Jim Battey

Philip Morris International (Switzerland)

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Philip Leder

Harvard University

Rebecca Taub

Madrigal Pharmaceuticals (United States)

Gilbert Lenoir

Fondation ARC pour la Recherche sur le Cancer

Christopher Moulding

Harvard University

William S. Murphy

Washington University in St. Louis

Lothar Hennighausen

National Institutes of Health

Ulrich Siebenlist

National Institute of Allergy and Infectious Diseases

Huntington Potter

University of Colorado Anschutz Medical Campus

Timothy A. Stewart

University of West Florida

David A. Clayton

University of Leicester

Cooperative Institutions

National Institutes of Health

National Cancer Institute

Harvard University

Philip Morris International (Switzerland)

Howard Hughes Medical Institute

Center for Cancer Research

Brigham and Women's Hospital

The University of Texas Southwestern Medical Center

Johns Hopkins University

Boston Children's Hospital

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

A processed human immunoglobulin epsilon gene has moved to chromosome 9.

Proceedings of the National Academy of Sciences (1982)

Jim Battey Edward E. Max Wesley O. McBride Daniel Swan Philip Leder

Processed genes--genes that resemble processed RNA transcripts rather than interrupted genomic sequences--have been identified as dispersed members of several gene families. Here we describe a processed gene that is one of the three human IgE-like sequences present in the human genome. The processed IgE gene has precisely lost its three intervening sequences, thereby fusing its four coding domains. The homology of the gene to its functional counterpart ends in an adenine-rich tail followed by an 11-base-pair sequence that is directly repeated 150 base pairs 5' to its first coding domain. In addition, the processed gene is located on human chromosome 9 rather than on chromosome 14, the site of the active immunoglobulin locus. The structure and evident mobility of this sequence support the concept that sequences can move about in the genome via RNA intermediates and that processed genes are a prominent feature of genomic structure.

Homology

Coding region

Gene density

Gene prediction

10.1073/pnas.79.19.5956

Cite

Citations (84)

The transcription map of mouse mitochondrial DNA

Cell (1978)

Jim Battey

Heavy strand

Coding strand

Restriction fragment

Transcription bubble

10.1016/0092-8674(78)90309-4

Cite

Citations (90)

Activation and somatic mutation of the translocated c-myc gene in Burkitt lymphoma cells

Cell (1984)

Rebecca Taub Christopher Moulding Jim Battey William S. Murphy Thomas J. Vasicek

Breakpoint

Burkitt's lymphoma

10.1016/0092-8674(84)90227-7

Cite

Citations (335)

TRANSCRIPTION PATTERN OF DROSOPHILA MELANOGASTER MITOCHONDRIAL DNA11This investigation was supported by grant no. NP-9E from the American Cancer Society and grant no. CA-12312-08 from the National Cancer Institute. J.B. and J.L.R.R. are Medical Scientist Training Program Fellows of the National Institute of General Medical Sciences (GM-07365-03) and D.A.C. is a Faculty Research Awardee of the American Cancer Society (FRA-136).

Elsevier eBooks (1979)

Jim Battey John L.R. Rubenstein David A. Clayton

10.1016/b978-0-12-198780-0.50032-5

Cite

Citations (2)

Chromatin structure and protein binding in the putative regulatory region of the c-myc gene in burkitt lymphoma

Cell (1984)

Ulrich Siebenlist Lothar Hennighausen Jim Battey Philip Leder

Burkitt's lymphoma

Lymphoblast

10.1016/0092-8674(84)90368-4

Cite

Citations (443)

Translocalions Among Antibody Genes in Human Cancer

Routledge eBooks (2019)

Philip Leder Jim Battey Gilbert Lenoir Christopher Moulding William S. Murphy

Geneticists have become increasingly aware of the fact that genes move, that they change position within and between chromosomes, and that they thus alter their relationships to one another with important regulatory and structural consequences. The discovery of oncogenes, originally noted as transforming genes carried or activated by retroviruses, combined with a growing understanding of transcriptional control mechanisms, provided the basis for two molecular models that could explain how a translocation might induce malignancy. Both recombinational events occurring during immunocyte maturation have important implications with regard to the regulated expression of the immunoglobulin (Ig) genes. The activity of the c-myc gene as measured by the steady-state level of c-myc mRNA is elevated in a number of human non-Burkitt tumors. The Ig loci involved in the translocations have a very special property: they undergo site- or region-specific recombination that is critical for the development of antibody diversity.

