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{{Short description|British-American biochemist}} |
{{Short description|British-American biochemist}} |
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'''Roger J. Davis.''' American biochemist and molecular biologist Roger J. Davis, Ph.D., F.R.S. was born in Britain. He is the H. Arthur Smith Endowed Chair and serves as Professor and Chair of the Program in Molecular Medicine at the [[University of Massachusetts]] Chan Medical School.<ref>https://www.umassmed.edu/davislab/lab-members/biography-of-roger-davis/</ref>. His work focuses on [[signaling pathways]] related to [[cellular stress]],including the c-Jun N-terminal kinase (JNK) pathway. Davis molecularly cloned human JNK <ref name=":3">{{cite journal | url=https://pubmed.ncbi.nlm.nih.gov/8137421/ | pmid=8137421 | date=1994 | last1=Dérijard | first1=B. | last2=Hibi | first2=M. | last3=Wu | first3=I. H. | last4=Barrett | first4=T. | last5=Su | first5=B. | last6=Deng | first6=T. | last7=Karin | first7=M. | last8=Davis | first8=R. J. | title=JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain | journal=Cell | volume=76 | issue=6 | pages=1025–1037 | doi=10.1016/0092-8674(94)90380-8 }}</ref> and has used biochemical, molecular, and mouse model techniques to study the physiological roles and molecular mechanisms of JNK <ref>{{cite journal | pmid=24647229 | date=2014 | last1=Sabio | first1=G. | last2=Davis | first2=R. J. | title=TNF and MAP kinase signalling pathways | journal=Seminars in Immunology | volume=26 | issue=3 | pages=237–245 | doi=10.1016/j.smim.2014.02.009 | pmc=4099309 }}</ref><ref name=":4">{{cite journal | url=https://linkinghub.elsevier.com/retrieve/pii/S0092-8674(00)00116-1 | pmid=11057897 | doi=10.1016/S0092-8674(00)00116-1 | title=Signal Transduction by the JNK Group of MAP Kinases | date=2000 | last1=Davis | first1=Roger J. | journal=Cell | volume=103 | issue=2 | pages=239–252 }}</ref>. The goal of his laboratory is to identify molecular targets within stress signaling pathways that can be used to develop treatments for diseases linked to cellular [[inflammation]], including [[cancer]], [[metabolic disorders]], and ischemia, his lab seeks to identify molecular targets within stress signaling pathways<ref>{{cite journal |last1=Hotamisligil |first1=G. S. |last2=Davis |first2=R. J. |date=2016 |title=Cell Signaling and Stress Responses |url=https://cshperspectives.cshlp.org/content/8/10/a006072.long |journal=Cold Spring Harbor Perspectives in Biology |volume=8 |issue=10 |pages=a006072 |doi=10.1101/cshperspect.a006072 |pmc=5046695 |pmid=27698029}}</ref>. |
'''Roger J. Davis.''' American biochemist and molecular biologist Roger J. Davis, Ph.D., F.R.S. was born in Britain. He is the H. Arthur Smith Endowed Chair and serves as Professor and Chair of the Program in Molecular Medicine at the [[University of Massachusetts]] Chan Medical School.<ref>https://www.umassmed.edu/davislab/lab-members/biography-of-roger-davis/</ref>. His work focuses on [[signaling pathways]] related to [[cellular stress]],including the c-Jun N-terminal kinase (JNK) pathway. Davis molecularly cloned human JNK <ref name=":3">{{cite journal | url=https://pubmed.ncbi.nlm.nih.gov/8137421/ | pmid=8137421 | date=1994 | last1=Dérijard | first1=B. | last2=Hibi | first2=M. | last3=Wu | first3=I. H. | last4=Barrett | first4=T. | last5=Su | first5=B. | last6=Deng | first6=T. | last7=Karin | first7=M. | last8=Davis | first8=R. J. | title=JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain | journal=Cell | volume=76 | issue=6 | pages=1025–1037 | doi=10.1016/0092-8674(94)90380-8 }}</ref> and has used biochemical, molecular, and mouse model techniques to study the physiological roles and molecular mechanisms of JNK <ref>{{cite journal | pmid=24647229 | date=2014 | last1=Sabio | first1=G. | last2=Davis | first2=R. J. | title=TNF and MAP kinase signalling pathways | journal=Seminars in Immunology | volume=26 | issue=3 | pages=237–245 | doi=10.1016/j.smim.2014.02.009 | pmc=4099309 }}</ref><ref name=":4">{{cite journal | url=https://linkinghub.elsevier.com/retrieve/pii/S0092-8674(00)00116-1 | pmid=11057897 | doi=10.1016/S0092-8674(00)00116-1 | title=Signal Transduction by the JNK Group of MAP Kinases | date=2000 | last1=Davis | first1=Roger J. | journal=Cell | volume=103 | issue=2 | pages=239–252 }}</ref>. The goal of his laboratory is to identify molecular targets within stress signaling pathways that can be used to develop treatments for diseases linked to cellular [[inflammation]], including [[cancer]], [[metabolic disorders]], and ischemia, his lab seeks to identify molecular targets within stress signaling pathways<ref>{{cite journal |last1=Hotamisligil |first1=G. S. |last2=Davis |first2=R. J. |date=2016 |title=Cell Signaling and Stress Responses |url=https://cshperspectives.cshlp.org/content/8/10/a006072.long |journal=Cold Spring Harbor Perspectives in Biology |volume=8 |issue=10 |pages=a006072 |doi=10.1101/cshperspect.a006072 |pmc=5046695 |pmid=27698029}}</ref>. |
