David Baltimore

Research summary

NF-κB transcriptional regulation, retroviral and tumorigenic biology, and post-transcriptional immune control organise this corpus. The 1988 Science paper identified IκB, a 60–70 kDa inhibitor that holds NF-κB in the cytosol of cells not expressing immunoglobulin κ light chain, requiring dissociating agents such as sodium deoxycholate to release NF-κB DNA-binding activity; the fractionated inhibitor inactivated NF-κB from various sources, including nuclei of phorbol-ester-treated cells, in a specific, saturable, and reversible manner, and the cytoplasmic localisation of the NF-κB/IκB complex was supported by enucleation experiments [4]. The 1996 Science paper showed that RelA-deficient mouse fibroblasts and macrophages suffer significantly reduced viability when treated with TNF-α, while RelA+/+ cells are unaffected; cytotoxicity was mediated through TNF receptor 1, and reintroduction of RelA into RelA−/− fibroblasts restored survival, demonstrating an essential role for NF-κB in preventing TNF-α-induced cell death [2]. The 2006 PNAS paper profiled 200 microRNAs in human monocytes and found that miR-146a/b, miR-132, and miR-155 are endotoxin-responsive; promoter analysis identified miR-146a as an NF-κB-dependent gene whose induction by microbial components and pro-inflammatory cytokines positions it as a post-transcriptional negative regulator of innate immune signalling proteins [1]. The 1990 Science paper showed that murine bone marrow infected with a retrovirus encoding the Philadelphia-chromosome-derived P210 bcr/abl protein and transplanted into irradiated syngeneic recipients produced hematologic malignancies including a chronic-myelogenous-leukemia-like myeloproliferative syndrome, providing direct experimental evidence that P210bcr/abl can induce CML in vivo [5]. The 1993 PNAS paper introduced BOSC 23, a transient-transfection 293T-derived ecotropic packaging line that produces >10^6 infectious-unit/ml helper-free retroviral supernatants within 72 hours of CaPO4 transfection, with no detectable replication-competent virus; the system enables high-titre delivery of retroviral vectors carrying genes that are difficult to propagate in stable producer lines [3]. The five works together build a coherent programme connecting transcription-factor regulation [4,2], post-transcriptional regulation by miRNAs in immune signalling [1], experimental retroviral leukemogenesis [5], and the reagent infrastructure that enables high-titre retroviral delivery for gene-transfer experiments [3].

Recent publications

1. NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses2006 · Proceedings of the National Academy of Sciences · 4254 citationsDOI
2. An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death1996 · Science · 3074 citationsDOI
3. NF-κB: Ten Years After1996 · Cell · 3011 citationsDOI
4. Multiple nuclear factors interact with the immunoglobulin enhancer sequences1986 · Cell · 2788 citationsDOI
5. A new DNA binding and dimerization motif in immunoglobulin enhancer binding, daughterless, MyoD, and myc proteins1989 · Cell · 2731 citationsDOI
6. Production of high-titer helper-free retroviruses by transient transfection.1993 · Proceedings of the National Academy of Sciences · 2312 citationsDOI
7. IκB: a Specific Inhibitor of the NF-κB Transcription Factor1988 · Science · 2181 citationsDOI
8. Induction of Chronic Myelogenous Leukemia in Mice by the P210 bcr/abl Gene of the Philadelphia Chromosome1990 · Science · 2177 citationsDOI
9. An inducible transcription factor activates expression of human immunodeficiency virus in T cells1987 · Nature · 2078 citationsDOI
10. Viral RNA-dependent DNA Polymerase: RNA-dependent DNA Polymerase in Virions of RNA Tumour Viruses1970 · Nature · 2026 citationsDOI

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External profiles

• ORCID: https://orcid.org/0000-0001-8723-8190
• OpenAlex: openalex.org

Profile compiled from public sources (Researchmap, OpenAlex, The University of Tokyo faculty directory). Last refreshed 2026-05. Report incorrect information.