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Condie E. Carmack

Researcher at Agilent Technologies

Publications -  24
Citations -  4988

Condie E. Carmack is an academic researcher from Agilent Technologies. The author has contributed to research in topics: Antibody & Antigen. The author has an hindex of 19, co-authored 24 publications receiving 4900 citations. Previous affiliations of Condie E. Carmack include University of Colorado Boulder & University of Pennsylvania.

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Resolution and characterization of pro-B and pre-pro-B cell stages in normal mouse bone marrow.

TL;DR: Functional analysis demonstrates that the proliferative response to IL-7, an early B lineage growth factor, is restricted to S7+ stages and, furthermore, that an additional, cell contact-mediated signal is essential for survival of Fr.
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Antigen-specific human antibodies from mice comprising four distinct genetic modifications

TL;DR: Transgenic mice that express human IgM, IgG and Igκ in the absence of mouse IgM or Igκ are developed that contain human sequence transgenes that undergo V(D)J joining, heavy-chain class switching, and somatic mutation to generate a repertoire of human sequence immunoglobulins.
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Expression of anti-DNA immunoglobulin transgenes in non-autoimmune mice.

TL;DR: By generating anti-DNA transgenic mice, the question of whether DNA-specific B cells are regulated in normal (non-autoimmune) mice is addressed and it is suggested that as a consequence of their self-reactive cells being developmentally arrested.
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A transgenic mouse that expresses a diversity of human sequence heavy and light chain immunoglobulins

TL;DR: The transgenic animals described in this paper represent a potential source of human sequence antibodies for in vivo therapeutic applications and the construction of these miniloci and the composition of the CDR3 repertoire generated by the transgenic mice are described.
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Human immunoglobulin transgenes undergo rearrangement, somatic mutation and class switching in mice that lack endogenous IgM.

TL;DR: The upper limit of the cis-acting sequences necessary to direct heavy chain class switching and somatic mutation is defined - the sequences included within the transgene are sufficient to direct class switch recombination of the class-switched heavy chain genes.