L
Laurie H. Glimcher
Researcher at Harvard University
Publications - 469
Citations - 73810
Laurie H. Glimcher is an academic researcher from Harvard University. The author has contributed to research in topics: T cell & Major histocompatibility complex. The author has an hindex of 135, co-authored 466 publications receiving 68983 citations. Previous affiliations of Laurie H. Glimcher include University Health Network & Cornell University.
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Journal ArticleDOI
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Umut Ozcan,Qiong Cao,Erkan Yilmaz,Ann-Hwee Lee,Neal N. Iwakoshi,Esra Özdelen,Gurol Tuncman,Cem Z. Görgün,Laurie H. Glimcher,Gökhan S. Hotamisligil +9 more
TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).
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A novel transcription factor, T-bet, directs Th1 lineage commitment.
Susanne J. Szabo,Sean T Kim,Gina L. Costa,Xiankui Zhang,C. Garrison Fathman,Laurie H. Glimcher +5 more
TL;DR: T-bet initiates Th1 lineage development from naive Thp cells both by activating Th1 genetic programs and by repressing the opposing Th2 programs, as evidenced by the simultaneous induction of IFNgamma and repression of IL-4 and IL-5.
Journal ArticleDOI
XBP-1 Regulates a Subset of Endoplasmic Reticulum Resident Chaperone Genes in the Unfolded Protein Response
TL;DR: It is suggested that the IRE1/XBP-1 pathway is required for efficient protein folding, maturation, and degradation in the ER and imply the existence of subsets of UPR target genes as defined by their dependence on XBP- 1.
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B7-1 and B7-2 costimulatory molecules activate differentially the Th1/Th2 developmental pathways: Application to autoimmune disease therapy
Vijay K. Kuchroo,Mercy Prabhu Das,Julia A. Brown,Ann M. Ranger,Scott S. Zamvil,Raymond A. Sobel,Howard L. Weiner,Nasrin Nabavi,Laurie H. Glimcher +8 more
TL;DR: Interaction of B 7-1 and B7-2 with shared counterreceptors CD28 and CTLA-4 results in very different outcomes in clinical disease by influencing commitment of precursors to a Th1 or Th2 lineage.
Journal ArticleDOI
XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease
Arthur Kaser,Ann-Hwee Lee,Andre Franke,Jonathan N. Glickman,Sebastian Zeissig,Herbert Tilg,Edward E. S. Nieuwenhuis,Darren E. Higgins,Stefan Schreiber,Laurie H. Glimcher,Richard S. Blumberg +10 more
TL;DR: It is reported that XBP1 deletion in intestinal epithelial cells (IECs) results in spontaneous enteritis and increased susceptibility to induced colitis secondary to both Paneth cell dysfunction and an epithelium that is overly reactive to inducers of IBD such as bacterial products (flagellin) and TNFalpha.