Dr. Jennifer Elizabeth Garrus (born 1973)


Born in Columbus, Ohio on October 6, 1973 to James and Karen Garrus. [HL003S][GDrive]

Dr. Jennifer Garrus, age 45, of Thornton, Colorado, passed away on October 17, 2018 [HL003S][GDrive]


Jennifer Garrus Professional - LinkedIN profile

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Results-oriented Scientific Leader with 12 years of experience in drug discovery, translational medicine and clinical development. Proven track record managing matrix teams providing lead optimization, translational research and Phase 1/2 support for multiple programs. Known for flexibility, performing in a self-directed environment and as team member while managing junior scientists. Recognized as an effective communicator, drawing on broad knowledge base and employing team-oriented leadership to deliver results. [...]


  • Merck - Senior Clinical Scientist

    • Employed Aug 2017 – Present

    • Employment Duration 2 yrs 9 mos

    • Location Greater Denver Area

  • ExecuPharm - Senior Clinical Scientist on assignment to Merck

    • Employed May 2016 – Jul 2017

    • Employment Duration 1 yr 3 mos

    • Location Greater Denver Area

  • Biodesix, Inc. - Senior Manager, Clinical Development/Translational Medicine

    • Employed Dec 2013 – Apr 2016

    • Employment Duration 2 yrs 5 mos

    • Location Boulder, CO

      • Collaborated with stakeholders on the design, execution and analysis of studies to elucidate the mechanism of action of VeriStrat®, a prognostic and predictive serum proteomics test for advanced non-small cell lung cancer patients

      • Wrote scientific proposals for nonclinical research projects, analyzed biomarker and clinical outcome data and prepared scientific reports for internal and external audiences.

  • Array BioPharma (Total Duration 6 yrs 7 mos)

    • Research Investigator

      • Employed Oct 2012 – Aug 2013 ( 11 mos )

      • Location Boulder, Colorado

      • Developed Phase 2 strategies to identify nucleic acid and protein-based response biomarkers in plasma and bone marrow of patients with hematologic malignancies for two programs.

      • Managed Translational Operations group, enabling all aspects of clinical sample management for 8 concurrent clinical trials (e.g., creation of PK / biomarker sampling kits, generation of site training materials, sample tracking, and facilitating outsourcing activities).

      • Created biomarker sections of clinical protocols and clinical study reports.

      • Supervised scientific and operations staff.

    • Senior Research Scientist

      • Employed Oct 2009 – Sep 2012 ( 3 yrs )

      • Location Boulder, Colorado

      • Provided strategic, scientific and operational leadership of cross-functional teams supporting one IND-stage and 3 clinical stage programs.

      • Led biomarker team for CSF-1R inhibitor program demonstrating pharmacodynamic activity in blood / serum / urine in Ph 1 patients with solid tumors.

      • Coordinated predictive biomarker strategy and oversaw sample analyses (in house and outsourced) identifying protein-based plasma biomarkers related to disease, age or clinical benefit from treatment with p38 / Tie2 inhibitor in patients with MDS in Phase 1 study.

      • Supervised IHC / immunoassay PD biomarker assay development and clinical sample analyses demonstrating mechanistic and functional target inhibition by p38 / Tie2 inhibitor in MDS patient bone marrow and plasma samples from Phase 1 study.

      • Defined potential clinical development strategies for selective HER2 inhibitor.

      • Wrote biomarker sections of clinical protocols, Investigator’s brochures, informed consent forms and clinical study reports.

      • Prepared presentations and technical report sections of business development documents.

      • Supervised scientific staff.

    • Title Research Scientist

      • Employed Feb 2007 – Sep 2009 ( 2 yrs 8 mos )

      • Location Boulder, Colorado

      • Provided strategic, scientific and operational leadership for 2 clinical stage programs.

      • Developed Phase 1 biomarker strategy and coordinated outsourcing of tumor biopsy IHC analyses, demonstrating target inhibition and confirming possible sensitivity marker in breast cancer patients treated with HER2 inhibitor.

      • Performed and directed nonclinical research supporting development paths of small molecule ErbB inhibitors in solid tumor indications.

      • Generated / implemented biomarker strategies for Phase 1 clinical trials,

      • Created sample collection manuals, conducted clinical site training on laboratory procedures.

      • Supervised scientific staff.

  • Myriad Genetics/Myriad Pharmaceuticals

    • Total Duration 3 yrs 9 mos

    • Title Scientist II

      • Employed May 2005 – Jan 2007 ( 1 yr 9 mos )

      • Served as Project Leader and managed multidisciplinary lead optimization effort delivering a small molecule HIV-1 maturation inhibitor IND candidate.

