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'''Jamey Marth''', [[Ph.D.]], is a molecular and cellular biologist. He is currently on the faculty of the [[Sanford Burnham Prebys Medical Discovery Institute|SBP Medical Discovery Institute]] in [[La Jolla, California]].<ref name=":0">{{Cite web|title=Jamey Marth, Ph.D. {{!}} SBP|url=https://www.sbpdiscovery.org/our-scientists/jamey-marth-phd|access-date=2021-07-14|website=www.sbpdiscovery.org}}</ref>
'''Jamey Marth''', [[Ph.D.]], is a molecular and cellular biologist. He is currently on the faculty of the [[Sanford-Burnham-Prebys Medical Research Institute|SBP Medical Discovery Institute]] of [[La Jolla, California|La Jolla]] and the [[University of California, Santa Barbara]]. Dr. Marth is Director of the Center for Nanomedicine and an adjunct Professor in the Department of Molecular, Cellular and Developmental Biology.<ref name="Forbes">{{cite news | last=Hardy| first=Quentin| title =Big Data's People-Changing Machine| work = [[Forbes (magazine)|Forbes]]| date =11 July 2011 | url =https://www.forbes.com/sites/quentinhardy/2011/07/11/big-datas-people-changing-machine/| access-date =29 April 2015}}</ref><ref name="Futurity">{{cite news | last=Foulsham| first=George| title =Fatty diet triggers diabetes onslaught | publisher = Futurity| date =16 August 2011 | url =http://www.futurity.org/fatty-diet-triggers-diabetes-onslaught/ | access-date =12 March 2015}}</ref> He is also the inaugural recipient of the [[Carbon]] Chair of Biochemistry and Molecular Biology and the recipient of the Mellichamp Chair of Systems Biology.<ref name="SD">{{cite news | title =Biomedical scientist discovers method to increase survival in sepsis | publisher = [[Science Daily]]| date =25 November 2013 | url =https://www.sciencedaily.com/releases/2013/11/131125164818.htm | access-date =12 March 2015}}</ref>
His research has largely focused on [[Cell biology|molecular cell biology]] and, in particular, how protein [[glycosylation]] contributes to the origins of common diseases including [[diabetes]], [[sepsis]], [[colitis]], and [[autoimmunity]].<ref name="UC">{{cite news | title =Pioneering research on type 2 diabetes | publisher = [[University of California]]| date =4 January 2013 | url =http://health.universityofcalifornia.edu/2013/01/04/pioneering-research-on-type-2-diabetes/ | access-date =12 March 2015}}</ref> His research is also credited with the conception and co-development of [[Cre-Lox recombination]] as a form of conditional [[mutagenesis]] in living mammals.<ref name="Nature">{{cite journal |last=Wadman |first=Meredith |date=27 August 1998 |title=DuPont opens up access to genetics tool |url=http://beta.industrydocuments.library.ucsf.edu/documentstore/h/l/j/b//hljb0088/hljb0088.pdf |journal=[[Nature (journal)|Nature]] |volume=394 |issue=819 |pages=819 |doi=10.1038/29607 |access-date=12 March 2015 |pmid=9732857 |s2cid=4431441 |doi-access=free }}{{Dead link|date=April 2020 |bot=InternetArchiveBot |fix-attempted=yes }}</ref>
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==Education==
Marth earned a Ph.D. in [[Pharmacology]] from the [[University of Washington]] in 1987.<ref name="MCDB">{{cite web |title=Jamey Marth |url=https://www.mcdb.ucsb.edu/people/faculty/jamey-marth |website=MCDB |publisher=UC Santa Barbara |access-date=3 December 2019}}</ref> During his time at Washington as a graduate student, he was mentored by [[Roger M. Perlmutter]] and [[Edwin G. Krebs]].{{Citation needed|date=April 2017}} Marth was Perlmutter's first graduate student.<ref name="BIO">{{cite web |url=https://www.mcdb.ucsb.edu/people/faculty/marth |title=Jamey Marth|author=<!--Staff writer(s); no by-line.--> |website=www.mcdb.uscb.com |publisher=[[University of California, Santa Barbara]] |access-date=12 March 2015}}</ref><ref name="AAI">{{cite news | title =The American Association of Immunologists Oral History Project | publisher =[[Journal of Immunology|American Association of Immunologists]] | date =23 January 2013 | url =https://www.aai.org/About/History/Notable_Members/pdfs/OHP/Transcripts/Trans-Inv_017-Perlmutter_Roger_M-2013_Final.pdf | access-date =12 March 2015 | archive-url =https://web.archive.org/web/20160102005322/http://www.aai.org/About/History/Notable_Members/pdfs/OHP/Transcripts/Trans-Inv_017-Perlmutter_Roger_M-2013_Final.pdf | archive-date =2 January 2016 | url-status =dead }}</ref> Marth's first faculty position after earning his doctorate was at the [[University of British Columbia]]'s Biomedical Research Centre in [[Vancouver]], [[British Columbia]], [[Canada]].<ref name="UCSD">{{cite news | title =Cellular and Molecular Medicine - 2009 Annual Report | publisher = [[University of California, San Diego]]| date =2009 | url =http://healthsciences.ucsd.edu/som/cmm/about/Documents/AnnualReport2009.pdf | access-date =12 March 2015}}</ref><ref name="Journal">{{cite journal |last1=Richards |first1=James D. |last2=Gold |first2=Michael R.|last3=Hourihane |first3=Sharon L. |last4=DeFranco |first4=Anthony L. |last5=Matsuuchi| first5=Linda| date=15 March 1996 |title=Reconstitution of B Cell Antigen Receptor-induced Signaling Events in a Nonlymphoid Cell Line by Expressing the Syk Protein-tyrosine Kinase |journal= [[Journal of Biological Chemistry]]|volume=271 |issue= 11|pages= 6458–6466|doi=10.1074/jbc.271.11.6458 |pmid=8626447 |doi-access=free }}</ref>


