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Adrian F. Arechiga
Researcher at University of California, Irvine
Publications - 14
Citations - 1212
Adrian F. Arechiga is an academic researcher from University of California, Irvine. The author has contributed to research in topics: FADD & Death domain. The author has an hindex of 10, co-authored 14 publications receiving 1156 citations. Previous affiliations of Adrian F. Arechiga include Benaroya Research Institute.
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Journal ArticleDOI
Genetic Variation in PTPN22 Corresponds to Altered Function of T and B Lymphocytes
Mary Rieck,Adrian F. Arechiga,Suna Onengut-Gumuscu,Carla J. Greenbaum,Patrick Concannon,Jane H. Buckner +5 more
TL;DR: It is demonstrated that homozygosity for this variant results in a profound deficit in T cell responsiveness to Ag stimulation, and the presence of the variant allele is associated with an increase in circulating memory T cells.
Journal ArticleDOI
FADD and caspase-8 control the outcome of autophagic signaling in proliferating T cells
Bryan D. Bell,Sabrina Leverrier,Brian M. Weist,Ryan H. Newton,Adrian F. Arechiga,Keith A. Luhrs,Naomi S. Morrissette,Craig M. Walsh +7 more
TL;DR: It is suggested that FADD and casp8 form a feedback loop to limit autophagy and prevent this salvage pathway from inducing RIPK1-dependent necroptotic cell death, thereby averting necrosis and inflammation in vivo.
Journal ArticleDOI
Cutting Edge: The PTPN22 Allelic Variant Associated with Autoimmunity Impairs B Cell Signaling
Adrian F. Arechiga,Tania Habib,Yantao He,Xian Zhang,Zhong Yin Zhang,Andrew Funk,Jane H. Buckner +6 more
TL;DR: It is shown that B cell signal transduction is impaired in individuals who express the PTPN22 1858T variant, which is suggested to alter BCR signaling and implicate B cells in the mechanism by which the P TPN22 2018T variant contributes to autoimmunity.
Journal Article
Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin.
TL;DR: Results suggest that Bcr-Abl may regulate translation of critical targets in CML cells via mTOR, and provide a rationale for testing the combination of mTOR inhibitors with the Abl kinase inhibitor imatinib in patients with CML.
Journal ArticleDOI
The requirements for Fas-associated death domain signaling in mature T cell activation and survival.
TL;DR: Results show that, in a highly regulated fashion, FADD, and most likely caspases, can transduce either a signal for survival or one that leads directly to apoptosis and that the balance between these opposing outcomes is crucial to adaptive immunity.