      • Developed cellular assays and performed compound characterization, including resistance selection and mechanism of action studies.

      • Created IND-enabling documents.

      • Supervised scientific staff.

    • Title Scientist I

      • Employed May 2003 – Apr 2005 ( 2 yrs )

      • Provided scientific leadership and laboratory support for 2 antiviral lead optimization projects.

      • Developed and optimized cell-based assays and tested compounds, supporting structure-activity relationship studies of small molecule compounds for antiviral and oncology programs.

      • Managed Biosafety Level 3 (BSL3) laboratory.

      • Supervised scientific staff.

2018 (October 17) Passing -

See [HL003S][GDrive]

[...] Jennifer will be remembered for being highly intelligent, down to earth, gracious, kind, fun-loving, and for her huge, heart-warming smile – with her eyes always twinkling. She was very humble, despite being extremely accomplished in her personal and professional life. She was a devoted mother, a loving daughter and sister, a loyal friend, and a giving member of her community.

She and her family moved to Colorado when she was three years old. She lived there most of her life, aside from the 10 years she spent in Utah pursuing her PhD and working as a scientist.

As a young girl, Jennifer was precocious, and she remained curious, driven and ambitious throughout her life. She was a member of the National Honor Society at Arapahoe High School. She studied ballet, played competitive soccer, and enjoyed water sports throughout her childhood and teen years.

While earning her degree in Biochemistry from Colorado State University, she received numerous awards and certificates of recognition, as well as the distinguished Colorado Scholars Scholarship from the College of Natural Sciences.

After completing her PhD in Biochemistry, she was a Senior Clinical researcher, most recently at Merck. She was a tenacious leader and worker, managing teams who conducted critical research on cures for cancer and viruses.

She dedicated her personal time to raising her children with warmth and generosity; although she enjoyed gardening, hiking, and time with family and friends, her kids were her primary source of joy, meaning and purpose. [...] .


See [HW002P][GDrive] (Mentioned : [Dr. Wesley Ian Sundquist (born 1959)] here)

Patrick Gavin (February 7, 2019)I met Jenn through Brendan. I appreciated her commitment to bringing Brendan to practice and enjoyed speaking to her about life after practice while our kiddos played on the swing set. My heart goes out to Kiera and Brendan. He’s still my favorite soccer player I coached! What a wonderful kid, and I hope this arrives late but with heartfelt love. [...]
Ira von Carlowitz (February 7, 2019)Jenn, I miss you...Suzy and I are working hard at upholding the regular get-togethers you would always plan for us...Especially after we both left Array. [...]
Sam Li (November 29, 2018)I know Jenn since we were both graduate students in Utah, working in the same lab but on different research projects. Even though as a young graduate student, Jenn was clearly much more mature than most of us, both scientifically and socially. She was always cheerful and kind to people around her. Not only she was smart, quickly on top of her research project, she was also extremely humble and down to earth. Soon after Jenn joined the lab, we became good friends. I remember that one summer I was about to carry out a scientific project abroad. Not knowing what might lay ahead, I was anxious. While driving me to the airport, in her car Jenn said to me “You will be fine! keep doing what you think is right … Don’t forget to have some fish and chips.” That is Jenn! Always encouraging and cheerful, a friend one can count on.Throughout past twenty years, even though we were in different parts of world or country, we kept in touch. Every holiday season, I’d receive a beautiful card from Jenn. They were always handmade and in Jenn’s handwriting. In the cards, Jenn talked about her new home, her kids and her work, full of love and joy. Two years ago, I had a chance to visit Boulder and met Jenn! It was so good to see her again after many years. We had great time over dinner, talking about friends and families.I cannot believe Jenn has left us! There are only a few people who had made difference in my life. Jenn is one of them. She made me want to be a better person. Jenn will remain as my best friend. She will be deeply missed!
Wes Sundquist [Dr. Wesley Ian Sundquist (born 1959)] (November 25, 2018) Jenn was clearly wonderful in so many of her different roles - mom, family member, friend and colleague. My own perspective on Jenn's amazing character came primarily from our interactions as scientific colleague - it was my great fortune to be her thesis advisor in the department of Biochemistry at the University of Utah from about 1997-2001. It is hard to imagine a better graduate student than Jenn. She was talented, smart, determined, insightful, and helpful to everyone. And she had golden hands in lab. Jenn simply had a gift for planning and performing experiments to produce the best possible data and insights. Our laboratory studies the molecular virology of HIV. Viruses are obligate parasites - their genomes are too small to produce all of the activities that they need to replicate, and so they often usurp host cellular pathways to perform functions that they need. Discovering and characterizing such processes is one of the major goals of our research. While Jenn was a student in our lab, she led a team that discovered that HIV coopts a human cellular pathway called the ESCRT pathway to bud from cells. This was a major discovery that has since been extended to many other viruses and has had a major influence on the research directions of many leading virology labs. The paper that Jenn wrote on the topic (Garrus et al. Cell (2001) 107:55-65) remains by far the most cited paper that our lab has ever written, and it is not an exaggeration to say that her work changed the course of our research. Like so many others, I valued Jenn above all else for her wonderful personal attributes - kindness, strength, curiosity, warmth and generosity - but I also wanted to record that she was a stellar scientist who made important discoveries that most scientists can only hope for. She will be greatly missed.
Kristen Cordova (November 4, 2018)Jenn was an amazing person- thoughtful, kind, generous, modest, positive, loyal, and helpful… all of the qualities that you appreciate in a true friend. She was never mean and listened but never judged; she was always thankful. At her memorial, many people shared that she had helped them through tough times or helped to develop them professionally and I found that to be so very true in both regards. She was always there in the background, ready to help if asked, personally and professionally. We worked together at Biodesix and she was a bright light while I went through a rough time in my life. We used to walk together in the afternoons and talk about our day-to-day duties within the company, but we would also discuss our personal lives and the triumphs of our babies. She would crave Shamane’s bakery while pregnant with Keira and I was more than happy to walk and talk with her! We took our boys to the Butterfly pavilion together and they dug through the worm exhibit and held Rosie the spider while Jenn and I chatted about life. We attended a wedding up near Estes and she said to me, “can you tell I never do anything fancy?!” as she asked me questions about what to wear and what purse to bring! I was the newest scientist hired, but she asked my opinion on scientific things. She was so humble and so gracious. I would like to thank her family for all the light she brought into my life and am sending all of my love to her sweet babies as they grow. She was beautiful inside and out and she will be missed by many people, including me.