His research has largely focused on how protein [[glycosylation]] contributes to the origins of common diseases and syndromes including [[diabetes]], [[sepsis]], [[colitis]], and [[autoimmunity]].<ref name=":1">{{Cite web|date=2011-08-16|title=Fatty diet triggers diabetes onslaught|url=https://www.futurity.org/fatty-diet-triggers-diabetes-onslaught/|access-date=2021-07-14|website=Futurity|language=en-US}}</ref><ref name=":8">{{Cite web|title=Biomedical scientist discovers method to increase survival in sepsis|url=https://www.sciencedaily.com/releases/2013/11/131125164818.htm|access-date=2021-07-14|website=ScienceDaily|language=en}}</ref><ref>{{Cite journal|last=Marth|first=Jamey David|date=2020|title=Glycosylation in a Common Mechanism of Colitis and Sepsis|url=https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2020.34.s1.00176|journal=The FASEB Journal|language=en|volume=34|issue=S1|pages=1–1|doi=10.1096/fasebj.2020.34.s1.00176|issn=1530-6860}}</ref><ref name=":2">{{Cite web|title=Jamey Marth Honored for Research Linking Glycans to Diabetes, Lupus, Sepsis|url=https://www.newswise.com/articles/jamey-marth-honored-for-research-linking-glycans-to-diabetes-lupus-sepsis|access-date=2021-07-14|website=www.newswise.com|language=en}}</ref>
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==Career==
While in Vancouver, Marth and colleagues conceived and developed Cre-Lox recombination for conditional mutagenesis. This technology has enabled the study of gene function in specific cell types and at specific times among living animals.<ref name=Science1994>{{cite journal|last1=Gu|first1=H|last2=Marth|first2=JD|last3=Orban|first3=PC|last4=Mossmann|first4=H|last5=Rajewsky|first5=K|title=Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting|journal=Science|date=1 July 1994|pmid=8016642|volume=265|issue=5168|pages=103–6|doi=10.1126/science.8016642|s2cid=19838380|url=https://semanticscholar.org/paper/b85376ba4333d820ce5e5fbda47a6d28e1276277}}</ref><ref>{{cite journal|last1=Orban|first1=PC|last2=Chui|first2=D|last3=Marth|first3=JD|title=Tissue-and site-specific DNA recombination in transgenic mice|journal=Proc. Natl. Acad. Sci. USA|date=1992|pages=6861–6865|pmid=1495975|pmc=49604|volume=89|issue=15|doi=10.1073/pnas.89.15.6861}}</ref> In 1995, [[George Palade]] and [[Marilyn Farquhar]] (among others) recruited Marth to the [[University of California, San Diego]] (UCSD) in the Department of Cellular and Molecular Medicine. Upon his arrival, he was appointed as an Investigator of the [[Howard Hughes Medical Institute]]. Marth spent more than 14 years in this position at UCSD.<ref name="UCSD"/> His research at HHMI and UCSD helped bolster an already renowned [[glycobiology]] program that originated with [[Ajit Varki]] and later included [[Jeffrey Esko]].<ref name="GRTC">{{cite news | title =GRTC | publisher = aiHit Limited| url =https://www.aihitdata.com/company/0067CBCA/GRTC/overview | access-date =12 March 2015}}</ref>
In 2009, he accepted a position at the University of California, Santa Barbara and the Sanford-Burnham Medical Research Institute as the Director of the Center for Nanomedicine. He also then became the inaugural recipient of the Carbon Chair in Biochemistry and Molecular Biology and the recipient of the Mellichamp Chair of Systems Biology.<ref name="SD"/><ref name="UCSD"/> In his position as the Director of the Center of Nanomedicine, Marth and his team further explored the application of new delivery methods to directly visualize and treat disease, initially in collaboration with Center for Nanomedicine Co-Founder, Dr. Erkki Ruoslahti.<ref name="Nooz01">{{cite news | last=Zeller| first=Jeremy| title =UCSB's Center for Nanomedicine Plants Seeds of Economic Development in Goleta Valley | publisher = Noozhawk| date =10 January 2011 | url =http://www.noozhawk.com/article/010911_ucsb_center_for_nanomedicine/ | access-date =12 March 2015}}</ref><ref name="Nooz02">{{cite news | title =Envisioning Novel Approaches for Eye Disease: 'The New Medicine' at UCSB| publisher = Noozhawk| date =16 October 2012| url =http://www.noozhawk.com/article/101612_novel_approaches_eye_disease_at_ucsb| access-date =29 April 2015}}</ref>
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==Research==
Marth’s research is credited with the development of new methodologies and conceptual advances in understanding the origins of disease. His conception and co-development of Cre-Lox conditional mutagenesis has provided a means to further discover the mechanistic underpinnings of development and disease, and continues to be used by scientists worldwide.<ref name=CreLoxSauers>{{cite journal|last1=Saure|first1=B.|title=Cre/lox: one more step in the taming of the genome|journal=Endocrine|date=2002|pmid=12624421|volume=19|issue=3|pages=221–8|doi=10.1385/endo:19:3:221|s2cid=29223716}}</ref> Prior to the development of conditional mutagenesis, the use of homologous recombination was limited to systemic gene targeting and mutation.<ref name="Nature"/> Marth's use of Cre-Lox conditional mutagenesis established the presence and functions of multiple and in some cases previously unknown enzymes participating in protein glycosylation, an area of research that has become a focus of exploration in how common diseases originate.<ref name="Journal03">{{cite journal |last1=Hennet |first1=T. |last2=Hagen |first2=F.K.|last3=Tabak |first3=L.A. |last4=Marth |first4=J.D. | date=1995 |title=T cell-specific deletion of a polypeptide N-acetylgalactosaminyltransferase gene by site-directed recombination. |journal= [[Proceedings of the National Academy of Sciences of the United States of America|Proc. Natl. Acad. Sci. USA]]|volume=92 |issue=26 |pages= 12070–4|doi= 10.1073/pnas.92.26.12070|pmid=8618846 |pmc=40298}}</ref> Marth has further used Cre-Lox conditional mutagenesis to establish a reproducible method for obtaining animal models of essential X chromosome-linked genes.