A non-leaky Artemis-deficient mouse that accurately models the human severe combined immune deficiency phenotype, including resistance to hematopoietic stem cell transplantation.
暂无分享,去创建一个
M. Cowan | Kanal Singh | S. Yannone | E. Dunn | Zheng Xiao | Imran S. Khan
[1] M. Nussenzweig,et al. T-independent type II immune responses generate memory B cells , 2006, The Journal of experimental medicine.
[2] Yunmei Ma,et al. The DNA-dependent Protein Kinase Catalytic Subunit Phosphorylation Sites in Human Artemis* , 2005, Journal of Biological Chemistry.
[3] S. Bhattacharyya,et al. B7.2-/- mature dendritic cells generate T-helper 2 and regulatory T donor cells in fetal mice after in utero allogeneic bone marrow transplantation. , 2005, Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation.
[4] David J. Chen,et al. Artemis deficiency confers a DNA double-strand break repair defect and Artemis phosphorylation status is altered by DNA damage and cell cycle progression. , 2005, DNA repair.
[5] A. Feeney,et al. Targeted Disruption of the Artemis Murine Counterpart Results in SCID and Defective V(D)J Recombination That Is Partially Corrected with Bone Marrow Transplantation1 , 2005, The Journal of Immunology.
[6] A. Makrigiannis,et al. Mapping of the BALB/c Ly49 cluster defines a minimal natural killer cell receptor gene repertoire. , 2004, Genomics.
[7] M. Nussenzweig,et al. Ku70/Ku80 and DNA-dependent Protein Kinase Catalytic Subunit Modulate RAG-mediated Cleavage , 2004, Journal of Biological Chemistry.
[8] Goberdhan P Dimri,et al. Control of the Replicative Life Span of Human Fibroblasts by p16 and the Polycomb Protein Bmi-1 , 2003, Molecular and Cellular Biology.
[9] F. Alt,et al. Leaky Scid phenotype associated with defective V(D)J coding end processing in Artemis-deficient mice. , 2002, Molecular cell.
[10] J. Demengeot,et al. A new statistical method for quantitative analyses: application to the precise quantification of T cell receptor repertoires. , 2002, Journal of immunological methods.
[11] E. Salido,et al. A Founder Mutation in Artemis, an SNM1-Like Protein, Causes SCID in Athabascan-Speaking Native Americans1 , 2002, The Journal of Immunology.
[12] M. Gellert. V(D)J recombination: RAG proteins, repair factors, and regulation. , 2002, Annual review of biochemistry.
[13] F. Alt,et al. The Mechanism and Regulation of Chromosomal V(D)J Recombination , 2002, Cell.
[14] Yunmei Ma,et al. Hairpin Opening and Overhang Processing by an Artemis/DNA-Dependent Protein Kinase Complex in Nonhomologous End Joining and V(D)J Recombination , 2002, Cell.
[15] A. Fischer,et al. Artemis, a Novel DNA Double-Strand Break Repair/V(D)J Recombination Protein, Is Mutated in Human Severe Combined Immune Deficiency , 2001, Cell.
[16] H. Pabst,et al. Bone marrow transplantation for T−B− severe combined immunodeficiency disease in Athabascan-speaking native Americans , 2001, Bone Marrow Transplantation.
[17] S. Anderson,et al. Identification of the Ly49L protein: evidence for activating counterparts to inhibitory Ly49 proteins , 2000, Journal of leukocyte biology.
[18] D. Schatz,et al. The RAG proteins and V(D)J recombination: complexes, ends, and transposition. , 2000, Annual review of immunology.
[19] A. Fischer,et al. A new gene involved in DNA double-strand break repair and V(D)J recombination is located on human chromosome 10p. , 2000, Human molecular genetics.
[20] K. Schwarz,et al. DNA ligase IV is essential for V(D)J recombination and DNA double-strand break repair in human precursor lymphocytes. , 1998, Molecular cell.
[21] P. Jeggo,et al. Targeted disruption of the catalytic subunit of the DNA-PK gene in mice confers severe combined immunodeficiency and radiosensitivity. , 1998, Immunity.
[22] M. Lieber,et al. Antigen receptor gene rearrangement. , 1998, Current opinion in immunology.
[23] D. Drayna,et al. The gene for severe combined immunodeficiency disease in Athabascan-speaking Native Americans is located on chromosome 10p. , 1998, American journal of human genetics.
[24] Molly A Bogue,et al. Ku86-Deficient Mice Exhibit Severe Combined Immunodeficiency and Defective Processing of V(D)J Recombination Intermediates , 1996, Cell.
[25] S. Lewis,et al. The mechanism of V(D)J joining: lessons from molecular, immunological, and comparative analyses. , 1994, Advances in immunology.
[26] M. Zöller,et al. The sizes of the CDR3 hypervariable regions of the murine T-cell receptor beta chains vary as a function of the recombined germ-line segments. , 1993, Proceedings of the National Academy of Sciences of the United States of America.