"M) 1. 10/17/2018 Jennifer Garrus (45) was stabbed to death by her husband of fifteen years Michael Ellison (46). They had attended divorce proceedings the day before and had been reported be arguing the morning of the murder. Ellison attempted to kill himself after stabbing his wife to death by jumping out of their second story window. He survived but broke his leg. Thornton, Adams County. "

Jan 18, 2004 (Jan 18) - Scence Magazine - " TSG101: An Antiviral Target with a Murky Past / Viruses hijack a host protein that normally sorts the trash "

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Ebola (above) is a killer virus that may commandeer cellular protein-sorting pathways through TSG101.

Viruses can't do much without a host. They propagate by usurping cellular machinery, and much of an infection's misery is due to the immune response. But conventional therapies, without much luck, essentially have targeted one-half of the infection equation: the foreign invader. Now, researchers increasingly are setting their sights on the host's role.

Investigators recently attempted to mitigate the host immune response and the associated collateral damage (see sidebar). Some explore a complementary approach: to cut off access to the cellular pathway that a virus commandeers to mass-produce, specifically, the route used to bud from the cell. Doing so, without impairing the host, could provide a powerful new broad-spectrum antiviral agent. "Conventional antivirals are highly specific, and pathogens can mutate to insensitivity," says Stanley Cohen, professor of genetics and medicine at Stanford University. "But if one can attack host genes required for pathogens to be pathogenic, resistance is less likely. One can affect the pathogenicity of the virus."


Cohen, who with Herbert W. Boyer in the early 1970s essentially founded recombinant DNA technology, says he might have zeroed in on what may become the first such "host-oriented" therapeutic target: Tumor Susceptibility Gene 101. Despite its moniker, TSG101 may have less to do with cancer than first thought, and everything to do with the vacuolar protein-sorting pathway that ferries excess cell-surface receptors to lysosomes, the enzyme-filled sacs that dismantle debris. Certain killer viruses, including HIV, Ebola, and Marburg, hijack this transport system using TSG101 protein to cloak themselves in membranous escape pods. At least three biotech companies are developing drugs to target TSG101, which Cohen dubs "the getaway driver for viral release." But a clinical future awaits clarification of its obfuscated origins as a tumor suppressor.