<ref>{{cite journal|last1=Shafi|first1=R|last2=Iver|first2=SP|last3=Ellies|first3=LG|last4=O'Donnell|first4=N|last5=Marek|first5=KW|last6=Chui|first6=D|last7=Hart|first7=GW|last8=Marth|first8=JD|title=The O-GlcNAc transferase gene resides on the X chromosome and is essential for embryonic stem cell viability and mouse ontogeny|journal=Proc Natl Acad Sci USA|date=23 May 2000|pmid=10801981|doi=10.1073/pnas.100471497|pmc=18502|volume=97|issue=11|pages=5735–9}}</ref> These studies further explained how [[glycan]] linkages contribute to the origins of disease at the metabolic and cellular levels.<ref name="CEN"/><ref name="Journal02">{{cite journal |last1=Ellies |first1=L.G. |last2=Tsuboi |first2=S.|last3=Petryniak |first3=B. |last4=Lowe |first4=J.B. |last5=Fukuda| first5=M.| last6=Marth| first6=J.D.| date=1998 |title=Core 2 O-glycan biosynthesis distinguishes between selectin ligands essential for leukocyte homing and inflammation |journal= [[Immunity (journal)|Immunity]]|volume=9 |issue=6 |pages= 881–90|doi= 10.1016/s1074-7613(00)80653-6| pmid=9881978|doi-access=free }}</ref><ref name="Immune">{{cite book | last =Edelson | first =Stephen B. |author2=Deborah Mitchell | title =What Your Doctor May Not Tell You About(TM): Autoimmune Disorders: The Revolutionary Drug-free Treatments for Thyroid Disease, Lupus, MS, IBD, Chronic | publisher =[[Grand Central Publishing]] | date =2003 | url = https://books.google.com/books?id=QBbn2kVKLxIC&pg=PT60&lpg=PT60&dq=%22jamey+marth%22#v=onepage | isbn =978-0446679244 }}</ref>
Marth's early studies of glycosylation and glycan linkages revealed a profound effect on immunity and contributed to the genesis of the related field of glycoimmunology.<ref name="CEN">{{cite news | last=Borman| first=Stu| title =Sugar Medicine | publisher =[[Chemical and Engineering News]]| date =30 July 2007 | url =https://pubs.acs.org/cen/coverstory/85/8531cover.html | access-date =12 March 2015}}</ref> Marth's lab further discovered relationships between aberrant glycan linkages and autoimmune diseases including the fact that the exposure of cryptic immature glycan linkages in mammals could initiate chronic sterile inflammation leading to the development of autoimmunity.<ref name=Chietallvivogenetic>{{cite journal|last1=Chui|first1=Daniel|title=Genetic remodeling of protein glycosylation in vivo induces autoimmune disease|journal=Proc Natl Acad Sci USA|date=30 January 2001|pmid=11158608|display-authors=etal|pmc=14722|volume=98|issue=3|pages=1142–7|doi=10.1073/pnas.98.3.1142}}</ref> Marth's research has shown that the occurrence of autoimmune conditions (such as [[lupus]]) in mammals can be caused by the presence of abnormal glycan structures within the body.<ref>{{cite journal|last1=Green|first1=R.S.|title=Mammalian N-glycan branching protects against innate immune self-recognition and inflammation in autoimmune disease pathogenesis|journal=Immunity|date=27 August 2007|pages=308–20|display-authors=etal|pmid=17681821|doi=10.1016/j.immuni.2007.06.008|volume=27|issue=2|url=https://escholarship.org/content/qt5mw8r91q/qt5mw8r91q.pdf?t=lnrzra}}</ref>
Marth's laboratory has also taken a close look at the molecular and cellular bases of type 2 diabetes and the role that protein glycosylation has in the origin of the disease. Their research showed that the malfunction of [[Pancreas|pancreatic]] [[beta cells]] was the major contributor to disease onset. Their research indicated that genetic variation was unlikely to be the cause of obesity-associated type 2 diabetes in humans. Instead, their models suggested that metabolic alterations of pancreatic beta cells due to an elevation of fatty acids in obesity disabled [[glucose]] sensing, resulting in [[hyperglycemia]] with glucose intolerance. Marth’s laboratory further found that this pathway was induced in human patients with type 2 diabetes and was responsible for a significant amount of insulin resistance present in obesity-associated diabetes.<ref name="Futurity"/><ref name="UC"/><ref name="BBC">{{cite news | last=Gallagher| first=James| title =Fat 'disrupts sugar sensors causing type 2 diabetes' | publisher = [[BBC]]| date =14 August 2011 | url =https://www.bbc.com/news/health-14503480 | access-date =12 March 2015}}</ref>
The pathological features of sepsis have also been the subject of research by Marth's laboratory. Marth and colleagues discovered the first physiological purpose of the Ashwell-Morell Receptor (AMR), a [[hepatocyte]] [[lectin]] discovered by [[Gilbert Ashwell]] and Anatol Morell. Their studies revealed both a biological purpose of the receptor and how to use it for therapeutic purposes in pneumococcal sepsis.<ref name="SD"/>
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In 2008, Dr. Marth published an enumeration of the building blocks of life, all of which fall under the 4 types of [[macromolecules]] present in all cells (glycans, [[lipids]], [[nucleic acids]], and proteins).<ref name="UCSD2">{{cite news | last=Kain| first=Debra| title =Do 68 Molecules Hold the Key to Understanding Disease?| publisher = UC San Diego News Center| date =3 September 2008 | url =http://ucsdnews.ucsd.edu/archive/newsrel/health/09-0868Molecules.asp| access-date =29 April 2015}}</ref> This concept is becoming a feature of modern cell biology texts.<ref>{{cite book|last1=Alberts|first1=Bruce|last2=Johnson|first2=Alexander|last3=Lewis|first3=Julian|last4=Raff|first4=Martin|last5=Roberts|first5=Keither|last6=Walter|first6=Peter|title=Molecular Biology of the Cell|date=2002|publisher=Garland Science|isbn=978-0815332183|edition=5th}}</ref> Marth and other colleagues have called attention to the fact that only half of these macromolecules are encoded in the genome, suggesting that a more holistic and rigorous approach is needed to fully understand cell biology and the origins of disease.<ref name="ZDN">{{cite news | last=Piquepaille| first=Roland| title =68 molecular building blocks of life| publisher =[[ZDNet]]| date =8 September 2008 | url =http://www.zdnet.com/article/68-molecular-building-blocks-of-life/| access-date =29 April 2015}}</ref>


