Haplionsufficiency of B cell linker protein enhances B cell signaling defects in mice expressing a limiting dosage of Bruton's tyrosine kinase
スポンサーリンク
概要
- 論文の詳細を見る
- 2003-03-01
著者
-
WITTE Owen
Howard Hughes Medical Institute, and Department of Microbiology, Immunology and Molecular Genetics,
-
Satterthwaite Anne
Simmons Arthritis Research Center Department Of Internal Medicine And Center For Immunology Ut South
-
Witte Owen
Howard Hughes Medical Institute And Department Of Microbiology Immunology And Molecular Genetics Uni
-
Chan Andrew
Division Of Rheumatology Department Of Internal Medicine Washington University School Of Medicine
-
WHYBURN Kindsey
Simmons Arthritis Research Center, Department of Internal Medicine and Center for Immunology, UT Sou
-
HALCOMB Kristina
Simmons Arthritis Research Center, Department of Internal Medicine and Center for Immunology, UT Sou
-
CONTRERAS Cristina
Simmons Arthritis Research Center, Department of Internal Medicine and Center for Immunology, UT Sou
-
PAPPU Rajita
Division of Rheumatology, Department of Internal Medicine, Washington University School of Medicine
-
Pappu Rajita
Division Of Rheumatology Department Of Internal Medicine Washington University School Of Medicine
-
Whyburn Kindsey
Simmons Arthritis Research Center Department Of Internal Medicine And Center For Immunology Ut South
-
Halcomb Kristina
Simmons Arthritis Research Center Department Of Internal Medicine And Center For Immunology Ut South
-
Contreras Cristina
Simmons Arthritis Research Center Department Of Internal Medicine And Center For Immunology Ut South
関連論文
- Bruton's tyrosine kinase is required for signaling the CD79b-mediated pro-B to pre-B cell transition
- Haplionsufficiency of B cell linker protein enhances B cell signaling defects in mice expressing a limiting dosage of Bruton's tyrosine kinase