Editing David Baltimore (section)

=== Caltech Laboratory (1997–2019) ===
Baltimore's laboratory at Caltech focused on two major research areas: understanding the development and functioning of the mammalian immune system and translational studies creating viral vectors to make the immune system more effective in resisting cancer. Their basic studies went in two directions: understanding the diverse activity of the NF-κB transcription factor, and understanding the normal and pathologic functions of microRNA.

==== Translational Science Initiatives ====
A primary focus of Baltimore's lab was use of gene therapy methods to treat HIV and cancer.<ref name=":5">{{Cite web|date=2010-05-21|title=David Baltimore|url=https://www.broadinstitute.org/bios/david-baltimore|access-date=2021-04-14|website=Broad Institute|language=en}}</ref> In the early 2000s one of Baltimore's graduate students, Lili Yang, developed a [[lentivirus]] vector that allowed for the cloning of genes for two chains of TCR. Recognizing its potentially profound implications for enhancing immunity, Baltimore developed a translational research initiative within his laboratory called "Engineering Immunity." The Bill and Melinda Gates Foundation awarded the program with a Grand Challenge Grant, and he used the funding to divide the initiative into four research programs and hire additional lab staff to lead each one. Two of the research programs sparked gene therapy start-up companies, Calimmune and Immune Design Corp, founded in 2006 and 2008 respectively.<ref>{{Cite web|title=Calimmune, Inc.|date=June 27, 2015 |url=https://www.linkedin.com/company/calimmune-inc}}</ref><ref>{{Cite web|title=Immune Design Corp - Company Profile and News|url=https://www.bloomberg.com/profile/company/IMDZ:US|access-date=2021-04-14|website=Bloomberg.com|language=en}}</ref> A third program focused on the development of an HIV vaccine, and eventually lead to clinical trials at NIH.<ref name=":1" /> In 2009 Baltimore became director of the Joint Center for Translational Medicine, a shared initiative between Caltech and UCLA aimed at developing bench to bedside medicine.<ref name=":5" />

==== MicroRNA Research ====
A focus of Baltimore's lab from his arrival at Caltech to the lab's closure in 2018 was understanding the role of [[microRNA]] in the immune system.<ref name=":1" /> MicroRNAs provide fine control over gene expression by regulating the amount of protein made by particular messenger RNAs.<ref name="CaltechBio">{{cite web|title=David Baltimore|url=https://www.bbe.caltech.edu/content/david-baltimore|website=Division of Biology and Biological Engineering|publisher=Caltech|access-date=May 25, 2015|archive-url=https://web.archive.org/web/20160601234446/http://www.bbe.caltech.edu/content/david-baltimore|archive-date=June 1, 2016|url-status=dead}}</ref>
In recent research led by [[Jimmy Zhao]], Baltimore's team has discovered a small RNA molecule called microRNA-146a (miR-146a) and bred a strain of mice that lacks miR146a.  They have used the miR146a(-) mice as a model to study the effects of chronic inflammation on the activity of hematopoietic stem cells (HSCs).  Their results suggest that microRNA-146a protects HSCs during chronic inflammation, and that its lack may contribute to blood cancers and bone marrow failure.<ref name="Dish2013">{{cite news|title=RNA Molecule Protects Stem Cells During Inflammation|url=https://beyondthedish.wordpress.com/2013/06/11/rna-molecule-protects-stem-cells-during-inflammation/|access-date=May 25, 2015|work=Beyond the Dish|date=June 11, 2013}}</ref>

===== Splicing Control Research =====
Another concentration within Baltimore's lab in recent years was control of inflammatory and immune responses, specifically splicing control of gene expression after inflammatory stimuli.<ref name=":5" /> In 2013 they discovered that ordered expression of genes following an inflammatory stimulus was controlled by splicing, not transcription as previously supposed.<ref>{{cite journal | vauthors = Hao S, Baltimore D | title = RNA splicing regulates the temporal order of TNF-induced gene expression | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 110 | issue = 29 | pages = 11934–9 | date = July 2013 | pmid = 23812748 | doi = 10.1073/pnas.1309990110 | pmc = 3718113 | bibcode = 2013PNAS..11011934H | doi-access = free }}</ref> This led to further discoveries that delayed splicing was caused by introns, with the revelation that RNA-binding protein BUD13 acts at this intron to increase the amount of successful splicing (2 articles by Luke Frankiw published in 2019 and 2020).<ref>{{cite journal | vauthors = Frankiw L, Majumdar D, Burns C, Vlach L, Moradian A, Sweredoski MJ, Baltimore D | title = BUD13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7 | language = English | journal = Molecular Cell | volume = 73 | issue = 4 | pages = 803–814.e6 | date = February 2019 | pmid = 30639243 | doi = 10.1016/j.molcel.2018.11.038 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Frankiw L, Mann M, Li G, Joglekar A, Baltimore D | title = Alternative splicing coupled with transcript degradation modulates OAS1g antiviral activity | journal = RNA | volume = 26 | issue = 2 | pages = 126–136 | date = February 2020 | pmid = 31740586 | pmc = 6961538 | doi = 10.1261/rna.073825.119 }}</ref>

In an autobiographical piece published in Annual Review Immunology in 2019, Baltimore announced that half of his lab space at Caltech would be taken over by a new assistant professor in Fall 2018, and his current lab group would be the last. "I have been involved in research for 60 years, and I think it is time to leave the field to younger people."<ref name=":1" />