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Richard Longnecker

Researcher at Northwestern University

Publications -  217
Citations -  14947

Richard Longnecker is an academic researcher from Northwestern University. The author has contributed to research in topics: Epstein–Barr virus & Virus. The author has an hindex of 60, co-authored 210 publications receiving 14197 citations. Previous affiliations of Richard Longnecker include University of Michigan & Brigham and Women's Hospital.

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Induction of bcl-2 expression by Epstein-Barr virus latent membrane protein 1 protects infected B cells from programmed cell death.

TL;DR: By DNA transfection into human B cells, it is shown that protection from apoptosis is conferred through expression of a single EBV latent protein, the latent membrane protein LMP 1, and it is demonstrated that L MP 1 mediates this effect by up-regulating expression of the cellular oncogene bcl-2.
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Epstein-Barr Virus LMP2A Drives B Cell Development and Survival in the Absence of Normal B Cell Receptor Signals

TL;DR: LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2a possesses a constitutive signaling activity in nontransformed cells.
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CDC42 and CDC43, two additional genes involved in budding and the establishment of cell polarity in the yeast Saccharomyces cerevisiae.

TL;DR: It is reported here that temperature-sensitive mutants defective in genes CDC42 and CDC43, like cdc24 mutants, fail to bud but continue growth at restrictive temperature, and thus arrest as large unbudded cells, supporting the hypothesis that the events associated with budding and those of the nuclear cycle represent two independent pathways within the cell cycle.
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Herpesvirus entry: an update.

TL;DR: The purpose of this review is to summarize recent findings on the entry of alpha- and gammaherpesviruses and on structure-function studies of their entry receptors and viral ligands.
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Btk/tec kinases regulate sustained increases in intracellular ca2+ following b-cell receptor activation

TL;DR: Results suggest that Btk maintains increased intracellular calcium levels by controlling a Tg‐sensitive, IP3‐gated calcium store(s) that regulates store‐operated calcium entry.