10.4324/9780429050329-30

Cite

Citations (0)

Chromatin Structural Changes in the Putative Regulatory Region of c-myc Accompany the Translocation in a Burkitt Lymphoma

Current topics in microbiology and immunology (1984)

Ulrich Siebenlist Lothar Hennighausen Jim Battey Philip Leder

Immunoglobulin heavy chain

10.1007/978-3-642-69860-6_31

Cite

Citations (1)

Chromatin Structure of the Human c-myc Oncogene: Definition of Regulatory Regions and Changes in Burkitt’s Lymphomas

Hämatologie und Bluttransfusion (1985)

Ulrich Siebenlist Lothar Hennighausen Jim Battey Philip Leder

Transcription

10.1007/978-3-642-70385-0_53

Cite

Citations (1)

A translocated human c-myc oncogene is altered in a conserved coding sequence.

Proceedings of the National Academy of Sciences (1986)

William S. Murphy Jacob Sarid Rebecca Taub Thomas J. Vasicek Jim Battey

We have cloned and characterized a c-myc (now designated MYC) oncogene that had been translocated into the mu switch region of the immunoglobulin heavy chain locus in a Burkitt lymphoma cell line. The breakpoint of the translocation occurs within the first intron of the c-myc gene, thereby separating the untranslocated first exon from the two coding exons. Transcription from the translocated gene arises from a cryptic promoter within the first intron, which produces a 438-nucleotide untranslated 5' region. The amino acid sequence of the protein encoded by the c-myc gene has been substantially altered. In particular, a compensating set of frameshift mutations alters a string of 24 amino acids in a region of the protein tightly conserved in human, mouse, and chicken c-myc genes as well as in the human N-myc and L-myc oncogenes. Despite this, the mutated gene retains a reduced transforming ability in a rat embryo fibroblast focus-formation assay.

Coding region

10.1073/pnas.83.9.2939

Cite

Citations (55)

Structural analysis of both products of a reciprocal translocation between c-myc and immunoglobulin loci in Burkitt lymphoma

Nucleic Acids Research (1985)

Christopher Moulding Aaron P. Rapoport P Goldman Jim Battey Gilbert Lenoir

Journal Article Structural analysis of both products of a reciprocal translocation between c-myc and immunoglobulin loci in Burkitt lymphoma Get access Christopher Moulding, Christopher Moulding Search for other works by this author on: Oxford Academic PubMed Google Scholar Aaron Rapoport, Aaron Rapoport Search for other works by this author on: Oxford Academic PubMed Google Scholar Paula Goldman, Paula Goldman Search for other works by this author on: Oxford Academic PubMed Google Scholar Jim Battey, Jim Battey Search for other works by this author on: Oxford Academic PubMed Google Scholar Gilbert M. Lenoir, Gilbert M. Lenoir 1International Agency for Research on Cancer150 Cours Albert-Thomas, 69372 Lyon, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Philip Leder Philip Leder Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 13, Issue 6, 25 March 1985, Pages 2141–2152, https://doi.org/10.1093/nar/13.6.2141 Published: 25 March 1985 Article history Received: 27 December 1984 Accepted: 05 February 1985 Published: 25 March 1985

Immunoglobulin heavy chain

Recombination signal sequences

Reciprocal

Gene rearrangement

10.1093/nar/13.6.2141

Cite

Citations (16)