Jessica L. Kelliher
Researcher
Also affiliated: University of Illinois Urbana-Champaign (2016–2020); Fred Hutch Cancer Center (2019); Cancer Research Center (2019)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Research by Jessica L. Kelliher focuses on understanding molecular mechanisms underlying cellular processes, particularly those related to DNA repair and T cell function. Her work has investigated the roles of specific proteins, such as RNF168 and UBA80, in regulating histone ubiquitination and DNA repair pathways. Kelliher has also explored how metabolic factors influence T cell activity, examining the role of PCK2 in supporting T cell effector functions in challenging environments and its potential manipulation to enhance immunotherapy responses. Her publications demonstrate a focus on proteomic analysis and the dynamics of protein turnover to identify key regulators in cellular processes like T cell exhaustion and persistence. Kelliher's research network includes extensive collaborations with colleagues at the University of Arkansas for Medical Sciences, with whom she shares multiple publications.
Metrics
- h-index: 8
- Publications: 13
- Citations: 729
Selected Publications
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762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments (2025)
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236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response (2025)
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277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion (2025)
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392 Donor-intrinsic proteomic programs shape CAR-T cell persistence across a longitudinal killing assay (2025)
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Comprehensive Analysis of Proteome Turnover Dynamics During T Cell Exhaustion (2025)
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376 Inhibition of GSK3β-mediated 53BP1 T334 phosphorylation in T cells enhances infiltration and cytotoxicity against head and neck squamous cell carcinoma (2024)
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319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion (2024)
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929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells (2024)
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932 Defining the role for PCK2 in T-cell metabolic plasticity (2024)
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Evolved histone tail regulates 53BP1 recruitment at damaged chromatin (2024)
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1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response (2023)
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304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors (2023)
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1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma (2023)
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UBA80 and UBA52 fine-tune RNF168-dependent histone ubiquitination and DNA repair (2023)
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New answers to the old RIDDLE: RNF168 and the DNA damage response pathway (2021)
Collaboration Network
Top Collaborators
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin
- 1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
Showing 5 of 13 shared publications
- 1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
Showing 5 of 11 shared publications
- 1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
Showing 5 of 10 shared publications
- 1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
Showing 5 of 10 shared publications
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
Showing 5 of 6 shared publications
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- Comprehensive Analysis of Proteome Turnover Dynamics During T Cell Exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- Comprehensive Analysis of Proteome Turnover Dynamics During T Cell Exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- New answers to the old RIDDLE: RNF168 and the DNA damage response pathway
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin
- UBA80 and UBA52 fine-tune RNF168-dependent histone ubiquitination and DNA repair
- 1020 Proteomic analysis of T cell exhaustion unveils differential modulation of the DNA damage response
- 1211 Defining the role of PCK2 in T cell metabolic plasticity in Glioblastoma
- 932 Defining the role for PCK2 in T-cell metabolic plasticity
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- 304 Discovering T cell proteome turnover dynamics to enhance persistence in solid tumors
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- 319 Comprehensive analysis of proteome turnover dynamics during T cell exhaustion
- Comprehensive Analysis of Proteome Turnover Dynamics During T Cell Exhaustion
- 277 Proteome turnover dynamics analysis uncovers E3 ligases that enhance T-cell persistence during exhaustion
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin
- UBA80 and UBA52 fine-tune RNF168-dependent histone ubiquitination and DNA repair
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