Surjit K. Datta
Baylor College of Medicine
28 Papers
455 Citations
Surjit K. Datta is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Bone marrow & Adenosine deaminase. The author has an hindex of 11, co-authored 28 publications. Previous affiliations of Surjit K. Datta include University of Texas Health Science Center at Houston & National Institutes of Health.
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Papers
Adenosine Deaminase-deficient Mice Generated Using a Two-stage Genetic Engineering Strategy Exhibit a Combined Immunodeficiency
TL;DR: The use of a two-stage genetic engineering strategy is reported to generate ADA-deficient mice that retain many features associated with ADA deficiency in humans, including a combined immunodeficiency, and these mice have provided in vivo information into the metabolic basis for the immune phenotype associated withADA deficiency.
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The Use of Enzyme Therapy to Regulate the Metabolic and Phenotypic Consequences of Adenosine Deaminase Deficiency in Mice: DIFFERENTIAL IMPACT ON PULMONARY AND IMMUNOLOGIC ABNORMALITIES *
Michael R. Blackburn,Melissa B. Aldrich,Jonathan B. Volmer,Wilma Chen,Hongyan Zhong,Susan J. Kelly,Michael S. Hershfield,Surjit K. Datta,Rodney E. Kellems +8 more
TL;DR: It is suggested that the pulmonary and immune phenotypes are separable and are related to the severity of metabolic disturbances in these tissues and the mechanisms underlying the immunodeficiency and pulmonary phenotypes associated with ADA deficiency.
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Genetic susceptibility and resistance to diet-induced atherosclerosis and hyperlipoproteinemia.
TL;DR: Data indicate that genetic resistance to diet-induced aortic atherosclerosis in mice is correlated with capacity to prevent large increases in serum cholesterol, to suppress abnormal a- and pre-R-migrating lipoproteins, and to maintain elevated serum apolipoprotein E/total lipoprotein protein ratios.
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Diverse Genetic Regulatory Motifs Required for Murine Adenosine Deaminase Gene Expression in the Placenta
Daqing Shi,John H. Winston,Michael R. Blackburn,Surjit K. Datta,Surjit K. Datta,Gerri Hanten,Rodney E. Kellems +6 more
TL;DR: It is found that multiple protein binding motifs are necessary for Ada expression in the placenta, and mutations in the potential protein binding sites and footprinting regions resulted in loss of placental expression in transgenic mice.
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Metabolic and Immunologic Consequences of Limited Adenosine Deaminase Expression in Mice
TL;DR: Mice with limited ADA expression exhibited profound disturbances in purine metabolism, including thymus-specific accumulations of deoxyadenosine and dATP, and inhibition of S-adenosylhomocysteine hydrolase in theThymus, spleen, and, to a lesser extent, the liver.
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