Discovering TSG101 in 1996 was the first fruit of random homozygous knockout (RHKO) technology, an antisense technique that identifies genes by a particular function, in this case, cellular transformation.1 Dampening TSG101 expression transformed murine 3T3 fibroblasts, which caused metastatic tumors in nude mice. The encoded protein bore the hallmarks of a transcription factor, but the links to carcinogenesis turned out to be indirect.


In 2000, experimental roads converged to flesh out the role of TSG101. Beth Agresta, a graduate student working with molecular geneticist Carol Carter, State University of New York, Stony Brook, was screening for cellular proteins that interact with HIV proteins. "She got several hits and wrote her thesis on one, but continued to check the database to see if there was any more information. One day, there was," recalls Carter. That was TSG101. Carter and Cohen collaborated to get at protein function.

Soon, another graduate student in Carter's group, Lynn Ver-Plank, identified the major viral core protein Gag as HIV's binding site for TSG101.2 Gag lets mature viruses bud from cells. At about the same time, Jennifer Garrus, a graduate student with biochemist [Dr. Wesley Ian Sundquist (born 1959)], University of Utah School of Medicine, Salt Lake City, blocked TSG101 with small interfering RNA, halting HIV budding. When she restored gene function, budding resumed.3

Gag and TSG101 attach by ubiquitin tags, and the host protein then escorts the viral emissary into the vacuolar protein-sorting pathway. But instead of being carted away to digestive doom in the lysosome, Gag proteins attach by their bound TSG101s to bits of cell membrane, ultimately becoming packaged into mature virions.

Yeast provided another connection. Also in 2000, University of Utah biologist Markus Babst and Scott Emr, a Howard Hughes Medical Institute investigator at the University of California, San Diego, found that TSG101 has a yeast counterpart, Vps23.4 Vps23/TSG101 is a subunit of a complex, called ESCRT-I, which binds and sorts ubiquitin-tagged molecules. They tested Cohen's TSG101 mutant cell line for protein transport defects and found trafficking phenotypes, says Babst.

The solid link to intracellular protein transport may explain the dual role of TSG101 in carcinogenesis and viral infection. The pathway normally recycles cell-surface receptors, including growth-factor receptors. Silence TSG101, and these receptors aren't sent to the lysosomal garbage dumps; instead they accumulate at the cell surface like uncollected trash. There, the receptors transduce too many signals to divide, and runaway mitosis results.

But the cancer connection still is not as clear as some researchers would like. "The role of TSG101 in cancer has been quite elusive," says [Dr. Wesley Ian Sundquist (born 1959)], citing a retracted report on TSG101 mutations in cancer patients.5 And Kay-Uwe Wagner, at the Eppley Institute for Research in Cancer and Allied Diseases at the University of Nebraska Medical Center, Omaha, used knockout mice to show that TSG101 is essential for embryo implantation but not tumor suppression.6 She also reexamined the original 1996 tumorigenic cell line and found "whopping levels" of TSG101.7 She blames Cohen's use of an immortal cell line. "Nobody was able to repeat these transformation studies in other cell lines," she says.


Still, Cohen maintains that TSG101 makes a good antiviral target. He and former postdoctoral researcher Limin Li cofounded the company Functional Genetics, which is developing a viral budding inhibitor based on TSG101's action.

But the jump from promising target in cell culture to antiviral development will not be easy. Such a drug probably would block normal ESCRT function as well, says Babst. "This could result in a tumorigenic phenotype." Effects could be wide-ranging. "I'm worried about the potential that a TSG101 inhibitor would exhibit general cytotoxicity," suggests Sundquist, who also works with Myriad Pharmaceuticals in Salt Lake City.

Even if TSG101 never overcomes its tainted beginnings, it may still pioneer host-oriented therapeutics, for there may be unknown aspects of the viral subversion of TSG101 to exploit. Concludes Carter: "That's what one goes after – to understand the process, what the virus does to divert the machinery – and target that."

Ricki Lewis rickilewis@nasw.org is a freelance writer in Scotia, NY.

Fight the Flu, Ignore the Bug

At the start of this year's particularly worrisome flu sea-son, researchers at London Imperial college in the United Kingdom posed a comforting thought. Suppose the bug's nasty symptoms could be avoided without vaccination or antiviral drugs by targeting the immune responses responsible for influenza's misery. Their tests on mice showed positive results, they say. Maybe so, say the skeptics, but that doesn't prove how humans would respond.

The Imperial College researchers have found that a receptor molecule called OX40 is overexpressed in T cells responding to a viral infection, but not in the remaining T-cell population.1 The receptor can be blocked using an OX40-immunoglobulin fusion protein called OX40:Ig. This, the researchers say, should temper overzealous immune responses in the lungs.

