View source for Anjana Rao

{{Short description|Indian-American molecular biologist}}
'''Anjana Rao''' is a [[Cell biology|cellular]] and [[Molecular biology|molecular biologist]] of Indian ethnicity, working in the US. She uses [[immune cells]] as well as other types of cells to understand [[intracellular signaling]] and [[gene expression]]. Her research focuses on how signaling pathways control gene expression.
== Education and career ==
Rao earned her master’s degree in physics from [[Osmania University]] in India, her Ph.D. in Biophysics from [[Harvard University]], and completed a postdoctoral fellowship at the [[Dana–Farber Cancer Institute|Dana-Farber Cancer Institute]].<ref name=":0">(n.d.). Retrieved from http://www.calcimedica.com/rao-bio.html</ref><ref name=":1">Anjana Rao. (2019, July 25). Retrieved from https://www.aiche.org/community/bio/anjana-rao</ref> She was a Professor of [[Pathology]] at Harvard Medical School until 2010, when she moved to be professor at the [[La Jolla Institute for Immunology]] and adjunct professor in [[Pharmacology]] at the [[University of California, San Diego|University of California San Diego]].<ref name=":0" /> With her collaborator [[Patrick Hogan (biologist)|Patrick Hogan]] (also professor at the La Jolla Institute for Immunology), she is a cofounder of the company Calcimedica.<ref name=":0" /><ref name=":1" /> She spent eight years on the Jane Coffin Childs Board of Scientific Advisors, a Foundation that supports cancer research, specifically research focusing on controlling the growth and development of cancer cells.<ref>Anjana Rao Retires from the JCC Board of Scientific Advisors. (2018, May 16). Retrieved from https://www.jccfund.org/blog/anjana-rao-retires-jcc-board-scientific-advisors/</ref> She is also a member of the Scientific Advisory Board of the [[Cancer Research Institute]], a non-profit organization that supports scientific research on cancer immunotherapy, one of the most promising cancer treatments currently available.<ref>{{Cite web|title=CRI Scientific Advisory Council|url=https://www.cancerresearch.org/about-cri/scientific-leadership|access-date=2021-01-29|website=Cancer Research Institute|language=en}}</ref>
== Awards ==
{{BLP unreferenced section|date=July 2023}}
Rao has been elected to the [[National Academy of Sciences|US National Academy of Sciences]], the [[American Academy of Arts and Sciences]], and the [[American Association for the Advancement of Science]]. She is a member of the [[American Association of Immunologists]] and the [[American Society for Biochemistry and Molecular Biology]].
== Research ==
Rao’s early research at Harvard was focused on [[NFAT]] (<u>N</u>uclear <u>F</u>actor of <u>A</u>ctivated <u>T</u>-cells) transcription factors, which she discovered with postdoctoral fellows Jugnu Jain and Pat McCaffrey and collaborator Patrick Hogan.<ref name=":2">Rao, A., Luo, C., & Hogan, P.G. (1997). Transcription factors of the NFAT family: regulation and function. ''Annual review of immunology'', ''15''(1), 707-747.</ref><ref name=":6">{{Cite journal|last1=Hogan|first1=P. G.|last2=Chen|first2=L.|last3=Nardone|first3=J.|last4=Rao|first4=A.|date=2003-09-15|title=Transcriptional regulation by calcium, calcineurin, and NFAT|journal=Genes & Development|volume=17|issue=18|pages=2205–2232|doi=10.1101/gad.1102703|pmid=12975316|issn=0890-9369|doi-access=free}}</ref> They showed that NFAT proteins were expressed by most immune cells, and were essential for transcription of genes important for an immune response.<ref name=":2" /><ref name=":6" /> They also showed that NFAT was regulated by calcium and the calcium-dependent phosphatase calcineurin, which removes phosphate groups from NFAT to allow it to enter into the nucleus of the cell, and that it partnered with the unrelated transcription factors Fos and Jun to turn on T cell activation.<ref name=":2" /><ref name=":6" />
