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Harvey F. Lodish, PhD
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Member, Whitehead Institute
Professor of Biology, MIT
Professor of Bioengineering, MIT
617.258.5216 phone
617.258.6768 fax
lodish@wi.mit.edu
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A leader in the field of membrane biology, Harvey F.
Lodish has isolated and cloned numerous proteins that
reside on the surface of cells and play a role in cell
growth, glucose transport, and fatty acid transport.
His results have important implications for the treatment
of cancer, diabetes, heart disease, and obesity. [
lodish research 220 kbps QuickTime]
Selected Achievements
• Isolated key genes involved in diabetes,
hypertension, leukemia, and obesity
• Lead author of the textbook Molecular Cell
Biology, now in its fifth edition and translated
into six languages
• Fellow of American Association for the Advancement
of Society (1986)
• Member of National Academy of Sciences (1987)
• Fellow of the American Academy of Arts and
Sciences (1999) |
His research focuses on several important areas at
the interface between molecular cell biology and medicine:
the development of red blood cells, isolating and growing
hematopoietic stem cells (rare adult bone marrow cells
capable of generating all blood and immune cells) [
hematopoietic stem cells 220 kbps QuickTime],
and the role of hormones produced by fat cells in boosting
fat and sugar metabolism and in affecting resistance
to insulin.
In 1988, the Lodish laboratory accomplished
pioneering work on erythropoietin (Epo), a hormone
produced
by the kidneys that controls the production of
red blood
cells; the group identified and cloned the Epo
receptor. The lab is working on an integrated picture
of Epo's
role in causing red blood cell progenitors to divide
rather than die off. Most recently, Lodish and
his colleagues have been probing how Epo causes survival
of stressed nerve cells.
Additionally, the Lodish
lab is studying hormones controlling fatty acid and
glucose metabolism,
broadening understanding
of obesity and type 2 diabetes. In 1995, the
lab cloned adipocyte complement-related protein (ACRP30),
a hormone
made exclusively by fat cells. The Lodish lab
later
showed that a fragment of ACRP30, called gACRP,
when administered in small doses causes profound
and sustained
weight loss in obese mice eating unlimited quantities
of fat and sugar. ACRP causes muscle to burn
fatty acids faster so they are not stored as fat and
also increases the metabolism of the sugar glucose.
Lodish
and colleagues continue to make advances in studying
the roles of this and other fat-cell hormones.
A Founding Member of the Whitehead Institute, Lodish
joined the MIT faculty in 1968 and has been a professor
of biology since 1976 and professor of bioengineering
since 1999. He earned his PhD at Rockefeller University
in 1966. He was elected a fellow of the American Association
for the Advancement of Science in 1986, a member of
the National Academy of Sciences in 1987, and a fellow
of the American Academy of Arts and Sciences in 1999.
Selected Publications
Chen, C-Z., L. Li, Lodish, H.F., and D. P. Bartel.
(2004). MicroRNAs modulate hematopoietic lineage
differentiation. Science 303, 83-86.
Bogan, J., N. Hendon, A. McKee, T-s Tsao, and Lodish,
H.F. (2003). Functional cloning of TUG as a regulator
of GLUT4 glucose transporter trafficking. Nature
425: 727 - 733.
Chen, C-Z., L. Li, M. Li, and Lodish, H.F. (2003).
The EndoglinPositive Sca-1Positive RhodamineLow
phenotype defines a near homogeneous population of long-term
repopulating hematopoietic stem cells. Immunity
19: 525 - 533.
Zhang, J., M. Socolovsky, A. W. Gross, and Lodish,
H.F. (2003). Role of Ras signaling in erythroid
differentiation of mouse fetal liver cells: functional
analysis by a flow cytometry-based novel culture system.
Blood 102: 3938 - 3946.
Tsao, T-s., E. Tomas, H. E. Murrey, C. Hug, D. H. Lee,
N. B. Ruderman, J. E. Heuser, and Lodish, H.F. (2003).
Role of disulfide bonds in Acrp30/adiponectin structure
and signaling specificity: Different oligomers activate
different signal transduction pathways. J. Biol.
Chem. 278: 50810 - 50817.
[lab]
[research summary]
[publications
(pubmed database)] |
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