Tracy Hussell and colleagues, who tested the drug on mice injected with influenza type A, found that clinical symptoms such as congestion and high body temperature were virtually eliminated. Hussell says there's no reason why the treatment could not be extended to humans, after symptoms have emerged. "Mice could show signs of illness for three days, and as soon as you administer this reagent, it stops clinical symptoms in their tracks."

In the future, humans could experience similar remission of symptoms, according to Alan Hay, director of the WHO Collaborating Centre for Reference and Research on Influenza at the UK National Institute for Medical Research. "It's interesting work, but it's early stages and needs further development," says Hay.

Brad Magor, assistant professor, Department of Biological Sciences (Immunogenetics), University of Alberta, is more dubious. "Mice are not natural hosts to influenza A, so their response to the pathogen is less likely to reflect that of a natural host such as a chicken, swine, or human." Magor says he's concerned that the body might permanently lose influenza-specific memory cells as a result of the treatment. He conceded, however, that blocking OX40 molecules showed significant promise for modulating immunity and inducing tolerance to engrafted organs.

Hussell says the group is focusing on the influenza treatment for now and is applying to the UK Medical Research Council and the Wellcome Trust for funding to begin human clinical trials. The Imperial College group collaborates with Xenova, a UK-based biotech that explores various therapeutic uses of OX40, including autoimmune disease and cancer.


The end of HIV-1 budding machinery

HIV-1 reprograms the cellular machinery and employs several unknown host proteins to bud from infected cells. In 5 October Cell, Jennifer Garrus and colleagues from University of Utah School of Medicine and Myriad Genetics, Salt Lake City show that the human tumor susceptibility gene 101 (Tsg101), which functions in vacuolar protein sorting (Vps) pathway, is critical to HIV-1 budding and the progression of the disease into full-blown AIDS.Garrus et al. used small interfering RNA to stop producti

Tudor Toma(t.toma@ic.ac.uk)

Oct 7, 2001

HIV-1 reprograms the cellular machinery and employs several unknown host proteins to bud from infected cells. In 5 October Cell, Jennifer Garrus and colleagues from University of Utah School of Medicine and Myriad Genetics, Salt Lake City show that the human tumor susceptibility gene 101 (Tsg101), which functions in vacuolar protein sorting (Vps) pathway, is critical to HIV-1 budding and the progression of the disease into full-blown AIDS.

Garrus et al. used small interfering RNA to stop production of Tsg101 in HIV infected human embryonic kidney cells lines. They found that Tsg101 depletion stopped HIV-1 replication at a late stage of the budding process. When they re-introduced Tsg101 in these cells, HIV-1 budding resumed. In addition, they showed that dominant negative mutant Vps4 proteins that inhibit vacuolar protein sorting also arrest HIV-1 budding (Cell 2001, 107:55-65).

New AIDS drugs that inactivate the Tsg101 protein may limit the amount of HIV virus in people who are infected. "This would be a whole new class of anti-HIV drugs," said Kenton Zavitz, a biochemist at Myriad who participated in the study.

oct 16 2016


ournal of Thoracic Oncology. 11(10):1736–1744, OCTOBER 2016

DOI: 10.1016/j.jtho.2016.05.038


PMID: 27448761

Issn Print: 1556-0864

Publication Date: October 2016

A Randomized Phase 2 Study Comparing the Combination of Ficlatuzumab and Gefitinib with Gefitinib Alone in Asian Patients with Advanced Stage Pulmonary Adenocarcinoma

Tony Mok;Sarayut Geater;Wu-Chou Su;Eng-Huat Tan;James Yang;Gee-Chen Chang;May Han;Philip Komarnitsky;Francis Payumo;Jennifer Garrus;Sandra Close;Keunchil Park;