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== Education ==
Marth earned a Ph.D. in [[Pharmacology]] from the [[University of Washington]] in 1987.<ref name=":0" /><ref>{{Cite web|date=2021-04-18|title=Jamey Marth {{!}} MCDB {{!}} UC Santa Barbara|url=https://web.archive.org/web/20210418193203/https:/www.mcdb.ucsb.edu/people/faculty/jamey-marth|access-date=2021-07-14|website=web.archive.org}}</ref> During his time at Washington as a graduate student, he was mentored by [[Roger M. Perlmutter]] and [[Edwin G. Krebs]].<ref name=":0" /> Marth was Perlmutter's first graduate student.<ref>{{Cite web|date=2016-01-02|title=Notable Members|url=https://web.archive.org/web/20160102005322/http:/www.aai.org/About/History/Notable_Members/pdfs/OHP/Transcripts/Trans-Inv_017-Perlmutter_Roger_M-2013_Final.pdf|url-status=live|access-date=2021-07-14|website=web.archive.org}}</ref>

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== Career ==
Following his time as a staff scientist at Oncogen Corporation in [[Seattle]], Marth was recruited to the founding faculty of the Biomedical Research Centre in [[Vancouver|Vancouver, British Columbia, Canada]], where he was also appointed as a professor in the Department of Medical Genetics at the University of British Columbia.<ref name=":0" /> In 1995, [[George Palade]] and [[Marilyn Farquhar]] (among others) recruited Marth to the [[University of California, San Diego]] (UCSD) in the Department of Cellular and Molecular Medicine.<ref name=":3">{{Cite web|date=2021-04-18|title=Jamey Marth {{!}} MCDB {{!}} UC Santa Barbara|url=https://web.archive.org/web/20210418193203/https:/www.mcdb.ucsb.edu/people/faculty/jamey-marth|access-date=2021-07-14|website=web.archive.org}}</ref> Upon his arrival, he was appointed as an Investigator of the [[Howard Hughes Medical Institute]].<ref name=":3" /> Marth spent more than 14 years in this position at UCSD. His research at HHMI and UCSD helped bolster an already renowned [[glycobiology]] program that originated with [[Ajit Varki]] and later included [[Jeffrey Esko]].<ref>{{Cite journal|last=Haltiwanger|first=Robert S.|date=2000-12-01|title=Essentials of Glycobiology. Ajit Varki , Richard Cummings , Jeffrey Esko , Hudson Freeze , Gerald Hart , Jamey Marth , Maarten Chrispeels , Ole Hindsgaul , James C. Paulson , John Lowe , Adriana Manzi , Leland Powell , Herman van Halbeek|url=https://www.journals.uchicago.edu/doi/abs/10.1086/393647|journal=The Quarterly Review of Biology|volume=75|issue=4|pages=451–452|doi=10.1086/393647|issn=0033-5770}}</ref><ref>{{Cite web|title=History - Glycobiology Research and Training Center, UC San Diego|url=https://medschool.ucsd.edu:443/research/GRTC/about/Pages/History.aspx|access-date=2021-07-14|website=UC San Diego Health Sciences|language=en-US}}</ref>

In 2009, he accepted a position at the University of California, Santa Barbara (UCSB) and the [[Sanford Burnham Prebys Medical Discovery Institute|Sanford-Burnham Medical Research Institute]] as the Director of the Center for Nanomedicine.<ref name=":3" /> He also then became the inaugural recipient of the Carbon Chair in Biochemistry and Molecular Biology and the recipient of the Mellichamp Chair of Systems Biology.<ref>{{Cite web|title=Faculty {{!}} Division of Mathematical Life and Physical Sciences - UC Santa Barbara|url=https://science.ucsb.edu/faculty|access-date=2021-07-14|website=science.ucsb.edu}}</ref><ref name=":2" />

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== Research ==
Marth’s research is credited with the development of methodologies applicable to investigating the origins of disease. His conception and co-development of Cre-Lox conditional mutagenesis has provided a means to further perceive the mechanistic underpinnings of disease, and continues to be used by scientists worldwide.<ref>{{Cite web|title=Floxed Mice - Cre-lox Recombination and Gene Targeting|url=https://www.genetargeting.com/floxed/lox-p/floxed-mice-cre/|access-date=2021-07-14|website=www.genetargeting.com|language=en-US}}</ref><ref>{{Cite web|last=Marth|first=J. D.|date=1996-05-01|title=Recent advances in gene mutagenesis by site-directed recombination.|url=https://www.jci.org/articles/view/118634/pdf|access-date=2021-07-14|website=www.jci.org|language=en}}</ref><ref>{{Cite journal|last=Gu|first=H.|last2=Marth|first2=J. D.|last3=Orban|first3=P. C.|last4=Mossmann|first4=H.|last5=Rajewsky|first5=K.|date=1994-07-01|title=Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting|url=https://pubmed.ncbi.nlm.nih.gov/8016642/|journal=Science (New York, N.Y.)|volume=265|issue=5168|pages=103–106|doi=10.1126/science.8016642|issn=0036-8075|pmid=8016642}}</ref> Prior to the development of conditional mutagenesis, the use of homologous recombination was limited to systemic gene targeting and mutation.<ref>{{Cite journal|last=Wadman|first=M.|date=1998-08-27|title=DuPont opens up access to genetics tool|url=https://pubmed.ncbi.nlm.nih.gov/9732857/|journal=Nature|volume=394|issue=6696|pages=819|doi=10.1038/29607|issn=0028-0836|pmid=9732857}}</ref> Marth's use of Cre-Lox conditional mutagenesis established the presence and functions of multiple and in some cases previously unknown enzymes participating in protein glycosylation, an area of research that has become a focus of exploration of the genetic and metabolic origins of disease.<ref name=":4">{{Cite web|last=News|first=Chemical & Engineering|title=Chemical & Engineering News: Cover Story - Sugar Medicine|url=http://pubsapp.acs.org/cen/coverstory/85/8531cover.html|access-date=2021-07-14|website=pubsapp.acs.org}}</ref><ref name=":5">{{Cite journal|date=2006-09-08|title=Glycosylation in Cellular Mechanisms of Health and Disease|url=https://www.sciencedirect.com/science/article/pii/S0092867406010865|journal=Cell|language=en|volume=126|issue=5|pages=855–867|doi=10.1016/j.cell.2006.08.019|issn=0092-8674}}</ref> Marth also used Cre-Lox mutagenesis to establish a reproducible method for obtaining animal models of essential X chromosome-linked genes.<ref>{{Cite journal|last=Shafi|first=Raheel|last2=Iyer|first2=Sai Prasad N.|last3=Ellies|first3=Lesley G.|last4=O'Donnell|first4=Niall|last5=Marek|first5=Kurt W.|last6=Chui|first6=Daniel|last7=Hart|first7=Gerald W.|last8=Marth|first8=Jamey D.|date=2000-05-23|title=The O-GlcNAc transferase gene resides on the X chromosome and is essential for embryonic stem cell viability and mouse ontogeny|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC18502/|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=97|issue=11|pages=5735–5739|issn=0027-8424|pmid=10801981}}</ref>