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Roger J. Davis. American biochemist and molecular biologist Roger J. Davis, Ph.D., F.R.S. was born in Britain. He is the H. Arthur Smith Endowed Chair and serves as Professor and Chair of the Program in Molecular Medicine at the University of Massachusetts Chan Medical School.[1]. His work focuses on signaling pathways related to cellular stress,including the c-Jun N-terminal kinase (JNK) pathway. Davis molecularly cloned human JNK [2] and has used biochemical, molecular, and mouse model techniques to study the physiological roles and molecular mechanisms of JNK [3][4]. The goal of his laboratory is to identify molecular targets within stress signaling pathways that can be used to develop treatments for diseases linked to cellular inflammation, including cancer, metabolic disorders, and ischemia, his lab seeks to identify molecular targets within stress signaling pathways[5].
His recent studies have focussed on the role of hepatic JNK in the development of the metabolic syndrome, which includes obesity, steatosis and insulin resistance) caused by the consumption of a high-fat diet [6]. His work investigates the JNK-dependent regulation of the nuclear hormone receptor complex PPARα/RXRα. These studies aim to identify potential therapeutic targets [7].

Academic Career
- Research Fellow, Queens’ College, Cambridge University (1983-1985)
- Damon Runyon Post-doctoral Fellow, University of Massachusetts Medical School, Worcester, MA 01655, USA (1984 -1985)[8].
- Assistant Professor, Department of Biochemistry, University of Massachusetts Medical School, (1985 – 1989)[9].
- Associate Professor, Department of Biochemistry, University of Massachusetts Medical School, (1989-1993)[9].
- Investigator, Howard Hughes Medical Institute Institute, Washington, DC, USA (1990 – 2019)[10].
- Professor, Program in Molecular Medicine, University of Massachusetts Medical School, (1993-present)[9].
- H. Arthur Smith Endowed Chair, Program in Molecular Medicine, University of Massachusetts Medical School, (2002-present) [9].
Research Contributions
Roger Davis was involved in the molecular cloning of human JNK, establishing that these kinases are part of the MAP kinase superfamily [2]. In particular, he worked on the stress kinase pathway, a signal transduction mechanism that helps cells sense external stimuli and adapt to changes [11].
He also contributed to identifying the MAP kinase kinases (MKK4 and MKK7) that activate JNK [12]. Later research showed that pro-inflammatory cytokines and environmental stress trigger the activation of the JNK pathway [4]. His group has used mouse models deficient in JNK1, JNK2, JNK3, MKK4, and MKK7 to study the roles of these kinases in vivo.
Additionally, he has studied transcription factors such as cJun, JunD, JunB, ATF2, Elk1, and NFAT4 that function downstream of JNK signaling. After JNK activation, these proteins play a role in controlling gene expression [13][14][15].
He has reported that JNK activation can cause cell death by apoptosis. This form of death is suppressed by activated AKT. JNK-mediated expression of TNF and JNK-mediated phosphorylation of the BH3-only proteins (Bim and Bmf) contribute to apoptosis caused by JNK activation. This form of cell death occurs during development (e.g. in the central nervous system) and in response to injury (e.g. excitotoxic stress and axotomy). JNK also contributes to tumor cell death and can suppress tumorigenesis [16][17][18][19].
He has also studied the role of JNK in the metabolic stress response to a high-fat diet. His group showed that JNK in the hypothalamus and pituitary gland suppresses energy expenditure and promotes obesity. In contrast, JNK in peripheral tissues causes insulin resistance. Examples include JNK-mediated inflammation via macrophage M1 polarization and tissue infiltration, hepatic JNK suppression of PPARα-mediated lipid oxidation and FGF21 action, and the role of adipose tissue JNK in modulating insulin sensitivity in both liver and fat tissue. These findings support a key role for JNK in the metabolic response to a high-fat diet [20][21][22][23].