+ Author Information

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Introduction:A randomized phase 2 study was designed to compare the combination of ficlatuzumab (AV-299), a humanized hepatocyte growth factor–neutralizing monoclonal antibody, plus gefitinib versus gefitinib monotherapy in a pulmonary adenocarcinoma population clinically enriched for EFGR tyrosine kinase inhibitor–sensitizing mutations.Methods:A total of 188 patients were randomized 1:1 to receive either gefitinib or ficlatuzumab plus gefitinib treatment. Patients who demonstrated disease control in the single-agent gefitinib arm were allowed to cross over to ficlatuzumab plus gefitinib treatment upon disease progression. Molecular analyses included tumor EGFR mutation status and retrospective proteomic testing using VeriStrat, a multivariate test based on mass spectrometry.Results:The addition of ficlatuzumab to gefitinib did not provide significant improvement over gefitinib monotherapy for the primary end point of overall response rate or the secondary end points of progression-free survival and overall survival. In the subgroup classified as VeriStrat poor, the addition of ficlatuzumab to gefitinib showed significant improvement in both progression-free survival and overall survival in both the intent-to-treat population and the subgroup with EGFR tyrosine kinase inhibitor–sensitizing mutations. For all patients, the most frequent adverse events were diarrhea, dermatitis acneiform, and paronychia.Conclusions:Although the trial showed no significant benefit from the addition of ficlatuzumab to gefitinib in the overall population of Asian patients with advanced-stage pulmonary adenocarcinoma, the biomarker data suggest that patients classified as VeriStrat poor may benefit from ficlatuzumab combination therapy.

HIV Gag mimics the Tsg101-recruiting activity of the human Hrs protein.

Pornillos O,

Higginson DS,

Stray KM,

Fisher RD,

Garrus JE,

Payne M,

He GP,

Wang HE,

Morham SG,

[Dr. Wesley Ian Sundquist (born 1959)]

Author information

The Journal of Cell Biology, 31 Jul 2003, 162(3):425-434

DOI: 10.1083/jcb.200302138 PMID: 12900394 PMCID: PMC2172688

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The HIV-1 Gag protein recruits the cellular factor Tsg101 to facilitate the final stages of virus budding. A conserved P(S/T)AP tetrapeptide motif within Gag (the "late domain") binds directly to the NH2-terminal ubiquitin E2 variant (UEV) domain of Tsg101. In the cell, Tsg101 is required for biogenesis of vesicles that bud into the lumen of late endosomal compartments called multivesicular bodies (MVBs). However, the mechanism by which Tsg101 is recruited from the cytoplasm onto the endosomal membrane has not been known. Now, we report that Tsg101 binds the COOH-terminal region of the endosomal protein hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs; residues 222-777). This interaction is mediated, in part, by binding of the Tsg101 UEV domain to the Hrs 348PSAP351 motif. Importantly, Hrs222-777 can recruit Tsg101 and rescue the budding of virus-like Gag particles that are missing native late domains. These observations indicate that Hrs normally functions to recruit Tsg101 to the endosomal membrane. HIV-1 Gag apparently mimics this Hrs activity, and thereby usurps Tsg101 and other components of the MVB vesicle fission machinery to facilitate viral budding.

HIV Gag mimics the Tsg101-recruiting activity of the human Hrs protein

Owen Pornillos,1 Daniel S. Higginson,1 Kirsten M. Stray,1 Robert D. Fisher,1 Jennifer E. Garrus,1 Marielle Payne,1 Gong-Ping He,2 Hubert E. Wang,2 Scott G. Morham,2 and [Dr. Wesley Ian Sundquist (born 1959)]1

Author information Article notes Copyright and License information

This article has been cited by other articles in PMC.


The HIV-1 Gag protein recruits the cellular factor Tsg101 to facilitate the final stages of virus budding. A conserved P(S/T)AP tetrapeptide motif within Gag (the “late domain”) binds directly to the NH2-terminal ubiquitin E2 variant (UEV) domain of Tsg101. In the cell, Tsg101 is required for biogenesis of vesicles that bud into the lumen of late endosomal compartments called multivesicular bodies (MVBs). However, the mechanism by which Tsg101 is recruited from the cytoplasm onto the endosomal membrane has not been known. Now, we report that Tsg101 binds the COOH-terminal region of the endosomal protein hepatocyte growth factor–regulated tyrosine kinase substrate (Hrs; residues 222–777). This interaction is mediated, in part, by binding of the Tsg101 UEV domain to the Hrs 348PSAP351 motif. Importantly, Hrs222–777 can recruit Tsg101 and rescue the budding of virus-like Gag particles that are missing native late domains. These observations indicate that Hrs normally functions to recruit Tsg101 to the endosomal membrane. HIV-1 Gag apparently mimics this Hrs activity, and thereby usurps Tsg101 and other components of the MVB vesicle fission machinery to facilitate viral budding.