Marth's early studies of glycosylation and glycan linkages revealed a profound effect on immunity and contributed to the genesis of the related sub-field termed glycoimmunology.<ref name=":6">{{Cite journal|last=Marth|first=Jamey D.|last2=Grewal|first2=Prabhjit K.|date=|title=Mammalian glycosylation in immunity|url=https://www.nature.com/articles/nri2417|journal=Nature Reviews Immunology|language=en|volume=8|issue=11|pages=874–887|doi=10.1038/nri2417|issn=1474-1741}}</ref><ref>{{Cite journal|last=Baum|first=Linda G.|last2=Crocker|first2=Paul R.|date=2009|title=Glycoimmunology: ignore at your peril!|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-065X.2009.00800.x|journal=Immunological Reviews|language=en|volume=230|issue=1|pages=5–8|doi=10.1111/j.1600-065X.2009.00800.x|issn=1600-065X}}</ref><ref name=":4" /> Marth's laboratory discovered connections between aberrant glycan linkages and autoimmune diseases including the fact that the exposure of cryptic immature glycan linkages in mammals could initiate chronic sterile inflammation leading to the development of autoimmunity.<ref name=":2" /><ref name=":5" /> Those findings indicated that autoimmunity can be precipitated by the presence of abnormal glycan structures within the body.<ref name=":6" /><ref>{{Cite journal|last=Green|first=Ryan S.|last2=Stone|first2=Erica L.|last3=Tenno|first3=Mari|last4=Lehtonen|first4=Eero|last5=Farquhar|first5=Marilyn G.|last6=Marth|first6=Jamey D.|date=2007-08-01|title=Mammalian N-glycan branching protects against innate immune self-recognition and inflammation in autoimmune disease pathogenesis.|url=https://escholarship.org/uc/item/5mw8r91q|journal=Immunity|language=en|volume=27|issue=2|pages=308–320|issn=1074-7613}}</ref>

Marth's laboratory has also taken a close look at the molecular and cellular bases of Type 2 diabetes and the role that protein glycosylation plays in the origin of the disease.<ref name=":7">{{Cite journal|last=Ohtsubo|first=Kazuaki|last2=Chen|first2=Mark Z|last3=Olefsky|first3=Jerrold M|last4=Marth|first4=Jamey D|date=2011-08-14|title=Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888087/|journal=Nature medicine|volume=17|issue=9|pages=1067–1075|doi=10.1038/nm.2414|issn=1078-8956|pmc=3888087|pmid=21841783}}</ref><ref>{{Cite web|title=UCSD Team Discovers Diabetes Trigger in Fatty Diet|url=https://health.ucsd.edu/news/2005/Pages/12_28_Marth.aspx|access-date=2021-07-14|website=UC Health - UC San Diego|language=en-US}}</ref> Their research demonstrated that acquired [[Pancreas|pancreatic]] [[Beta cells|beta cell]] dysfunction was the major contributor of disease onset and corroborated views that genetic variation was unlikely to be the primary cause of obesity-associated Type 2 diabetes in humans.<ref name=":7" /><ref>{{Cite web|title=How Fat and Obesity Cause Diabetes|url=https://www.news.ucsb.edu/2011/013098/how-fat-and-obesity-cause-diabetes|access-date=2021-07-14|website=The UCSB Current|language=en}}</ref> Instead, their findings revealed that altered pancreatic beta cell glycosylation resulting from elevated fatty acid levels in obesity disabled [[glucose]] sensing, resulting in [[hyperglycemia]] with glucose intolerance.<ref name=":1" /><ref>{{Cite web|date=2019-03-02|title=Pioneering research on type 2 diabetes - UC Health|url=https://web.archive.org/web/20190302100405/https:/health.universityofcalifornia.edu/2013/01/04/pioneering-research-on-type-2-diabetes/|url-status=live|access-date=2021-07-14|website=web.archive.org}}</ref> Marth’s research team further found that this pathway was induced in human patients with Type 2 diabetes and was responsible for a significant amount of the insulin resistance present in experimentally-induced obesity-associated diabetes.<ref name=":1" /><ref>{{Cite news|date=2011-08-14|title=Fat 'disrupts sugar sensors causing type 2 diabetes'|language=en-GB|work=BBC News|url=https://www.bbc.com/news/health-14503480|access-date=2021-07-14}}</ref>

The pathological underpinnings of inflammatory diseases including sepsis have also been the subject of research by Marth's laboratory.<ref name=":8" /><ref name=":2" /><ref>{{Cite journal|last=Yang|first=Won Ho|last2=Heithoff|first2=Douglas M.|last3=Aziz|first3=Peter V.|last4=Sperandio|first4=Markus|last5=Nizet|first5=Victor|last6=Mahan|first6=Michael J.|last7=Marth|first7=Jamey D.|date=2017-12-22|title=Recurrent Infection Progressively Disables Host Protection Against Intestinal Inflammation|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824721/|journal=Science (New York, N.Y.)|volume=358|issue=6370|doi=10.1126/science.aao5610|issn=0036-8075|pmc=5824721|pmid=29269445}}</ref> Marth and colleagues discovered the first physiological purpose of the Ashwell-Morell Receptor (AMR), a [[hepatocyte]] [[lectin]] discovered by [[Gilbert Ashwell]] and Anatol Morell.<ref>{{Cite journal|last=Grewal|first=Prabhjit K|last2=Uchiyama|first2=Satoshi|last3=Ditto|first3=David|last4=Varki|first4=Nissi|last5=Le|first5=Dzung T|last6=Nizet|first6=Victor|last7=Marth|first7=Jamey D|date=|title=The Ashwell receptor mitigates the lethal coagulopathy of sepsis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2853759/|journal=Nature medicine|volume=14|issue=6|pages=648–655|doi=10.1038/nm1760|issn=1078-8956|pmc=2853759|pmid=18488037}}</ref><ref name=":5" /> Their studies further identified how AMR function can be modulated for therapeutic purposes.<ref name=":8" />