Also while at Harvard, Rao, Hogan, and postdoctoral fellows Yousang Gwack and Stefan Feske, with colleagues Richard Lewis and Murali Prakriya at Stanford, discovered the molecular identity of [[Calcium release activated channel|<u>C</u>alcium <u>R</u>elease-<u>A</u>ctivated <u>C</u>alcium]] (CRAC) channels which are necessary for calcium to enter most cells in the body.<ref name=":3">Feske, S., Gwack, Y., Prakriya, M., Srikanth, S., Puppel, S. H., Tanasa, B., Hogan, P.G., Lewis, R.S., Daly, M. & Rao, A. (2006). A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function. ''Nature'', ''441''(7090), 179-185.</ref><ref>{{Cite journal|last1=Prakriya|first1=Murali|last2=Feske|first2=Stefan|last3=Gwack|first3=Yousang|last4=Srikanth|first4=Sonal|last5=Rao|first5=Anjana|last6=Hogan|first6=Patrick G.|date=2006-08-20|title=Orai1 is an essential pore subunit of the CRAC channel|url=http://dx.doi.org/10.1038/nature05122|journal=Nature|volume=443|issue=7108|pages=230–233|doi=10.1038/nature05122|pmid=16921383|bibcode=2006Natur.443..230P|s2cid=4310221|issn=0028-0836}}</ref> They discovered that an inherited immunodeficiency was caused by a mutation in the gene encoding the CRAC channel [[ORAI1]].<ref name=":3" /> The immunodeficiency was due to the role calcium activation plays in the translocation of NFAT proteins to the nucleus, which then turn on immune response genes including cytokine genes such as Interleukin-2.<ref>{{Cite journal|last1=Hogan|first1=Patrick G.|last2=Lewis|first2=Richard S.|last3=Rao|first3=Anjana|date=2010-03-01|title=Molecular Basis of Calcium Signaling in Lymphocytes: STIM and ORAI|journal=Annual Review of Immunology|volume=28|issue=1|pages=491–533|doi=10.1146/annurev.immunol.021908.132550|pmid=20307213|issn=0732-0582|pmc=2861828}}</ref> In the immunodeficient patients, the mutation in ORAI1 caused a complete loss of calcium entry and left the children susceptible to different kinds of infections.<ref name=":3" />
Just before moving from Harvard to the west coast, Rao discovered the [[TET enzymes|TET (<u>T</u>en-<u>E</u>leven <u>T</u>ranslocation) proteins]] with graduate student Mamta Tahiliani and collaborator Dr. L. Aravind.<ref name=":7">{{Cite journal|last1=Tahiliani|first1=M.|last2=Koh|first2=K. P.|last3=Shen|first3=Y.|last4=Pastor|first4=W. A.|last5=Bandukwala|first5=H.|last6=Brudno|first6=Y.|last7=Agarwal|first7=S.|last8=Iyer|first8=L. M.|last9=Liu|first9=D. R.|last10=Aravind|first10=L.|last11=Rao|first11=A.|date=2009-04-16|title=Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian DNA by MLL Partner TET1|journal=Science|volume=324|issue=5929|pages=930–935|doi=10.1126/science.1170116|pmid=19372391|issn=0036-8075|pmc=2715015|bibcode=2009Sci...324..930T}}</ref> They showed that all three TET proteins are enzymes that alter gene expression by oxidizing the methyl group of the “fifth base”, 5-hydroxymethylcytosine, and causing [[DNA demethylation]], replacement of 5-methylcytosine by cytosine.<ref name=":7" /><ref>{{Cite journal|last1=Ko|first1=Myunggon|last2=Huang|first2=Yun|last3=Jankowska|first3=Anna M.|last4=Pape|first4=Utz J.|last5=Tahiliani|first5=Mamta|last6=Bandukwala|first6=Hozefa S.|last7=An|first7=Jungeun|last8=Lamperti|first8=Edward D.|last9=Koh|first9=Kian Peng|last10=Ganetzky|first10=Rebecca|last11=Liu|first11=X. Shirley|date=2010-12-09|title=Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2|journal=Nature|volume=468|issue=7325|pages=839–843|doi=10.1038/nature09586|pmid=21057493|issn=0028-0836|pmc=3003755|bibcode=2010Natur.468..839K}}</ref> At the La Jolla Institute, her lab demonstrated the importance of TET enzymes in proper gene expression, both in various cells of the immune system and during embryonic development.<ref name=":8">{{Cite journal|last1=Lio|first1=Chan-Wang J.|last2=Yue|first2=Xiaojing|last3=López-Moyado|first3=Isaac F.|last4=Tahiliani|first4=Mamta|last5=Aravind|first5=L.