Publications
- Dérijard, B., et al. (1994). "JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain." Cell 76(6): 1025–1037. PMID: 8173421[2]
- Davis, R.J. (2000). "Signal transduction by the JNK group of MAP kinases." Cell 103(2): 239–252. PMID: 11057897.[4]
- Sabio, G., et al. (2008). "A stress signaling pathway in adipose tissue regulates hepatic insulin resistance." Science 322(5907): 1539-43. PMID: 19056984[20]
- Sabio, G., & Davis, R.J. (2010). "cJun NH2-terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance." Trends Biochem Sci 35(9): 490-6. PMID: 20452774[24]
Honors and Awards
- Damon Runyon Post-doctoral Fellow (1984–1985).[25]
- Howard Hughes Medical Institute, Investigator (1990–2019).[26]
- Chancellor's Medal for Excellence in Scholarship, University of Massachusetts Medical School (2012).[27]
- Steven C. Beering Award (2013).[28]
Elected Memberships
- Royal Society (London) (2002)[29].
- European Molecular Biology Organization (EMBO) (2010)[30].
- American Academy of Microbiology (2012)[31].
- American Association for the Advancement of Science (2012)[32]
- National Academy of Inventors National Academy of Inventors (2012)[33].
- National Academy of Sciences (2018)[34].
- American Academy of Arts & Sciences (2021)[35].
- National Academy of Medicine (2023)[36]
References
- ^ https://www.umassmed.edu/davislab/lab-members/biography-of-roger-davis/
- ^ a b c Dérijard, B.; Hibi, M.; Wu, I. H.; Barrett, T.; Su, B.; Deng, T.; Karin, M.; Davis, R. J. (1994). "JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain". Cell. 76 (6): 1025–1037. doi:10.1016/0092-8674(94)90380-8. PMID 8137421.
- ^ Sabio, G.; Davis, R. J. (2014). "TNF and MAP kinase signalling pathways". Seminars in Immunology. 26 (3): 237–245. doi:10.1016/j.smim.2014.02.009. PMC 4099309. PMID 24647229.
- ^ a b c Davis, Roger J. (2000). "Signal Transduction by the JNK Group of MAP Kinases". Cell. 103 (2): 239–252. doi:10.1016/S0092-8674(00)00116-1. PMID 11057897.
- ^ Hotamisligil, G. S.; Davis, R. J. (2016). "Cell Signaling and Stress Responses". Cold Spring Harbor Perspectives in Biology. 8 (10): a006072. doi:10.1101/cshperspect.a006072. PMC 5046695. PMID 27698029.
- ^ Sabio, Guadalupe; Das, Madhumita; Mora, Alfonso; Zhang, Zhiyou; Jun, John Y.; Ko, Hwi Jin; Barrett, Tamera; Kim, Jason K.; Davis, Roger J. (2008). "A Stress Signaling Pathway in Adipose Tissue Regulates Hepatic Insulin Resistance". Science. 322 (5907): 1539–1543. Bibcode:2008Sci...322.1539S. doi:10.1126/science.1160794. PMC 2643026. PMID 19056984.
- ^ Vernia, S.; Cavanagh-Kyros, J.; Garcia-Haro, L.; Sabio, G.; Barrett, T.; Jung, D. Y.; Kim, J. K.; Xu, J.; Shulha, H. P.; Garber, M.; Gao, G.; Davis, R. J. (2014). "The PPARα-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway". Cell Metabolism. 20 (3): 512–525. doi:10.1016/j.cmet.2014.06.010. PMC 4156535. PMID 25043817.
- ^ https://www.damonrunyon.org/sites/default/files/Awardees%20A-E.pdf Damon Runyon Post-doctoral Fellow
- ^ a b c d https://www.umassmed.edu/davislab/lab-members/roger-davis-biography/ Assistant Professor, Department of Biochemistry
- ^ https://www.hhmi.org/scientists/roger-j-davis Investigator, Howard Hughes Medical Institute
- ^ https://www.researchgate.net/publication/311770337_Cell_Signaling_and_Stress_Responses
- ^ Dérijard, Benoit; Raingeaud, Joël; Barrett, Tamera; Wu, I-Huan; Han, Jiahuai; Ulevitch, Richard J.; Davis, Roger J. (1995). "Independent Human MAP-Kinase Signal Transduction Pathways Defined by MEK and MKK Isoforms". Science. 267 (5198): 682–685. Bibcode:1995Sci...267..682D. doi:10.1126/science.7839144. PMID 7839144.
- ^ Dickens, Martin; Rogers, Jeffrey S.; Cavanagh, Julie; Raitano, Art; Xia, Zhengui; Halpern, Jocelyn R.; Greenberg, Michael E.; Sawyers, Charles L.; Davis, Roger J. (1997). "A Cytoplasmic Inhibitor of the JNK Signal Transduction Pathway". Science. 277 (5326): 693–696. doi:10.1126/science.277.5326.693. PMID 9235893.