⚫
In 2008, Marth published an initial enumeration of the building blocks of life, all of which fall under the four types of cellular [[macromolecules]] (glycans, [[lipids]], [[nucleic acids]], and proteins).<ref name=":9">{{Cite journal|last=Marth|first=Jamey D.|date=|title=A unified vision of the building blocks of life|url=https://www.nature.com/articles/ncb0908-1015|journal=Nature Cell Biology|language=en|volume=10|issue=9|pages=1015–1015|doi=10.1038/ncb0908-1015|issn=1476-4679}}</ref><ref>{{Cite web|title=Do 68 Molecules Hold the Key to Understanding Disease?|url=https://ucsdnews.ucsd.edu/archive/newsrel/health/09-0868Molecules.asp|access-date=2021-07-14|website=ucsdnews.ucsd.edu}}</ref> This accounting has become an educational feature of cell biology texts. Marth and other colleagues have called attention to the fact that only half of these macromolecules are encoded by the genome, suggesting that a more holistic approach is needed in biomedical research to fully understand and intervene in the origins and progression of disease.<ref name=":9" /><ref>{{Cite web|last=Piquepaille|first=Roland|title=68 molecular building blocks of life|url=https://www.zdnet.com/article/68-molecular-building-blocks-of-life/|access-date=2021-07-14|website=ZDNet|language=en}}</ref>

⚫
== Selected Publications ==


⚫
==Selected publications==
* {{cite journal | last1 = Grewal | first1 = P.K. | last2 = Aziz | first2 = P.Z. | last3 = Uchiyama | first3 = S. | last4 = Rubio | first4 = G.R. | last5 = Lardone | first5 = R.D. | last6 = Le | first6 = D. | last7 = Varki | first7 = N. | last8 = Nizet | first8 = V. | last9 = Marth | first9 = J.D. | year = 2013 | title = Inducing host protection in pneumococcal sepsis by preactivation of the Ashwell-Morell receptor | journal = Proc. Natl. Acad. Sci. USA | volume = 110 | issue = 50| pages = 20218–20223 | doi=10.1073/pnas.1313905110 | pmid=24284176 | pmc=3864324}}
* {{cite journal | last1 = Grewal | first1 = P.K. | last2 = Aziz | first2 = P.Z. | last3 = Uchiyama | first3 = S. | last4 = Rubio | first4 = G.R. | last5 = Lardone | first5 = R.D. | last6 = Le | first6 = D. | last7 = Varki | first7 = N. | last8 = Nizet | first8 = V. | last9 = Marth | first9 = J.D. | year = 2013 | title = Inducing host protection in pneumococcal sepsis by preactivation of the Ashwell-Morell receptor | journal = Proc. Natl. Acad. Sci. USA | volume = 110 | issue = 50| pages = 20218–20223 | doi=10.1073/pnas.1313905110 | pmid=24284176 | pmc=3864324}}
* {{cite journal | last1 = Ohtsubo | first1 = K. | last2 = Chen | first2 = M. Z. | last3 = Olefsky | first3 = J.M. | last4 = Marth | first4 = J.D. | year = 2011 | title = Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport | journal = Nat. Med. | volume = 17 | issue = 9| pages = 1067–1075 | doi=10.1038/nm.2414| pmid = 21841783 | pmc = 3888087 }}
* {{cite journal | last1 = Ohtsubo | first1 = K. | last2 = Chen | first2 = M. Z. | last3 = Olefsky | first3 = J.M. | last4 = Marth | first4 = J.D. | year = 2011 | title = Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport | journal = Nat. Med. | volume = 17 | issue = 9| pages = 1067–1075 | doi=10.1038/nm.2414| pmid = 21841783 | pmc = 3888087 }}
Line 75: Line 73:
* {{cite journal | last1 = Chui | first1 = D. | last2 = Sellakumar | first2 = G. | last3 = Green | first3 = R. | last4 = Sutton-Smith | first4 = M. | last5 = McQuistan | first5 = T. | last6 = Marek | first6 = K. | last7 = Morris | first7 = H. | last8 = Dell | first8 = A. | last9 = Marth | first9 = J.D. | year = 2001 | title = Genetic remodeling of protein glycosylation in vivo induces autoimmune disease | journal = Proc Natl Acad Sci USA | volume = 98 | issue = 3| pages = 1142–1147 | doi=10.1073/pnas.98.3.1142 | pmid=11158608 | pmc=14722}}
* {{cite journal | last1 = Chui | first1 = D. | last2 = Sellakumar | first2 = G. | last3 = Green | first3 = R. | last4 = Sutton-Smith | first4 = M. | last5 = McQuistan | first5 = T. | last6 = Marek | first6 = K. | last7 = Morris | first7 = H. | last8 = Dell | first8 = A. | last9 = Marth | first9 = J.D. | year = 2001 | title = Genetic remodeling of protein glycosylation in vivo induces autoimmune disease | journal = Proc Natl Acad Sci USA | volume = 98 | issue = 3| pages = 1142–1147 | doi=10.1073/pnas.98.3.1142 | pmid=11158608 | pmc=14722}}
* {{cite journal | last1 = Chui | first1 = D. | last2 = Oh-Eda | first2 = M. | last3 = Liao | first3 = Y.F. | last4 = Panneerselvam | first4 = K. | last5 = Lal | first5 = A. | last6 = Marek | first6 = K.W. | last7 = Freeze | first7 = H.H. | last8 = Moremen | first8 = K.W. | last9 = Fukuda | first9 = M.N. | last10 = Marth | first10 = J.D. | year = 1997 | title = Alpha-mannosidase-II deficiency results in dyserythropoiesis and unveils an alternate pathway in oligosaccharide biosynthesis | journal = Cell | volume = 90 | issue = 1| pages = 157–67 | doi=10.1016/s0092-8674(00)80322-0| pmid = 9230311 | s2cid = 6064567 | doi-access = free }}
* {{cite journal | last1 = Chui | first1 = D. | last2 = Oh-Eda | first2 = M. | last3 = Liao | first3 = Y.F. | last4 = Panneerselvam | first4 = K. | last5 = Lal | first5 = A. | last6 = Marek | first6 = K.W. | last7 = Freeze | first7 = H.H. | last8 = Moremen | first8 = K.W. | last9 = Fukuda | first9 = M.N. | last10 = Marth | first10 = J.D. | year = 1997 | title = Alpha-mannosidase-II deficiency results in dyserythropoiesis and unveils an alternate pathway in oligosaccharide biosynthesis | journal = Cell | volume = 90 | issue = 1| pages = 157–67 | doi=10.1016/s0092-8674(00)80322-0| pmid = 9230311 | s2cid = 6064567 | doi-access = free }}
* Hennet, T; Hagen, F K; Tabak, L A; Marth, J D (1995-12-19). "[https://pubmed.ncbi.nlm.nih.gov/8618846/ T-cell-specific deletion of a polypeptide N-acetylgalactosaminyl-transferase gene by site-directed recombination]". Proceedings of the National Academy of Sciences of the United States of America. 92 (26): 12070–12074. ISSN 0027-8424. PMID [https://pubmed.ncbi.nlm.nih.gov/8618846 8618846].

