Betty P.

Published
2007
Full Text
View/download PDF

34. Association of a common complement receptor 2 haplotype with increased risk of systemic lupus erythematosus

Author

Wua, Hui, Boackle, Susan A., Hanvivadhanakul, Punchong, Ulgiati, Daniela, Grossman, Jennifer M., Lee, Youngho, Shen, Nan, Abraham, Lawrence J., Mercer, Timothy R., Park, Elly, Hebert, Lee A., Rovin, Brad H., Birmingham, Dan J., Chang, Deh-Ming, Cheng, Chung Jen, McCurdy, Deborah, Badsha, Humeira M., Thong, Bernard Y.H., Chng, Hiok H., Arnett, Frank C., Wallace, Daniel J., Yu, C. Yung, Hahn, Bevra H., Cantor, Rita M., and Tsao, Betty P.

Subjects
Systemic lupus erythematosus -- Research, Single nucleotide polymorphisms -- Research, Disease susceptibility -- Research, Complement (Immunology) -- Research, Science and technology
Abstract

A genomic region on distal mouse chromosome 1 and its syntenic human counterpart 1q23-42 show strong evidence of harboring lupus susceptibility genes. We found evidence of linkage at 1q32.2 in a targeted genome scan of 1q21-43 in 126 lupus multiplex families containing 151 affected sibpairs (nonparametric linkage score 2.52, P = 0.006). A positional candidate gene at 1q32.2, complement receptor 2 (CR2), is also a candidate in the murine Sle1c lupus susceptibility locus. To explore its role in human disease, we analyzed 1,416 individuals from 258 Caucasian and 142 Chinese lupus simplex families and demonstrated that a common three-single-nucleotide polymorphism CR2 haplotype (rs3813946, rs1048971, rs17615) was associated with lupus susceptibility (P = 0.00001) with a 1.54-fold increased risk for the development of disease. Single-nucleotide polymorphism 1 (rs3813946), located in the 5' untranslated region of the CR2 gene, altered transcriptional activity, suggesting a potential mechanism by which CR2 could contribute to the development of lupus. Our findings reveal that CR2 is a likely susceptibility gene for human lupus at 1q32.2, extending previous studies suggesting that CR2 participates in the pathogenesis of systemic lupus erythematosus. linkage | disease susceptibility | antoimmunity | single-nucleotide polymorphisms | syntenic conservation

Published
2007

37. MRI Contributes to Accurate and Early Diagnosis of Non-Radiographic HLA-B27 Negative Axial Spondyloarthritis

Author

LU, CHUN-CHI, primary, Huang, Guo-Shu, additional, Lee, Tony Szu-Hsien, additional, Chao, En, additional, Chen, Hsiang-Cheng, additional, Yong-Si, Guo, additional, Shi-Jye, Chu, additional, Feng-Cheng, Liu, additional, Kao, San-Yuan, additional, Hou, Tsung-Yun, additional, Chen, Chen-Hung, additional, Chang, Deh-Ming, additional, and Lyu, Sin-Yi, additional

Published
2020
Full Text
View/download PDF

41. Association of PPP2CA polymorphisms with systemic lupus erythematosus susceptibility in multiple ethnic groups

Author

Tan, Wenfeng, Sunahori, Katsue, Zhao, Jian, Deng, Yun, Kaufman, Kenneth M., Kelly, Jennifer A., Langefeld, Carl D., Williams, Adrienne H., Comeau, Mary E., Ziegler, Julie T., Marion, Miranda C., Bae, Sang-Cheol, Lee, Joo Hyun, Lee, Ji-Seon, Chang, Deh-Ming, Song, Yeong Wook, Yu, Chack-Yung, Kimberly, Robert P., Edberg, Jeffrey C., Brown, Elizabeth E., Petri, Michelle A., Ramsey-Goldman, Rosalind, Vilá, Luis M., Reveille, John D., Alarcón-Riquelme, Marta E., Harley, John B., Boackle, Susan A., Stevens, Anne M., Scofield, Hal R., Merrill, Joan T., Freedman, Barry I., Anaya, Juan-Manuel, Criswell, Lindsey A., Jacob, Chaim O., Vyse, Timothy J., Niewold, Timothy B., Gaffney, Patrick M., Moser, Kathy L., Gilkeson, Gary S., Kamen, Diane L., James, Judith A., Grossman, Jennifer M., Hahn, Bevra H., Tsokos, George C., and Tsao, Betty P.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results