|last6=Rao|first6=Anjana|date=2020-01-22|title=TET methylcytosine oxidases: new insights from a decade of research|journal=Journal of Biosciences|language=en|volume=45|issue=1|pages=21|doi=10.1007/s12038-019-9973-4|issn=0973-7138|doi-access=free|pmc=7216820}}</ref> They also highlighted the role of TET proteins in suppressing cancer development, particularly in lymphoid, myeloid and other hematological malignancies,<ref name=":8" /> and outlined the potential for TET activators such as Vitamin C as targeted epigenetic therapy for these hematological malignancies.<ref>{{Cite journal|last1=Yue|first1=Xiaojing|last2=Rao|first2=Anjana|date=2020-09-17|title=TET family dioxygenases and the TET activator vitamin C in immune responses and cancer|url= |journal=Blood|volume=136|issue=12|pages=1394–1401|doi=10.1182/blood.2019004158|pmid=32730592|pmc=7498365|issn=0006-4971}}</ref>
As a continuation of their longstanding interest in NFAT and calcium signalling, Rao and Hogan have also performed research on T cell exhaustion.<ref>{{Cite journal|last1=Pereira|first1=Renata M.|last2=Hogan|first2=Patrick G.|last3=Rao|first3=Anjana|last4=Martinez|first4=Gustavo J.|date=2017-06-12|title=Transcriptional and epigenetic regulation of T cell hyporesponsiveness|journal=Journal of Leukocyte Biology|volume=102|issue=3|pages=601–615|doi=10.1189/jlb.2ri0317-097r|pmid=28606939|pmc=5557644|issn=0741-5400|doi-access=free}}</ref> With colleagues, they worked to define the term [[T-cell exhaustion|T cell exhaustion]], which was vaguely used to mean decreased immune responses due to overstimulation of T-cells by antigens.<ref name=":4">Blank, C.U., Haining, W.N., Held, W., Hogan, P.G., Kallies, A., Lugli, E., Lynn, R.C., Philip, M., Rao, A., Restifo, N.P. & Schietinger, A. (2019). Defining ‘T cell exhaustion’. ''Nature Reviews Immunology'', ''19''(11), 665-674.</ref> Their research specifically focuses on T cells found within tumors. They and their colleagues have shown that like normal T cells, [[Chimeric antigen receptor T cell|T cells with <u>C</u>himeric <u>A</u>ntigen <u>R</u>eceptors (CAR)]] become exhausted when residing in a tumor. They concluded that [[TOX]] and [[NR4A]] transcription factors play an important role in the exhaustion of T cells, and that inhibition or disruption of these transcription factors is a promising approach for cancer immunotherapy.<ref>{{Cite journal|last1=Chen|first1=Joyce|last2=López-Moyado|first2=Isaac F.|last3=Seo|first3=Hyungseok|last4=Lio|first4=Chan-Wang J.|last5=Hempleman|first5=Laura J.|last6=Sekiya|first6=Takashi|last7=Yoshimura|first7=Akihiko|last8=Scott-Browne|first8=James P.|last9=Rao|first9=Anjana|date=2019-02-27|title=NR4A transcription factors limit CAR T cell function in solid tumours|journal=Nature|volume=567|issue=7749|pages=530–534|doi=10.1038/s41586-019-0985-x|pmid=30814732|issn=0028-0836|pmc=6546093|bibcode=2019Natur.567..530C}}</ref><ref name=":5">{{cite journal|last1=Seo|first1=Hyungseok|last2=Chen|first2=Joyce|last3=González-Avalos|first3=Edahí|last4=Samaniego-Castruita|first4=Daniela|last5=Das|first5=Arundhoti|last6=Wang|first6=Yueqiang H.|last7=López-Moyado|first7=Isaac F.|last8=Georges|first8=Romain O.|last9=Zhang|first9=Wade|last10=Onodera|first10=Atsushi|last11=Wu|first11=Cheng-Jang|date=2019-06-18|title=TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8 + T cell exhaustion|journal=Proceedings of the National Academy of Sciences|volume=116|issue=25|pages=12410–12415|doi=10.1073/pnas.1905675116|issn=1091-6490|pmc=6589758|pmid=31152140|first12=Li-Fan|last12=Lu|first13=Patrick G.|last13=Hogan|first14=Avinash|last14=Bhandoola|first15=Anjana|last15=Rao|doi-access=free}}</ref>
== References ==
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[[Category:Osmania University alumni]]
[[Category:Harvard Medical School alumni]]
[[Category:Indian immunologists]]
[[Category:Year of birth missing (living people)]]
[[Category:Living people]]