==References==
== References ==
{{reflist|2}}
{{reflist}}


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Revision as of 09:58, 14 July 2021

Jamey Marth
Born
Sarasota, Florida
NationalityAmerican and Canadian
Alma materUniversity of Washington
Scientific career
FieldsMolecular biology
Cellular biology
InstitutionsSBP Medical Discovery Institute
UC Santa Barbara
Howard Hughes Medical Institute
UC San Diego
Doctoral advisorsRoger M. Perlmutter and Edwin G. Krebs

Jamey Marth, Ph.D., is a molecular and cellular biologist. He is currently on the faculty of the SBP Medical Discovery Institute in La Jolla, California.[1]

His research has largely focused on how protein glycosylation contributes to the origins of common diseases and syndromes including diabetes, sepsis, colitis, and autoimmunity.[2][3][4][5]

Education

Marth earned a Ph.D. in Pharmacology from the University of Washington in 1987.[1][6] During his time at Washington as a graduate student, he was mentored by Roger M. Perlmutter and Edwin G. Krebs.[1] Marth was Perlmutter's first graduate student.[7]

Career

Following his time as a staff scientist at Oncogen Corporation in Seattle, Marth was recruited to the founding faculty of the Biomedical Research Centre in Vancouver, British Columbia, Canada, where he was also appointed as a professor in the Department of Medical Genetics at the University of British Columbia.[1] In 1995, George Palade and Marilyn Farquhar (among others) recruited Marth to the University of California, San Diego (UCSD) in the Department of Cellular and Molecular Medicine.[8] Upon his arrival, he was appointed as an Investigator of the Howard Hughes Medical Institute.[8] Marth spent more than 14 years in this position at UCSD. His research at HHMI and UCSD helped bolster an already renowned glycobiology program that originated with Ajit Varki and later included Jeffrey Esko.[9][10]

In 2009, he accepted a position at the University of California, Santa Barbara (UCSB) and the Sanford-Burnham Medical Research Institute as the Director of the Center for Nanomedicine.[8] He also then became the inaugural recipient of the Carbon Chair in Biochemistry and Molecular Biology and the recipient of the Mellichamp Chair of Systems Biology.[11][5]

Research

Marth’s research is credited with the development of methodologies applicable to investigating the origins of disease. His conception and co-development of Cre-Lox conditional mutagenesis has provided a means to further perceive the mechanistic underpinnings of disease, and continues to be used by scientists worldwide.[12][13][14] Prior to the development of conditional mutagenesis, the use of homologous recombination was limited to systemic gene targeting and mutation.[15] Marth's use of Cre-Lox conditional mutagenesis established the presence and functions of multiple and in some cases previously unknown enzymes participating in protein glycosylation, an area of research that has become a focus of exploration of the genetic and metabolic origins of disease.[16][17] Marth also used Cre-Lox mutagenesis to establish a reproducible method for obtaining animal models of essential X chromosome-linked genes.[18]

Marth's early studies of glycosylation and glycan linkages revealed a profound effect on immunity and contributed to the genesis of the related sub-field termed glycoimmunology.[19][20][16] Marth's laboratory discovered connections between aberrant glycan linkages and autoimmune diseases including the fact that the exposure of cryptic immature glycan linkages in mammals could initiate chronic sterile inflammation leading to the development of autoimmunity.[5][17] Those findings indicated that autoimmunity can be precipitated by the presence of abnormal glycan structures within the body.[19][21]

Marth's laboratory has also taken a close look at the molecular and cellular bases of Type 2 diabetes and the role that protein glycosylation plays in the origin of the disease.[22][23] Their research demonstrated that acquired pancreatic beta cell dysfunction was the major contributor of disease onset and corroborated views that genetic variation was unlikely to be the primary cause of obesity-associated Type 2 diabetes in humans.[22][24] Instead, their findings revealed that altered pancreatic beta cell glycosylation resulting from elevated fatty acid levels in obesity disabled glucose sensing, resulting in hyperglycemia with glucose intolerance.[2][25] Marth’s research team further found that this pathway was induced in human patients with Type 2 diabetes and was responsible for a significant amount of the insulin resistance present in experimentally-induced obesity-associated diabetes.[2][26]

The pathological underpinnings of inflammatory diseases including sepsis have also been the subject of research by Marth's laboratory.[3][5][27] Marth and colleagues discovered the first physiological purpose of the Ashwell-Morell Receptor (AMR), a hepatocyte lectin discovered by Gilbert Ashwell and Anatol Morell.[28][17] Their studies further identified how AMR function can be modulated for therapeutic purposes.[3]

In 2008, Marth published an initial enumeration of the building blocks of life, all of which fall under the four types of cellular macromolecules (glycans, lipids, nucleic acids, and proteins).[29][30] This accounting has become an educational feature of cell biology texts. Marth and other colleagues have called attention to the fact that only half of these macromolecules are encoded by the genome, suggesting that a more holistic approach is needed in biomedical research to fully understand and intervene in the origins and progression of disease.[29][31]