Keywords: virus budding; virions; ubiquitin; vacuolar protein sorting; multivesicular body


The HIV Gag protein orchestrates viral assembly and budding, and forms the structural shell of the immature virus (for review see Göttlinger, 2001). Even in the absence of any other viral proteins, HIV-1 Gag can form extracellular virus-like particles (VLPs) that resemble authentic HIV virions. Efficient release of HIV-1 virions and Gag VLPs from most cell types requires the presence of a “late domain” located in the COOH-terminal Gag p6 region (Göttlinger et al., 1991; Huang et al., 1995; Demirov et al., 2002b). All HIV-1 strains contain the late domain tetrapeptide motif P(S/T)AP (where the second position can be either Ser or Thr; Fig. 1), which is a docking site for the cellular protein, tumor susceptibility gene 101 (Tsg101; for review see Pornillos et al., 2002c). Tsg101 appears to facilitate viral budding by recruiting additional cellular factors that can catalyze release of the enveloped virion. In addition to the P(S/T)AP sequence found in HIV-1 Gag, distinct late domain sequences have also been identified and characterized in several other enveloped RNA viruses. The best characterized of these is the PPXY motif (where X is any amino acid), which binds the Nedd4 protein family of ubiquitin E3 ligases (Xiang et al., 1996; Harty et al., 1999, 2001; Strack et al., 2000; Kikonyogo et al., 2001; Yasuda et al., 2002; Timmins et al., 2003).


J Biol Chem. 2004 Aug 20;279(34):36059-71. Epub 2004 Jun 23.

The human endosomal sorting complex required for transport (ESCRT-I) and its role in HIV-1 budding.

Stuchell MD1, Garrus JE, Müller B, Stray KM, Ghaffarian S, McKinnon R, Kräusslich HG, Morham SG, [Dr. Wesley Ian Sundquist (born 1959)]


Department of Biochemistry, University of Utah, Salt Lake City, Utah 84132-3201, USA.


Efficient human immunodeficiency virus type 1 (HIV-1) budding requires an interaction between the PTAP late domain in the viral p6(Gag) protein and the cellular protein TSG101. In yeast, Vps23p/TSG101 binds both Vps28p and Vps37p to form the soluble ESCRT-I complex, which functions in sorting ubiquitylated protein cargoes into multivesicular bodies. Human cells also contain ESCRT-I, but the VPS37 component(s) have not been identified. Bioinformatics and yeast two-hybrid screening methods were therefore used to identify four novel human proteins (VPS37A-D) that share weak but significant sequence similarity with yeast Vps37p and to demonstrate that VPS37A and VPS37B bind TSG101. Detailed studies produced four lines of evidence that human VPS37B is a Vps37p ortholog. 1) TSG101 bound to several different sites on VPS37B, including a putative coiled-coil region and a PTAP motif. 2) TSG101 and VPS28 co-immunoprecipitated with VPS37B-FLAG, and the three proteins comigrated together in soluble complexes of the correct size for human ESCRT-I ( approximately 350 kDa). 3) Like TGS101, VPS37B became trapped on aberrant endosomal compartments in the presence of VPS4A proteins lacking ATPase activity. 4) Finally, VPS37B could recruit TSG101/ESCRT-I activity and thereby rescue the budding of both mutant Gag particles and HIV-1 viruses lacking native late domains. Further studies of ESCRT-I revealed that TSG101 mutations that inhibited PTAP or VPS28 binding blocked HIV-1 budding. Taken together, these experiments define new components of the human ESCRT-I complex and characterize several TSG101 protein/protein interactions required for HIV-1 budding and infectivity.





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Michael Arthur Ellison

2018 (Oct 17) - Legal notice from District Attorney - "Thornton Man Charged with First-degree Murder in Stabbing Death of his Wife "

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17th Judicial District Attorney Dave Young announced Wednesday that Michael Arthur Ellison has been charged with first-degree murder after deliberation in the stabbing death of his wife in Thornton.

Thornton police found Jennifer Ellison, 45, dead at the couple’s home at 13154 Uinta Street in Thornton on October 17 after receiving a 911 call from Michael Ellison.

Ellison (DOB 02/25/72) was advised of the charges Wednesday in Adams County District Court. A preliminary hearing is set for December 31 in Division E of Adams County District Court.

The filing of a criminal charge is merely a formal accusation that an individual committed a crime under Colorado Laws. A defendant is presumed innocent until and unless proven guilty.

Michael Ellison - LinkedIn ( Apri 2020 )

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Research Scientist


Results-oriented scientist with 15 years of experience in lab management, design and execution of experiments and publication. Track record of leading laboratory personnel in multiple projects. Known for independent hypothesis creation and testing. An effective communicator with a broad knowledge base.

