Y. Gu

发表

Analysis of Time Series Gene Expression and DNA Methylation Reveals the Molecular Features of Myocardial Infarction Progression

X. Gu, Changlian Lu, Yanjun Zheng, 2022, Frontiers in Cardiovascular Medicine.

The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila trithorax, to the AF-4 gene

H. Alder, T. Nakamura, E. Canaani, 1992, Cell.

An altered 11-kilobase transcript in leukemic cell lines with the t(4;11)(q21;q23) chromosome translocation.

P. Nowell, C. Bloomfield, T. Nakamura, 1992, Cancer research.

Domains with transcriptional regulatory activity within the ALL1 and AF4 proteins involved in acute leukemia.

C. Croce, T. Nakamura, E. Canaani, 1995, Proceedings of the National Academy of Sciences of the United States of America.

Molecular cloning and characterization of the mouse and human TUSP gene, a novel member of the tubby superfamily.

C. Y. Wang, J. She, S. Eckenrode, 2001, Gene.

The interplay between nonhomologous end-joining and cell cycle checkpoint factors in development, genomic stability, and tumorigenesis.

F. Alt, R. DePinho, N. Sharpless, 2000, Cold Spring Harbor symposia on quantitative biology.

Nonhomologous end-joining proteins are required for V(D)J recombination, normal growth, and neurogenesis.

F. Alt, D. Ferguson, J. Chaudhuri, 1999, Cold Spring Harbor symposia on quantitative biology.

Analysis of the murine All-1 gene reveals conserved domains with human ALL-1 and identifies a motif shared with DNA methyltransferases.

C. Croce, H. Alder, T. Nakamura, 1993, Proceedings of the National Academy of Sciences of the United States of America.

Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs.

P. Nowell, N. Kamada, H. Alder, 1993, Proceedings of the National Academy of Sciences of the United States of America.

The (4;11)(q21;q23) chromosome translocations in acute leukemias involve the VDJ recombinase.

P. Nowell, C. Croce, H. Alder, 1992, Proceedings of the National Academy of Sciences of the United States of America.

ALL-1 partial duplication in acute leukemia.

M. Caligiuri, C. Bloomfield, C. Croce, 1994, Proceedings of the National Academy of Sciences of the United States of America.

Sequence analysis of the breakpoint cluster region in the ALL-1 gene involved in acute leukemia.

C. Croce, H. Alder, T. Nakamura, 1994, Cancer research.

Growth retardation and leaky SCID phenotype of Ku70-deficient mice.

F. Alt, Hwei-Ling Cheng, J. Manis, 1997, Immunity.

Ku70-deficient embryonic stem cells have increased ionizing radiosensitivity, defective DNA end-binding activity, and inability to support V(D)J recombination.

F. Alt, S. Jin, D. Weaver, 1997, Proceedings of the National Academy of Sciences of the United States of America.

Defective embryonic neurogenesis in Ku-deficient but not DNA-dependent protein kinase catalytic subunit-deficient mice.

F. Alt, D. Ferguson, J. Chun, 2000, Proceedings of the National Academy of Sciences of the United States of America.

ALL-1 tandem duplication in acute myeloid leukemia with a normal karyotype involves homologous recombination between Alu elements.

M. Caligiuri, C. Bloomfield, C. Croce, 1994, Cancer research.

Leucine-zipper dimerization motif encoded by the AF17 gene fused to ALL-1 (MLL) in acute leukemia.

C. Croce, K. Huebner, R. Berger, 1994, Proceedings of the National Academy of Sciences of the United States of America.

Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice.

F. Alt, W. Swat, T. Roberts, 2000, Proceedings of the National Academy of Sciences of the United States of America.

Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation.

P. Nowell, C. Croce, K. Huebner, 1993, Cancer research.