Selected Publications

References

  1. ^ a b c d "Jamey Marth, Ph.D. | SBP". www.sbpdiscovery.org. Retrieved 2021-07-14.
  2. ^ a b c "Fatty diet triggers diabetes onslaught". Futurity. 2011-08-16. Retrieved 2021-07-14.
  3. ^ a b c "Biomedical scientist discovers method to increase survival in sepsis". ScienceDaily. Retrieved 2021-07-14.
  4. ^ Marth, Jamey David (2020). "Glycosylation in a Common Mechanism of Colitis and Sepsis". The FASEB Journal. 34 (S1): 1–1. doi:10.1096/fasebj.2020.34.s1.00176. ISSN 1530-6860.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ a b c d "Jamey Marth Honored for Research Linking Glycans to Diabetes, Lupus, Sepsis". www.newswise.com. Retrieved 2021-07-14.
  6. ^ "Jamey Marth | MCDB | UC Santa Barbara". web.archive.org. 2021-04-18. Retrieved 2021-07-14.
  7. ^ "Notable Members" (PDF). web.archive.org. 2016-01-02. Retrieved 2021-07-14.{{cite web}}: CS1 maint: url-status (link)
  8. ^ a b c "Jamey Marth | MCDB | UC Santa Barbara". web.archive.org. 2021-04-18. Retrieved 2021-07-14.
  9. ^ Haltiwanger, Robert S. (2000-12-01). "Essentials of Glycobiology. Ajit Varki , Richard Cummings , Jeffrey Esko , Hudson Freeze , Gerald Hart , Jamey Marth , Maarten Chrispeels , Ole Hindsgaul , James C. Paulson , John Lowe , Adriana Manzi , Leland Powell , Herman van Halbeek". The Quarterly Review of Biology. 75 (4): 451–452. doi:10.1086/393647. ISSN 0033-5770.
  10. ^ "History - Glycobiology Research and Training Center, UC San Diego". UC San Diego Health Sciences. Retrieved 2021-07-14.
  11. ^ "Faculty | Division of Mathematical Life and Physical Sciences - UC Santa Barbara". science.ucsb.edu. Retrieved 2021-07-14.
  12. ^ "Floxed Mice - Cre-lox Recombination and Gene Targeting". www.genetargeting.com. Retrieved 2021-07-14.
  13. ^ Marth, J. D. (1996-05-01). "Recent advances in gene mutagenesis by site-directed recombination". www.jci.org. Retrieved 2021-07-14.
  14. ^ Gu, H.; Marth, J. D.; Orban, P. C.; Mossmann, H.; Rajewsky, K. (1994-07-01). "Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting". Science (New York, N.Y.). 265 (5168): 103–106. doi:10.1126/science.8016642. ISSN 0036-8075. PMID 8016642.
  15. ^ Wadman, M. (1998-08-27). "DuPont opens up access to genetics tool". Nature. 394 (6696): 819. doi:10.1038/29607. ISSN 0028-0836. PMID 9732857.
  16. ^ a b News, Chemical & Engineering. "Chemical & Engineering News: Cover Story - Sugar Medicine". pubsapp.acs.org. Retrieved 2021-07-14. {{cite web}}: |last= has generic name (help)
  17. ^ a b c "Glycosylation in Cellular Mechanisms of Health and Disease". Cell. 126 (5): 855–867. 2006-09-08. doi:10.1016/j.cell.2006.08.019. ISSN 0092-8674.
  18. ^ Shafi, Raheel; Iyer, Sai Prasad N.; Ellies, Lesley G.; O'Donnell, Niall; Marek, Kurt W.; Chui, Daniel; Hart, Gerald W.; Marth, Jamey D. (2000-05-23). "The O-GlcNAc transferase gene resides on the X chromosome and is essential for embryonic stem cell viability and mouse ontogeny". Proceedings of the National Academy of Sciences of the United States of America. 97 (11): 5735–5739. ISSN 0027-8424. PMID 10801981.
  19. ^ a b Marth, Jamey D.; Grewal, Prabhjit K. "Mammalian glycosylation in immunity". Nature Reviews Immunology. 8 (11): 874–887. doi:10.1038/nri2417. ISSN 1474-1741.
  20. ^ Baum, Linda G.; Crocker, Paul R. (2009). "Glycoimmunology: ignore at your peril!". Immunological Reviews. 230 (1): 5–8. doi:10.1111/j.1600-065X.2009.00800.x. ISSN 1600-065X.
  21. ^ Green, Ryan S.; Stone, Erica L.; Tenno, Mari; Lehtonen, Eero; Farquhar, Marilyn G.; Marth, Jamey D. (2007-08-01). "Mammalian N-glycan branching protects against innate immune self-recognition and inflammation in autoimmune disease pathogenesis". Immunity. 27 (2): 308–320. ISSN 1074-7613.
  22. ^ a b Ohtsubo, Kazuaki; Chen, Mark Z; Olefsky, Jerrold M; Marth, Jamey D (2011-08-14). "Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport". Nature medicine. 17 (9): 1067–1075. doi:10.1038/nm.2414. ISSN 1078-8956. PMC 3888087. PMID 21841783.
  23. ^ "UCSD Team Discovers Diabetes Trigger in Fatty Diet". UC Health - UC San Diego. Retrieved 2021-07-14.
  24. ^ "How Fat and Obesity Cause Diabetes". The UCSB Current. Retrieved 2021-07-14.
  25. ^ "Pioneering research on type 2 diabetes - UC Health". web.archive.org. 2019-03-02. Retrieved 2021-07-14.{{cite web}}: CS1 maint: url-status (link)
  26. ^ "Fat 'disrupts sugar sensors causing type 2 diabetes'". BBC News. 2011-08-14. Retrieved 2021-07-14.
  27. ^ Yang, Won Ho; Heithoff, Douglas M.; Aziz, Peter V.; Sperandio, Markus; Nizet, Victor; Mahan, Michael J.; Marth, Jamey D. (2017-12-22). "Recurrent Infection Progressively Disables Host Protection Against Intestinal Inflammation". Science (New York, N.Y.). 358 (6370). doi:10.1126/science.aao5610. ISSN 0036-8075. PMC 5824721. PMID 29269445.
  28. ^ Grewal, Prabhjit K; Uchiyama, Satoshi; Ditto, David; Varki, Nissi; Le, Dzung T; Nizet, Victor; Marth, Jamey D. "The Ashwell receptor mitigates the lethal coagulopathy of sepsis". Nature medicine. 14 (6): 648–655. doi:10.1038/nm1760. ISSN 1078-8956. PMC 2853759. PMID 18488037.
  29. ^ a b Marth, Jamey D. "A unified vision of the building blocks of life". Nature Cell Biology. 10 (9): 1015–1015. doi:10.1038/ncb0908-1015. ISSN 1476-4679.
  30. ^ "Do 68 Molecules Hold the Key to Understanding Disease?". ucsdnews.ucsd.edu. Retrieved 2021-07-14.
  31. ^ Piquepaille, Roland. "68 molecular building blocks of life". ZDNet. Retrieved 2021-07-14.
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