• Molecular Biology

• Biochemistry

• Cell Biology

• Scientific leadership

• Publication of peer reviewed studies


  • University of Colorado Denver - Senior Research Associate

    • Dates Employed 2013 – Present (7 yrs)

    • Location Aurora Colorado

    • Characterization of neutrophils from individuals treated with interferon gamma or cannabis

    • Analysis of neutrophils from patients with immune deficiency

    • Guidance, training and leadership for medical fellows and junior lab personnel

    • Preparation and submission of scientific manuscripts

    • Clinical study design

    • Development and use of myeloid cell function assays

    • Coordination of a bioinformatics group and a genomics core facility to measure drug induced changes in mRNA profiles in myeloid cells

    • Design/use of colorimetric, luminescent and fluorescent-96 well assays

    • Review of microarray data to derive biological insights

    • Correlation of mRNA and protein expression changes

  • Bonfills Blood Center - Post Doctoral Fellow

    • Dates Employed 2008 – 2013 ( 5 years )

    • Location Denver Colorado

    • Characterization of the role of peroxiredoxin 6 (Prdx6) in modulating the oxidative burst of neutrophils.

    • Analysis of neutrophils from patients with immune deficiency

    • Genetic manipulation of model cell lines to achieve depletion of Prdx6

    • Re-expression of wild type and mutant Prdx6 in knockdown cell lines

    • Luminescence and colorimetric based assays of oxidase activity

    • Over-expression and purification of wild type and mutant Prdx6

    • In vitro enzyme assays to characterize recombinant Prdx6 molecules

    • Training of undergraduate summer rotation students

    • Preparation and submission of scientific manuscripts

  • University of Utah - Postdoctoral Associate

    • Dates Employed 2002 – 2007

    • Characterization of novel peptide inhibitors of nicotinic acetylcholine receptors (nAChRs)

    • Lecturer, undergraduate biochemistry

    • RT-PCR, PCR and RACE-based discovery of novel toxin genes from marine snails

    • Chemical preparation of synthetic peptide toxins

    • Xenopus oocyte two electrode voltage clamp to characterize receptor-subtype-specificity of peptide toxins

    • Characterization of receptor-toxin interactions by mutagenesis.

    • Writing and submitting manuscripts and addressing reviewer comments

    • Supervision and training of junior laboratory personnel

  • University of Utah - Graduate student

    • Dates Employed 1998 – 2001 (3 years )

    • Location Greater Salt Lake City Area

    • Graduate Student: University of Utah Biology Department, Salt Lake City

      • Thesis Project: Natural and combinatorial peptide toxins

      • Discovery of a novel, non-competitive peptide antagonist of the alpha7 nAChR

      • Cloning toxin genes from marine snails

      • Use of multiple techniques in molecular biology, cell biology and biochemistry including PCR, mutagenesis, subcloning, mammalian cell culture, transient transfections, cDNA preparation, RACE, reverse phase HPLC (analytical and preparative) and radio-ligand binding assays

  • Teaching assistant, undergraduate Biochemistry


  • University of Utah - Degree Name Doctor of Philosophy - PhD - Field Of Study Biochemistry and Molecular Biology - Dates attended or expected graduation 1996 – 2001

  • University of Bath - Degree Name Bachelor of Science - BS - Field Of Study Biochemistry - Dates attended or expected graduation 1991 – 1995

MyLife - Profile as of April 2020

PDF at [HL003U][GDrive] / Image at [HL003V][GDrive]

Summary: Michael Ellison's birthday is 07/25/1972 and is 47 years old. Previously city included Salt Lake City UT. Michael Arthur Ellison and Michael A Ellison are some of the alias or nicknames that Michael has used. We have lots of information about Michael: religious views are listed as Christian, ethnicity is Caucasian, and political affiliation is currently a registered Republican. Michael's relationship status is married. Alyssa Hoffman, Abigail Struska, Brandon Shaver, Nicholas Hoffman and Haylie Weston, and many others are family members and associates of Michael. Michael's reported annual income is about $70 - 79,999; with a net worth that tops $100,000 - $249,999. Read Full Summary

ARRREST ? ( 2018-11-01 03:57:52 )

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Arrest Report Overview: Michael Ellison

First Name: MICHAEL

Last Name: ELLISON

Gender: Male

Arrest Date: 2018-11-01 03:57:52

Age: 46

State: Colorado

County: Adams

Dob: 1972-07-25 00:00:00

Booking Date: 2018-11-01 15:57:52

Birth Year: 1972

Home sale

Home was sold in Jan 2020 - See Zillow - [HW002O][GDrive] - see below -