2,966 research outputs found
Colin Humphris
"Colin Humphris 2 Sqdrn. RAAF. 1941 - 1942 Author of - 'Trapped on Timor' (as a result of bombing of Darwin Feb. 19, 1942)".Colin Humphris. 2 Squadron, Royal Australian Air Force 1941 - 1942. Author of - 'Trapped on Timor' (as a result of bombing of Darwin February 19, 1942)
Interview with Colin Wilson, part 4, undated
Interview with Colin Wilson, part 4, features an interview with author Colin Wilson in which he discusses his views regarding society and art, his reclusive nature, and the intellectual and fantastical elements of his works, undated
Interview with Colin Wilson, part 2, undated
Interview with Colin Wilson, part 2, features an interview with author Colin Wilson in which he discusses his views regarding society and art, his reclusive nature, and the intellectual and fantastical elements of his works, undated
Providence College Faculty Author Series 2017-2018: D. Colin Jaundrill
In this installment of the Faculty Authors Series, D. Colin Jaundrill (History, Providence College) discusses his newest book, Samurai to Soldier: Remaking Military Service in Nineteenth-Century Japan
Providence College Faculty Author Series 2017-2018: D. Colin Jaundrill
In this installment of the Faculty Authors Series, D. Colin Jaundrill (History, Providence College) discusses his newest book, Samurai to Soldier: Remaking Military Service in Nineteenth-Century Japan
The cytotoxic lymphocyte protease, granzyme B, targets the cytoskeleton and perturbs microtubule polymerization dynamics
Granzyme B, a serine protease derived from cytotoxic T lymphocyte (CTL) and Natural Killer (NK) cell granules, plays an important role in coordinating apoptosis of CTL and NK target cells. Here, we report that granzyme B targets the cytoskeleton by cleaving and removing the acidic C-terminal tail of alpha-tubulin. Consistent with this, Granzyme B markedly enhanced rates of microtubule polymerization in vitro, most likely by removal of an autoinhibitory domain within the tubulin C terminus. Moreover, delivery of Granzyme B into HeLa target cells promoted dramatic reorganization of the microtubule network in a caspase-independent manner. These data reveal that granzyme B directly attacks a major component of the cell cytoskeleton, which may contribute to the incapacitation of target cells during CTL/NK-mediated killing
Interview with Colin Jerolmack
Colin Jerolmack is an Assistant Professor at New York University
in Sociology and Environmental Studies. He is the author of The
Global Pigeon (forthcoming) and an alumnus of the Robert Wood
Johnson Foundation Scholars in Health Policy Program at Harvard
University
Human and murine granzyme B exhibit divergent substrate preferences
The cytotoxic lymphocyte protease granzyme B (GzmB) can promote apoptosis through direct processing and activation of members of the caspase family. GzmB can also cleave the BH3-only protein, BID, to promote caspase-independent mitochondrial permeabilization. Although human and mouse forms of GzmB exhibit extensive homology, these proteases diverge at residues predicted to influence substrate binding. We show that human and mouse GzmB exhibit radical differences in their ability to cleave BID, as well as several other key substrates, such as ICAD and caspase-8. Moreover, pharmacological inhibition of caspases clonogenically rescued human and mouse target cells from apoptosis initiated by mouse GzmB, but failed to do so in response to human GzmB. These data demonstrate that human and murine GzmB are distinct enzymes with different substrate preferences. Our observations also illustrate how subtle differences in enzyme structure can radically affect substrate selection
Meeting Report – proteostasis in Ericeira
ABSTRACT
It was a sunny Ericeira, in Portugal, that received the participants of the EMBO Workshop on Proteostasis, from 17 to 21 November 2017. Most participants gave talks or presented posters concerning their most recent research results, and lively scientific discussions occurred against the backdrop of the beautiful Atlantic Ocean.
Proteostasis is the portmanteau of the words protein and homeostasis, and it refers to the biological mechanisms controlling the biogenesis, folding, trafficking and degradation of proteins in cells. An imbalance in proteostasis can lead to the accumulation of misfolded proteins or excessive protein degradation, and is associated with many human diseases. A wide variety of research approaches are used to identify the mechanisms that regulate proteostasis, typically involving different model organisms (yeast, invertebrates or mammalian systems) and different methodologies (genetics, biochemistry, biophysics, structural biology, cell biology and organismal biology). Around 140 researchers in the proteostasis field met in the Hotel Vila Galé, Ericeira, Portugal for the EMBO Workshop in Proteostasis, organized by Pedro Domingos (ITQB-NOVA, Oeiras, Portugal) and Colin Adrain (IGC, Oeiras, Portugal). In this report, we attempt to review and integrate the ideas that emerged at the workshop. Owing to space restrictions, we could not cover all talks or posters and we apologize to the colleagues whose presentations could not be discussed.</jats:p
Colin Fraser
Photograph - Colin Fraser (third from right) in a loaded scow leaving for Fort Chipewyan from Athabasca, Alberta. A group of men are also standing on the pie
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