Harvey F. Lodish

About

Harvey F. Lodish is a Professor of Biology and Biological Engineering at MIT and a Founding Member of the Whitehead Institute. Before closing his lab in 2020, his research focused on the development of red blood cells and the use of modified red cells for introducing novel therapeutics into the human body, as well as the development of brown and white fat cells. He has been a leader in molecular cell biology and biotechnology entrepreneurship for over five decades. His early research concentrated on the regulation of messenger RNA translation and the biogenesis of plasma membrane glycoproteins. Beginning in the 1980s, his work involved cloning and characterizing many proteins, microRNAs, and long noncoding RNAs important for red cell development and function. His laboratory was the first to clone and sequence mRNAs encoding hormone receptors, mammalian glucose transport proteins, and proteins involved in adipose cell formation and function. He identified and characterized several genes and proteins involved in insulin resistance and stress responses in adipose cells. Throughout his career, he has mentored hundreds of students and postdoctoral fellows and continues to teach classes on biotechnology. He has received numerous awards, including the Wallace H. Coulter Award for Lifetime Achievement in Hematology and the Donald Metcalf Award, and is a member of the National Academy of Sciences and the American Academy of Arts and Sciences.

Research topics

• Biology
• Cell biology
• Molecular biology
• Chemistry
• Biochemistry

Selected publications

• Enhanced phosphocholine metabolism is essential for terminal erythropoiesis

  Blood · 2018-04-30 · 57 citations

  articleOpen accessSenior author

  Red cells contain a unique constellation of membrane lipids. Although much is known about regulated protein expression, the regulation of lipid metabolism during erythropoiesis is poorly studied. Here, we show that transcription of PHOSPHO1, a phosphoethanolamine and phosphocholine phosphatase that mediates the hydrolysis of phosphocholine to choline, is strongly upregulated during the terminal stages of erythropoiesis of both human and mouse erythropoiesis, concomitant with increased catabolism…

  PublisherOA PDFDOI

• FAM210B is an erythropoietin target and regulates erythroid heme synthesis by controlling mitochondrial iron import and ferrochelatase activity

  Journal of Biological Chemistry · 2018-10-26 · 46 citations

  articleOpen access

  -deficient murine erythroid cells and zebrafish morphants. Genetic complementation experiments revealed that FAM210B is not a mitochondrial iron transporter but is required for adequate mitochondrial iron import to sustain heme synthesis and iron-sulfur cluster formation during erythroid differentiation. FAM210B was also required for maximal ferrochelatase activity in differentiating erythroid cells. We propose that FAM210B functions as an adaptor protein that facilitates the formation of an oli…

  PublisherOA PDFDOI

• Rate of Progression through a Continuum of Transit-Amplifying Progenitor Cell States Regulates Blood Cell Production

  Developmental Cell · 2019-02-28 · 38 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Phosphocholine accumulation and PHOSPHO1 depletion promote adipose tissue thermogenesis

  Proceedings of the National Academy of Sciences · 2020-06-17 · 25 citations

  articleOpen accessCorresponding

  Phosphocholine phosphatase-1 (PHOSPHO1) is a phosphocholine phosphatase that catalyzes the hydrolysis of phosphocholine (PC) to choline. Here we demonstrate that the PHOSPHO1 transcript is highly enriched in mature brown adipose tissue (BAT) and is further induced by cold and isoproterenol treatments of BAT and primary brown adipocytes. In defining the functional relevance of PHOPSPHO1 in BAT thermogenesis and energy metabolism, we show that PHOSPHO1 knockout mice are cold-tolerant, with higher…

  PublisherOA PDFDOI

• An adipose lncRAP2-Igf2bp2 complex enhances adipogenesis and energy expenditure by stabilizing target mRNAs

  iScience · 2021-12-24 · 19 citations

  articleOpen accessCorresponding

  interactome analyses, we show that lncRAP2 forms complexes with proteins that stabilize mRNAs and modulate translation, among them Igf2bp2. Surveying transcriptome-wide Igf2bp2 client mRNAs in white adipocytes reveals selective binding to mRNAs encoding adipogenic regulators and energy expenditure effectors, including adiponectin. These same target proteins are downregulated when either Igf2bp2 or lncRAP2 is downregulated, hindering adipocyte lipolysis. Proteomics and ribosome profiling show thi…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01DK037571

  NIH · $1.2M · 1991

• NIH Grant R01AI022347

  NIH · $269k · 1986

• NIH Grant R01GM035012

  NIH · $1.8M · 1994

Frequent coauthors

• Mike Hennessy

  Target (United States)

  320 shared

• Nora A. Janjan

  STATinMED (United States)

  320 shared

• Sonali M. Smith

  320 shared

• Angela J. Fought

  Mayo Clinic

  320 shared

• Tara Ghalambor

  University of Arizona

  320 shared

• Nikia R. McFadden

  University of California Davis Medical Center

  320 shared

• Kirk E. Cahill

  Loyola University Chicago

  320 shared

• Whitney Ly

  University of North Carolina Health Care

  320 shared

Awards & honors

• Wallace H. Coulter Award for Lifetime Achievement in Hematol…
• Donald Metcalf Award, International Society for Experimental…
• American Society for Cell Biology WICB Sandra K. Masur Senio…
• Pioneer Award, Diamond Blackfan Anemia Foundation, 2016
• Mentor Award in Basic Science, American Society of Hematolog…

Similar researchers at Massachusetts Institute of Technology

• Rudolf Jaenischh-295
• Robert A. Weinbergh-291
• Susumu Tonegawah-237