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Rona J. Mogil

Researcher at La Jolla Institute for Allergy and Immunology

Publications -  8
Citations -  2291

Rona J. Mogil is an academic researcher from La Jolla Institute for Allergy and Immunology. The author has contributed to research in topics: Apoptosis & T cell. The author has an hindex of 7, co-authored 8 publications receiving 2248 citations.

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Journal ArticleDOI

Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas

TL;DR: This work shows that the Fas/CD95 receptor, which can transduce a potent apoptotic signal when ligated, is rapidly expressed following activation of T-cell hybridomas, as is its functional, membrane-bound ligand8.
Book ChapterDOI

The end of the (cell) line: methods for the study of apoptosis in vitro.

TL;DR: This chapter describes cell death assays that are based on the observation that apoptosis is accompanied by DNA fragmentation, either into the classical “ladder” pattern of 200 bp integer multiples, 50kb fragments, or single-stranded DNA cleavage.
Journal ArticleDOI

Fas (CD95) participates in peripheral T cell deletion and associated apoptosis in vivo

TL;DR: Experiments on peripheral deletion in mice carrying the lpr/lpr defect, which has been shown to be due to defective production of the CD95/Fas molecule, suggest that cells with the highest levels of Fas are preferentially deleted.
Journal ArticleDOI

Role of Acidic Sphingomyelinase in Fas/CD95-mediated Cell Death

TL;DR: Using genetically engineered mice deficient in the aSMase gene (aSMase−/−), it is found that thymocytes, concanavalin A-activated T cells, and lipopolysaccharide-activated B cells derived from both aSMases were equally sensitive to Fas-mediated cell death, triggered by either anti-Fas antibody or Fas ligand in vitro.
Journal Article

Role of DNA fragmentation in T cell activation-induced apoptosis in vitro and in vivo.

TL;DR: An essential role for DNA fragmentation as an irreversible step in activation-induced apoptosis in T cell hybridomas and during T cell development is supported, in which inhibition of DNA fragmentation does not prevent loss of cell viability.