- ^ Whitmarsh, Alan J.; Cavanagh, Julie; Tournier, Cathy; Yasuda, Jun; Davis, Roger J. (1998). "A Mammalian Scaffold Complex That Selectively Mediates MAP Kinase Activation". Science. 281 (5383): 1671–1674. Bibcode:1998Sci...281.1671W. doi:10.1126/science.281.5383.1671. PMID 9733513.
- ^ Whitmarsh, A. J.; Kuan, C. Y.; Kennedy, N. J.; Kelkar, N.; Haydar, T. F.; Mordes, J. P.; Appel, M.; Rossini, A. A.; Jones, S. N.; Flavell, R. A.; Rakic, P.; Davis, R. J. (2001). "Requirement of the JIP1 scaffold protein for stress-induced JNK activation". Genes & Development. 15 (18): 2421–2432. doi:10.1101/gad.922801. PMC 312784. PMID 11562351.
- ^ Tournier, Cathy; Hess, Patricia; Yang, Derek D.; Xu, Jie; Turner, Tod K.; Nimnual, Anjaruwee; Bar-Sagi, Dafna; Jones, Stephen N.; Flavell, Richard A.; Davis, Roger J. (2000). "Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway". Science. 288 (5467): 870–874. Bibcode:2000Sci...288..870T. doi:10.1126/science.288.5467.870. PMID 10797012.
- ^ Lei, Kui; Davis, Roger J. (2003). "JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis". Proceedings of the National Academy of Sciences. 100 (5): 2432–2437. Bibcode:2003PNAS..100.2432L. doi:10.1073/pnas.0438011100. PMC 151358. PMID 12591950.
- ^ Hübner, A.; Barrett, T.; Flavell, R. A.; Davis, R. J. (2008). "Multisite phosphorylation regulates Bim stability and apoptotic activity". Molecular Cell. 30 (4): 415–425. doi:10.1016/j.molcel.2008.03.025. PMC 2453504. PMID 18498746.
- ^ Das, Madhumita; Sabio, Guadalupe; Jiang, Feng; Rincón, Mercedes; Flavell, Richard A.; Davis, Roger J. (2009). "Induction of Hepatitis by JNK-Mediated Expression of TNF-α". Cell. 136 (2): 249–260. doi:10.1016/j.cell.2008.11.017. PMC 2794880. PMID 19167327.
- ^ a b Sabio, Guadalupe; Das, Madhumita; Mora, Alfonso; Zhang, Zhiyou; Jun, John Y.; Ko, Hwi Jin; Barrett, Tamera; Kim, Jason K.; Davis, Roger J. (2008). "A Stress Signaling Pathway in Adipose Tissue Regulates Hepatic Insulin Resistance". Science. 322 (5907): 1539–1543. Bibcode:2008Sci...322.1539S. doi:10.1126/science.1160794. PMC 2643026. PMID 19056984.
- ^ Sabio, G.; Cavanagh-Kyros, J.; Barrett, T.; Jung, D. Y.; Ko, H. J.; Ong, H.; Morel, C.; Mora, A.; Reilly, J.; Kim, J. K.; Davis, R. J. (2010). "Role of the hypothalamic–pituitary–thyroid axis in metabolic regulation by JNK1". Genes & Development. 24 (3): 256–264. doi:10.1101/gad.1878510. PMC 2811827. PMID 20080940.
- ^ Han, Myoung Sook; Jung, Dae Young; Morel, Caroline; Lakhani, Saquib A.; Kim, Jason K.; Flavell, Richard A.; Davis, Roger J. (2013). "JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation". Science. 339 (6116): 218–222. Bibcode:2013Sci...339..218H. doi:10.1126/science.1227568. PMC 3835653. PMID 23223452.
- ^ Vernia, S.; Cavanagh-Kyros, J.; Garcia-Haro, L.; Sabio, G.; Barrett, T.; Jung, D. Y.; Kim, J. K.; Xu, J.; Shulha, H. P.; Garber, M.; Gao, G.; Davis, R. J. (2014). "The PPARα-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway". Cell Metabolism. 20 (3): 512–525. doi:10.1016/j.cmet.2014.06.010. PMC 4156535. PMID 25043817.
- ^ Sabio, G.; Davis, R. J. (2010). "CJun NH2-terminal kinase 1 (JNK1): Roles in metabolic regulation of insulin resistance". Trends in Biochemical Sciences. 35 (9): 490–496. doi:10.1016/j.tibs.2010.04.004. PMC 2975251. PMID 20452774.
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