Laurie Glimcher

Laurie H. Glimcher, a member of the National Academy of Sciences, is the incoming Dean of the Weill Cornell Medical College. She will succeed Antonio M. Gotto Jr. in January 2012.[1]

Glimcher is Irene Heinz Given Professor of Immunology at the Harvard School of Public Health, and Professor of Medicine at Harvard Medical School.[2] and is a specialist in osteoporosis.[1] She received her bachelors degree from Radcliffe College in 1972 and her M.D. from Harvard in 1976.

Her research, according to her biography at Harvard, "uses biochemical and genetic approaches to elucidate the molecular pathways that regulate CD4 T helper cell development and activation. ... The Glimcher laboratory defined the genetic bases of both IL-4 and IFNg expression in T cells. They identified the proto-oncogene c-maf as the transcription factor responsible for Th2-specific IL-4 expression [and]...discovered the first Th1-specific transcription factor, T-bet and demonstrated that this single factor is a master-regulator of IFNg gene expression and the Th1 phenotype." [2]

She is reported by the Chronicle of Higher Education to have " extensive ties to two pharmaceutical companies, Merck and Bristol-Myers Squibb.[1][3] According to the New York Times, since 1997 she has been on the Board of Bristol-Myers Squibb , and "received $244,5000 in compensation for 2010" and "1.4 million in deferred share units" [1] Her research at Harvard has been paritally funded by a three-year contract with Merck, "the company that makes Fosamax".[1] She is also on the Board of the Waters Corporation, af lab equipment manufacturer.[1] In this article, she "defended her outside interests, saying they presented no conflict as long as they were transparent. She said she wanted to 'leverage the strengths of everyone,' whether scientists, pharmaceutical companies or biotechnology companies. 'There should be no silos between all of these different strengths,' " [1]

Contents

Memberships

Awards

She was honored by a symposium at Harvard on April 15, 2011, titled " “A Commitment to Lineage: A Symposium in Celebration of Laurie Glimcher,.[4]

Selected recent publications

jointly with other members of her laboratory:
Ho I-C, Hodge MR, Rooney JW, Glimcher LH. 1996. The proto-oncogene c-maf is responsible for tissue-specific expression of interleukin-4. Cell 85:973-83.

Szabo SJ, Kim ST, Costa GL, Zhang X, Fathman GC, Glimcher LH. 2000. A novel transcription factor, T-bet, directs Th1 lineage commitment. Cell 100:655-69.

Reimold AM, Iwakoshi NN, Manis J, Vallabhajosyula P, Szomolanyi-Tsuda E, Gravallese EM, Friend D, Grusby MJ, Alt F, Glimcher LH. 2001. Plasma cell differentiation requires transcription factor XBP-1. Nature 412:300-7.

Szabo SJ, Sullivan BM, Stemmann C, Satoskar AR, Sleckman BP, Glimcher LH. 2002. Distinct effects of T-bet in TH1 lineage commitment and IFN-gamma production in CD4 and CD8 T cells. Science 295:338-42.

Finotto S, Neurath MF, Glickman JN, Qin S, Lehr HA, Green FH, Ackerman K, Haley K, Galle PR, Szabo SJ, Drazen JM, De Sanctis GT, Glimcher LH. 2002. Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet. Science 295:336-8.

Maldonado RA, Irvine DJ, Schreiber R, Glimcher LH. 2004. A role for the immunological synapse in lineage commitment of CD4 lymphocytes. Nature 431:527-32.

Hwang ES, Szabo SJ, Schwartzberg PL, Glimcher LH. 2005. T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3. Science 307:430-3.

Wang J, Fathman JW, Lugo-Villarino G, von Andrian U, Dorfman DM, Glimcher LH. 2006. Transcription factor T-bet regulates inflammatory arthritis through its function in dendritic cells. Journal of Clinical Investigation 16(2):414-21.

Jones DC, Wein MN, Oukka M, Hofstaetter JG, Glimcher MJ, Glimcher LH. 2006. Regulation of adult bone mass by the zinc finger adapter protein Schnurri-3. Science 312(5777):1223-7.

Garrett W, Lord GM, Punit S, Lugo G, Mazmanian S, Ito S, Glickman J, Glimcher LH. 2007. Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. Cell 131:33-45.

Lee Ah, Scapa EF, Cohen DE, Glimcher LH. 2008. Regulation of hepatic lipogenesis by the transcription factor XBP1. Science 320(5882):1492-6.

Kaser A, Lee AH, Franke A, Glickman JN, Zeissig S, Tilg H, Nieuwenhuis EES, Higgins DE, Schreiber S, Glimcher LH, Blumberg RS. 2008. Transcription factor XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease. Cell 134:743-56.

Garrett W, Punit S, Gallini C, Michaud M, Zhang D, Sigrist K, Lord G, Glickman J, Glimcher LH. 2009. Colitis-associated colorectal cancer driven by T-bet deficiency in dendritic cells. Cancer Cell 16(3):208-19.

Hetz C, Thielen P, Matus S, Nassif M, Court F, María Cuervo AM, Martinez G, Kiffin R, Brown R, Glimcher LH. 2009. XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy. Genes and Development 23(19):2294-306. PMCID: 2758741.

Garrett WS, Gordon J, Glimcher LH. 2010. Homeostasis and inflammation in the Intestine. Cell 140(6):859-70.

Greenblatt MB, Shim JH, Zou W, Sitara D, Schweitzer M, Hu D, Lotinun S, Sano Y, Baron R, Park JM, Simon A, Xie M, Schneider MD, Zhai B, Gygi S, Davis R, Glimcher LH. 2010. A p 38 MAPK pathway essential for bone homeostasis.Journal of Clinical Investigation 120(7):2457-73.

Garrett WS, Gallini CA, Yatsunenko T, Michaud M, DuBois A, Delaney ML, Punit S, Karlsson M, Bry L, Glickman JN, Gordon JI, Onderdonk AB, Glimcher LH. 2010. Enterobacteriaceae act in concert with a gut microbiota to induce both spontaneous and maternally-transmitted colitis. Cell Host Microbe (in press).

References

External links