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Patrick G. Hogan

Researcher at Harvard University

Publications -  34
Citations -  7912

Patrick G. Hogan is an academic researcher from Harvard University. The author has contributed to research in topics: NFAT & Transcription factor. The author has an hindex of 27, co-authored 34 publications receiving 7579 citations. Previous affiliations of Patrick G. Hogan include La Jolla Institute for Allergy and Immunology & Boston Children's Hospital.

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Transcriptional regulation by calcium, calcineurin, and NFAT

TL;DR: The NFAT family of transcription factors encompasses five proteins evolutionarily related to the Rel/NF B family, and it is clear that NFAT activates transcription of a large number of genes during an effective immune response.
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Orai1 is an essential pore subunit of the CRAC channel

TL;DR: It is shown that Orai1 is a plasma membrane protein, and that CRAC channel function is sensitive to mutation of two conserved acidic residues in the transmembrane segments, which reduces Ca2+ influx, increases current carried by monovalent cations, and renders the channel permeable to Cs+.
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Structure of the DNA-binding domains from NFAT, Fos and Jun bound specifically to DNA

TL;DR: In this paper, a 2.7-A-resolution crystal structure of the DNA-binding domains of NFAT, Fos and Jun, in a quaternary complex with a DNA fragment containing the distal antigen-receptor response element from the interleukin-2 gene promoter, shows an extended interface between NFAT and AP-1.
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Concerted dephosphorylation of the transcription factor NFAT1 induces a conformational switch that regulates transcriptional activity.

TL;DR: The data suggest that dephosphorylation promotes NFAT1 activation by increasing the probability of an active conformation, in a manner analogous to that by which depolarization increases the open probability of voltage-gated ion channels.
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Isolation of the cyclosporin-sensitive T cell transcription factor NFATp

TL;DR: The molecular cloning of NFATp should allow detailed analysis of a T cell transcription factor that is central to initiation of the immune response.